Tesi: "Kidney glomerulus Diseases"

1

Wang, Yang. "Murine adriamycin-induced nephropathy : the roles of cell-mediated immunity and CD4+ T-lymphocytes." Thesis, The University of Sydney, 2000. https://hdl.handle.net/2123/27827.

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2

Leung, Chi-kam Joseph, and 梁志錦. "The pathogenesis of IgA nephropathy: the roleof IgA molecule and the nature of IgA receptors." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B29744908.

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3

Wootton, Andrew. "The glomerular basement membrane and nephritis /." Title page, contents and abstract only, 1985. http://web4.library.adelaide.edu.au/theses/09PH/09phw918.pdf.

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4

Cavaglieri, Rita de Cássia. "Terapia com células tronco derivadas do líquido amniótico humano na nefropatia crônica experimental: é possível bloquear a progresso da doença renal estabelecida?" Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/5/5148/tde-09052018-101720/.

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Abstract (sommario):

Células tronco mesenquimais (CTm) apresentam potencial para tratamento da doença renal pela possibilidade de promover regeneração tecidual e recuperação funcional, possivelmente por seus efeitos parácrinos. Na última década, o líquido amniótico foi descrito como uma fonte promissora de extração e isolamento de CTm. Alguns estudos mostraram o efeito renoprotetor das CTm derivadas do líquido amniótico (CTmLA) na doença renal aguda e crônica, quando inoculadas precocemente. Entretanto, ainda não foi estudado o efeito da administração de CTmLA em modelo experimental de doença renal crônica (DRC) com a lesão já estabelecida, situação esta que reproduz melhor a apresentação clínica da doença nos pacientes. Assim, o objetivo do presente estudo foi analisar o efeito da inoculação de CTmLA na região subcapsular renal no modelo de DRC já estabelecido. As CTmLA foram obtidas de pacientes no segundo trimestre de gestação e isoladas através da sua capacidade de aderência ao plástico. A caracterização das CTm foi feita por citometria de fluxo e pela diferenciação celular in vitro. O modelo de DRC utilizado foi o de nefrectomia 5/6 (Nx) que, pela perda de massa renal, evolui com hipertensão arterial, proteinúria, glomeruloesclerose, fibrose intersticial e perda progressiva da função renal. Quinze dias após a indução do modelo, estas alterações já são marcantes e agravam-se com 30 dias. Foram realizados 2 protocolos experimentais: no protocolo I, os animais Nx com DRC estabelecida receberam dose única de CTmLA (5x105) na região subcapsular renal e foram acompanhados por 30 e 60 dias de experimento. No protocolo II, os animais Nx com DRC estabelecida receberam duas doses de CTmLA (5x105) na região subcapsular renal, no 15° e 30° dia após a nefrectomia 5/6, e foram acompanhados por 30 dias, totalizando 60 dias de experimento. Os animais foram subdivididos nos grupos: Sham, ratos submetidos à cirurgia fictícia; Sham+CTmLA, ratos submetidos à Sham que receberam CTmLA; Nx, ratos submetidos à nefrectomia 5/6; Nx+CTmLA, ratos Nx que receberam CTmLA. Para verificar a localização das CTmLA no tecido renal foi realizada a hibridização in situ para cromossomo XY. Foram realizadas análises dos parâmetros clínicos e laboratoriais, além de análise histológica, imunohistoquímica, PCR em tempo real e multiplex. Resultados: as CTmLA cultivadas mostraram grande capacidade de aderência, crescimento em colônia e de diferenciação em células osteogênicas, adipogênicas e condrogênicas. A análise por citometria mostrou-se positiva para CD29, CD44, CD90 e CD105, com uma pequena população de células de CD14, CD34, CD45 e CD117, confirmando a presença preponderante de CTm. Protocolo I: Após 30 dias, a inoculação de CTmLA, dose única, preveniu a elevação da pressão arterial, da proteinúria, da glomeruloesclerose, recuperando a expressão dos marcadores de podócitos, WT-1 e sinaptopodina. Entretanto, não houve efeito benéfico nos níveis de creatinina sérica e na fibrose intersticial, após 30 e 60 dias. O tratamento com CTmLA promoveu uma diminuição marcante do número de macrófagos e uma discreta queda dos leucócitos no infiltrado inflamatório renal, além da diminuição do número de miofibroblastos no interstício renal. Citocinas pró-inflamatórias foram encontradas em menor concentração no tecido renal dos animais que receberam CTmLA (IL-1beta, TNF-alfa, MCP-1 e RANTES). Não houve alteração significativa das citocinas Th1 e Th2, exceto por um aumento da IL-4 nos animais tratados com CTmLA. Os animais que foram acompanhados por 60 dias tiveram uma melhora da proteinúria, da glomeruloesclerose, diminuição do infiltrado de macrófagos e uma melhora da expressão de WT-1. Não foram observadas diferenças estatísticas nos parâmetros de creatinina sérica e fibrose intersticial, aos 30 e 60 dias. Protocolo II: Nos animais que receberam a segunda dose de CTmLA e foram acompanhados por 60 dias observou-se prevenção da elevação da pressão arterial e da proteinúria, além de uma marcante diminuição da fibrose intersticial. Em conclusão, o presente estudo mostrou, pela primeira vez, que a terapia com CTmLA foi capaz de induzir renoproteção nos animais com doença renal crônica estabelecida. O tratamento com CTmLA pode representar uma nova abordagem terapêutica bloqueando a progressão da doença renal crônica Mesenchymal stem cells (mSC) represent therapeutic potential for the treatment of renal diseases, due to their ability to induce tissue regeneration and functional recovery. Human amniotic fluid stem cells (AFmSC) are a class of fetal, pluripotent stem cells, which present characteristics intermediate between embryonic and adult stem cells. These cells are characterized by the expression of mesenchymal stem cells markers. In addition, they have the ability to differentiate into lineages of all embryonic germ layers. They also show high proliferative rates, but do not induce tumor formation. Therefore, AFmSC are considered to be a very promising cell source and these characteristics have generated a great interest concerning their potential renoprotective effects. The aim of this study was to analyze the effects of AFmSC in an experimental model of chronic kidney disease, the 5/6 nephrectomy model (Nx), after the disease has been established, in order to more closely resemble the clinical settings in humans. AFmSC derived from second-trimester amniocentesis were isolated by plastic adhesion. After 4-7 passages, AFmSC characteristics were confirmed by flow cytometry and by their ability to differentiate into osteogenic, adipogenic and chondrogenic lineages. Two experimental protocols were performed: In protocol I, rats underwent 5/6 nephrectomy (Nx) or sham surgery at day 0, received at day 15 a single dose of hAFmSC (5x105 cells) injected under the renal capsule and were studied at day 30 and 60 days. In protocol II, rats underwent Nx or sham surgery, and received at days 15 and 30, two doses of hAFmSC (5x105 cells) injected under the renal capsule, and were studied at day 60. In both protocols, the animals were subdivided into four groups: Sham, rats submitted to fictitious surgery; Sham+hAFmSC, Sham rats that received hAFmSC; Nx, rats submitted to nephrectomy 5/6; Nx+hAFmSC, Nx rats receiving hAFmSC. The hAFmSC were followed in the renal tissue by in situ hybridization for XY chromosome. In all the groups, clinical and histological parameters were analyzed by immunohistochemistry and real-time PCR. Results: AFmSC cultivated demonstrated an ability to adhere to plastic, to grow in colonies and to differentiate in osteogenic, adipogenic and chondrogenic cells. Quantitative analysis of cell markers by flow cytometry showed that isolated cells were positive for CD29, CD44, CD90 and CD105, with a small population of cells positive for CD14, CD34, CD45 and CD117, confirming a preponderant presence of mSC. Protocol I: After 30 days, the single dose of hAFmSC significantly reduced the blood pressure levels, proteinuria, glomerulosclerosis and improved the expression of podocytes markers, WT-1 and synaptopodin. A marked decrease on the number of macrophages and a discrete decrease of leucocyte infiltration, as well as a reduction of interstitial myofibroblasts was observed. Treatment with hAFmSC significantly reduced some proinflammatory cytokines (IL1beta, TNF-alpha, MCP-1 and RANTES). No significant difference in Th1 or Th2 cytokines was observed, except for IL-4 increase in Nx rats treated with hAFmSC. At 60 days of follow-up, Nx rats treated with hAFmSC presented reduced proteinuria, glomerulosclerosis and macrophages besides increase in WT-1 expression. No improvements were observed on serum creatinine and of interstitial fibrosis, after 30 and 60 days. Protocol II: Inoculation of two doses of hAFmSC in Nx rats improved blood pressure levels, proteinuria and interstitial fibrosis at day 60. In conclusion, the present study demonstrated, for the first time, that hAFmSC induced renoprotection in animals with established chronic kidney disease. Treatment with hAFmSC may represent a novel therapeutic approach for blocking the progression of chronic kidney disease

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5

Brittain, Alison Louise. "Growth Hormone (GH) and the Glomerular Podocyte." Ohio University / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1554208861914841.

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6

Sousa, Mauri Félix de. ""Efeitos renais da haploinsuficiência do gene Pkd1 (Polycystic kidney disease 1) em camundongos"." Universidade de São Paulo, 2005. http://www.teses.usp.br/teses/disponiveis/5/5148/tde-21122005-163447/.

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Vários estudos mostram que na doença renal policística autossômica dominante os cistos surgem a partir de um mecanismo de "dois-golpes". A patogênese das manifestações não-císticas, contudo, é pouco compreendida. Neste estudo usamos uma linhagem de camundongos endogâmica com uma mutação nula em Pkd1, onde animais heterozigotos apresentam formação cística renal mínima até 40 semanas de idade. O clearance de inulina e o número de glomérulos foram menores em machos Pkd1+/- que Pkd1+/+, enquanto o volume glomerular médio foi maior em heterozigotos. A excreção urinária de NO2/NO3 não diferiu significantemente entre os dois grupos. Avaliamos a osmolalidade urinária máxima em machos e fêmeas Pkd1+/- and Pkd1+/+, porém não foi detectada diferença significante entre os grupos heterozigoto e selvagem. Nossos resultados oferecem evidência direta de que a haploinsuficiência de Pkd1 resulta em anormalidades anatômicas e funcionais renais e sugerem que o estado haploinsuficiente de Pkd1 possa resultar na redução do número de néfrons por diminuir a ramificação tubular renal durante a nefrogênese Several studies show that in autosomal dominant polycystic kidney disease cysts arise through a "two-hit" mechanism. The pathogenesis of non-cystic features, however, is poorly understood. In this study we used an inbred mouse line with a null mutation of Pkd1, where heterozygotes had minimal renal cyst formation up to 40 weeks of age. Inulin clearance and the number of glomeruli were lower in Pkd1+/- than in Pkd1+/+ males, while a higher average glomerular volume was observed in heterozygotes. The urinary excretion of NO2/NO3 did not significantly differ between the two groups. Maximal urinary osmolality was evaluated in Pkd1+/- and Pkd1+/+ males and females, but no significant difference was detected between the heterozygous and the wild type groups. Our results provide direct evidence that haploinsufficiency for Pkd1 results in anatomic and functional abnormalities of the kidney and suggest that Pkd1 haploinsufficiency may result in a reduced number of nephrons by diminishing renal tubule branching during nephrogenesis

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7

Baboolal, Keshwar. "The renin angiotensin system in experimental renal disease." Thesis, King's College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.336469.

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8

Randles, Michael. "Proteomic analyses of kidney glomerular extracellular matrix in health and disease." Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/proteomic-analyses-of-kidney-glomerular-extracellular-matrix-in-health-and-disease(a39fe408-db06-4d80-b97b-4e0651bf7bc3).html.

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Glomerular filtration is a vital physiological process removing waste products from the circulation and this process occurs across the glomerular filtration barrier (GFB). The cells and extracellular matrix (ECM), which form this barrier, are exposed to forces during ultrafiltration and special adaptation is required to withstand these forces. Dysfunction in cellular adhesion machinery or ECM assembly within the GFB causes loss of selective glomerular filtration, however, the mechanisms governing these processes are poorly understood. To this end we sought to characterise the glomerular ECM and adhesion machinery using high throughput mass spectrometry (MS)-based proteomics. MS of human glomerular ECM identified a highly complex extracellular niche, revealing the potential involvement of novel ECM proteins in glomerular development and disease processes. Furthermore we identified that glomerular cells in culture had distinct ECM proteomes and interestingly, coculture experiments demonstrated that the ECM proteome was influenced by cellular crosstalk and had a closer resemblance to glomerular ECM in vivo. Protein network analyses of in vivo and in vitro ECM datasets revealed a common core of highly connected structural ECM proteins that may be important for glomerular ECM assembly. To understand how this ECM proteome altered in disease, we studied mice with mild glomerular dysfunction. Here, transcriptomic and proteomic analyses identified alterations in ECM composition and 3D electron microscopy revealed striking ultrastructural changes in glomerular ECM. MS-based proteomics was next applied to the analysis of glomerular podocyte adhesion complexes, leading to the discovery that the actin cytoskeletal regulators and trafficking machinery are recruited to adhesions sites in an ECM-ligand dependent manner. Furthermore, these differences functionally altered cell shape and adhesion strength. These same analyses were applied to podocyte cell-cell junctions, revealing an unexpected overlap of cell-ECM and cell-cell adhesion machinery. Overall, these findings demonstrate for the first time the complexity of the glomerular ECM and adhesion signalling complexes and reinforce the benefits of global, unbiased experimental approaches. In addition the results suggest that glomerular ECM composition, organisation and adhesion signalling are context dependent, and therefore, represent potential therapeutic targets.

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9

Sheerin, Neil Stephen. "Complement in the pathogenesis of immune mediated glomerular injury." Thesis, King's College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.313287.

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10

Stitt, Erin Maureen. "The Role of Podocyte Prostaglandin E2 and Angiotensin II Receptors in Glomerular Disease." Thesis, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/19800.

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The incidence of chronic kidney disease (CKD) is increasing. CKD is characterized by a gradual decrease in renal function leading to end stage renal disease (ESRD). Damage to the glomerular podocytes, is one of the first hallmarks of CKD. We hypothesized that podocyte prostaglandin E2 (PGE2) receptors contribute to the progression of glomerular injury in models of CKD. To test this hypothesis, transgenic mice were generated with either podocyte-specific overexpression or deletion of the PGE2 EP4 receptor (EP4pod+and EP4pod-/- respectively). Mice were next tested in the 5/6 nephrectomy (5/6 Nx) or angiotensin II (Ang II) models of CKD. These studies revealed increased proteinuria and decreased survival for EP4pod+ mice while EP4pod-/- mice were protected against the development of glomerular injury. Furthermore, our findings were supported by in vitro studies using cultured mouse podocytes where an adhesion defect was uncovered for cells overexpressing the EP4 receptor. Additionally, our investigations have demonstrated a novel synergy between angiotensin II AT1 receptors and prostaglandin E2 EP4 receptors. This was revealed by in vitro studies using isolated mouse glomeruli. There we were able to show that Ang II stimulation leads to increased expression of cyclooxygenase 2 (COX-2), the enzyme responsible for synthesis of PGE2, in a p38 mitogen activated protein kinase (MAPK) dependent fashion. Moreover increased PGE2 synthesis was measured in response to Ang II stimulation. We confirmed the presence of this synergy in our cultured mouse podocytes and showed an adhesion defect in response to Ang II stimulation which was COX-2 and EP4 dependent. These findings suggest that Ang II AT1 receptors and PGE2 EP4 receptors act in concert to exacerbate glomerulopathies. Studies using mice with either podocyte-specific overexpression of a dominant negative p38 MAPK or mice with global deletion of the EP1 receptor did not provide conclusive results as to their respective signaling involvement in podocyte injury. Altogether our findings provide novel insight for podocyte PGE2 EP4 and Ang II AT1 receptor signaling in models of CKD. These studies provide novel avenues for pursuing therapeutic interventions for individuals with progressive kidney disease.

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11

Dhaun, Neeraj. "Endothelin system & its antagonism in chronic kidney disease." Thesis, University of Edinburgh, 2012. http://hdl.handle.net/1842/6528.

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Since its discovery in 1988 the powerful vasoconstrictor endothelin-1 (ET-1) has been widely implicated in the pathophysiology of chronic kidney disease (CKD) as well as the cardiovascular disease with which it is associated. ET receptor antagonists have favourable effects in experimental models of these conditions and orally acting antagonists are now licensed for the treatment of pulmonary arterial hypertension. However, there is a paucity of human data regarding the role of ET-1 in CKD. In this thesis, I have therefore explored the utility of ET-1 as a biomarker in CKD, and, using selective ET receptor antagonists, the beneficial renal and cardiovascular effects of ET receptor antagonism in CKD. I have shown that as glomerular filtration rate (GFR) declines plasma ET-1 increases linearly whereas urinary ET-1 shows an exponential increase. Furthermore, urinary ET-1 may be a useful marker of disease activity in patients with lupus nephritis. Its levels are high in those with biopsy-proven active renal inflammation and these fall with treatment. I have shown that in subjects with stable non-diabetic proteinuric CKD, acute selective ETA receptor antagonism reduces blood pressure and arterial stiffness and that these systemic benefits are associated with an increase in renal blood flow and reduction in proteinuria. Importantly, these effects are seen on top of those achieved with maximal therapy with angiotensin converting enzyme inhibitors and/or angiotensin receptor blockers. Following a study confirming unchanged pharmacokinetics in CKD, I have used an oral selective ETA receptor antagonist to show that the reductions in BP, arterial stiffness and proteinuria seen in my acute studies are maintained longer term. This results of this study also suggest that the mechanism for the reduction in proteinuria is haemodynamic and relates to a reduction in GFR and filtration fraction. In summary, these studies suggest that ET-1 may act as a potential biomarker of renal inflammation, and confirm its role in the pathophysiology of the systemic and renal vasoconstriction seen in CKD. They also suggest that selective ETA receptor antagonism may provide a novel therapeutic approach in proteinuric CKD on top of standard therapies. Larger and longer term studies are now warranted to confirm this potential.

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12

Parry, Robin Geoffrey. "Cytokines in minimal change nephropathy." Thesis, University of Bristol, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341511.

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13

Kampa, Naruepon. "Renal scintigraphy in dogs : evaluation of glomerular filtration rate measurement by 99mTc-DTPA renogram /." Uppsala : Dept. of Biomedical Sciences and Public Health, Swedish University of Agricultural Sciences, 2006. http://epsilon.slu.se/200609.pdf.

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14

Boisvert, Naomi. "The Role of Ubiquitin C-Terminal Hydrolase L1 in Renal Function and Glomerular Disease." Thesis, Université d'Ottawa / University of Ottawa, 2017. http://hdl.handle.net/10393/36927.

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Ubiquitin C-terminal hydrolase L1 is a deubiquitinating enzyme that salvages ubiquitin from substrates and maintains intracellular ubiquitin pools. While the role of ubiquitin C-terminal hydrolase L1 is well characterized in neurons, there is an increasing scope of evidence to suggest that ubiquitin C-terminal hydrolase L1 also plays a role in renal function and glomerular disease, however, its specific role in these settings remains incompletely elucidated. In the present thesis we explored the role of ubiquitin C-terminal hydrolase L1 in a mouse model of glomerular disease, ACTN4-associated focal segmental glomerulosclerosis and the role of ubiquitin C-terminal hydrolase L1 in renal function. Deletion of ubiquitin C-terminal hydrolase L1 in a mouse model of ACTN4-associated focal segmental glomerulosclerosis significantly improved indices of podocyte injury, a likely result of ubiquitin pool attenuation and sustained α-actinin-4 levels. However, global ablation of ubiquitin C-terminal hydrolase L1 in mice led to altered renal hemodynamics, namely glomerular hyperfiltration, most likely attributed to nerve dysfunction and loss of arterial resistance. Finally, mice lacking ubiquitin C-terminal hydrolase L1 exhibited perturbations in phosphate homeostasis as these showed evidence of hyperphosphatemia and phosphaturia, indicating altered renal phosphate balance. Altogether, these data show that while ubiquitin C-terminal hydrolase L1 plays a maladaptive role in glomerular disease, it also functions as a crucial regulator of renal hemodynamics and renal phosphate handling, suggesting that it may have distinct functions in diseased and non-diseased kidneys.

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15

Xiao, Xue. "C3 glomerulopathy: exploring the role of the glomerular micro-environment in disease pathogenesis." Diss., University of Iowa, 2017. https://ir.uiowa.edu/etd/6019.

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C3 glomerulopathy (C3G) encompasses a group of severe renal diseases characterized by “dominant C3” deposition in the renal glomerulus. Patients typically present as nephritic nephrotics, with hematuria, hypertension, heavy proteinuria and edema. Within ten years of diagnosis, 50% of affected patients progress to end-stage renal disease and require dialysis or renal transplantation. No treatment is available to halt disease progression and thus both disease recurrence and allograft loss are common after transplantation. Genetic studies of C3G have firmly implicated dysregulation of the alternative pathway (AP) of complement in disease pathogenesis. In addition to genetic factors, acquired factors like autoantibodies can also exaggerate AP activity in the circulation to cause C3G. Although AP dysregulation in the circulation (i.e. fluid-phase dysregulation) has been well studied in these patients, AP activity in the glomerular microenvironment is not well understood. In this body of work, we used MaxGel, an ex-vivo surrogate for the glomerular extracellular matrix, to study AP activity and regulation. We showed that C3 convertase can be assembled on MaxGel and elucidated the dynamics of its formation and decay in the presence of complement regulators. We confirm that on MaxGel factor H (fH) inhibits C3 convertase formation and accelerates its decay, while properdin has a stabilizing effect. We also show that the complement factor H-related proteins (FHRs) are vital to the regulation of AP activity. Consistent with our MaxGel data, CFHR gene-fusion events have been reported as genetic drivers of disease in a few familial cases of C3G. One such familial case in which we identified and characterized the rearrangement event results from a novel CFHR5-CFHR2 fusion gene. The fusion gene is translated into a circulating FHR-5/-2 protein that consists of the first two SCRs of FHR-5 followed by all four SCRs of FHR-2. The structural repetition of SCR1-2 followed by another SCR1-2 motif facilitates the formation of complex FHR-1, FHR-2 and FHR-5 multimers, which have enhanced affinity for C3b and by out-competing fH, lead to impaired C3 convertase regulation in the glomerular microenvironment. Finally, we tested gene therapy as a tool to rescue the disease phenotype and restore fluid-phase AP complement control in a mouse model of C3G (Cfh-/-/huCR1-Tg mice). Using the piggyBac transposon system, we introduced a construct derived from complement regulator 1 (CR1) into Cfh-/-/huCR1-Tg mice. Delivery of sCR1-AC via hydrodynamic tail vein injection provided constitutive circulatory expression of sCR1-AC, and in animals followed for 6 months, we found that long-term expression of this complement regulator rescued the renal phenotype. These results suggest that sCR1 may be a potential therapy for patients with this disease.

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16

Duan, Erning. "The Effects of Heparin-binding EGF-like Growth Factor on The Development of Diabetic Renal Disease." Miami University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=miami1258581611.

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17

Kaiser, Tiffany E. "An Appropriate Assessment of Kidney Function In Patients with End Stage Liver Disease: Role of Cystatin C." University of Cincinnati / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1396532967.

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18

He, Jiang, Michael Shlipak, Amanda Anderson, Jason A. Roy, Harold I. Feldman, Radhakrishna Reddy Kallem, Radhika Kanthety, et al. "Risk Factors for Heart Failure in Patients With Chronic Kidney Disease: The CRIC (Chronic Renal Insufficiency Cohort) Study." WILEY, 2017. http://hdl.handle.net/10150/625054.

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Abstract (sommario):

Background-Heart failure is common in patients with chronic kidney disease. We studied risk factors for incident heart failure among 3557 participants in the CRIC (Chronic Renal Insufficiency Cohort) Study. Methods and Results-Kidney function was assessed by estimated glomerular filtration rate (eGFR) using serum creatinine, cystatin C, or both, and 24-hour urine albumin excretion. During an average of 6.3 years of follow-up, 452 participants developed incident heart failure. After adjustment for age, sex, race, and clinical site, hazard ratio (95% CI) for heart failure associated with 1 SD lower creatinine-based eGFR was 1.67 (1.49, 1.89), 1 SD lower cystatin C-based-eGFR was 2.43 (2.10, 2.80), and 1 SD higher log-albuminuria was 1.65 (1.53, 1.78), all P< 0.001. When all 3 kidney function measures were simultaneously included in the model, lower cystatin C-based eGFR and higher log-albuminuria remained significantly and directly associated with incidence of heart failure. After adjusting for eGFR, albuminuria, and other traditional cardiovascular risk factors, anemia (1.37, 95% CI 1.09, 1.72, P= 0.006), insulin resistance (1.16, 95% CI 1.04, 1.28, P= 0.006), hemoglobin A1c (1.27, 95% CI 1.14, 1.41, P< 0.001), interleukin-6 (1.15, 95% CI 1.05, 1.25, P= 0.002), and tumor necrosis factor-a (1.10, 95% CI 1.00, 1.21, P= 0.05) were all significantly and directly associated with incidence of heart failure. Conclusions-Our study indicates that cystatin C-based eGFR and albuminuria are better predictors for risk of heart failure compared to creatinine-based eGFR. Furthermore, anemia, insulin resistance, inflammation, and poor glycemic control are independent risk factors for the development of heart failure among patients with chronic kidney disease.

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19

Hassouneh, Ramzi. "Prostaglandin E2 Receptor 3 (EP3) Contributes to Polyuria, Glomerular Hyperfiltration, and Renal Injury in Diabetes." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/32773.

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Abstract (sommario):

Cyclooxygenases (COXs) and their main renal product, prostaglandin E2 (PGE2), regulate many physiological renal functions and are involved in the pathogenesis of diabetic kidney disease. The PGE2 receptor EP3 has been repeatedly shown to be upregulated during diabetes. Physiologically, EP3 is best recognized to act as a diuretic by antagonizing arginine-vasopressin (AVP)-mediated water reabsorption. Incidentally, the first renal manifestation of diabetes is polyuria, which may trigger a cascade of events leading to DN. We hypothesize that EP3 contributes to polyuria and kidney dysfunction during diabetes. We injected EP3-/- mice with streptozotocin (STZ) and evaluated their renal function 12-weeks post injection. EP3-/- STZ mice exhibit attenuated polyuria while exhibiting increased urine osmolality suggesting enhanced water reabsorption. Western blots reveal that EP3-/- STZ mice have increased expression of aquaporin-1 and aquaporin-2 as well as reduced urinary AVP excretion compared to STZ mice. However, salt transporters were equivalently increased in STZ and EP3-/- STZ mice. In vitro microperfusion shows that EP3 completely abrogates AVP-mediated water reabsorption in STZ cortical collecting ducts. Furthermore, EP3-/- STZ mice showed blunted renal COX-2 expression as well as reduced renal hypertrophy, glomerular hyperfiltration, and albuminuria. Taken together, the data suggests that EP3 contributes to polyuria during diabetes by inhibiting expression of aquaporins. Additionally, EP3 seems to contribute to renal COX-2 induction during diabetes. The lack of an increase in renal COX-2 protein levels in EP3-/- STZ mice may be protective by preventing further renal damage.

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20

Dehmer, Susanne. "Validation of Abbott Diagnostics turbidimetric cystatin C assay and enzymatic creatinine assay using the Architect c8000 analyzer." Thesis, Uppsala University, Department of Medical Biochemistry and Microbiology, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-105609.

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Objective: Estimation of glomerular filtration rate (GFR) is an important tool in the diagnosis and management of chronic kidney disease. Today creatinine is the most frequently used marker for kidney function though several studies indicate that cystatin C is a superior marker. The purpose of this study was to validate Abbott Diagnostics turbidimetric cystatin C assay and enzymatic creatinine assay.Methods: The validation was performed by studies of CV for the two methods and correlations between the two and other available methods for assessing GFR. The stability of cystatin C at room temperature was also evaluated.Results: Both methods showed good precision. The Abbott cystatin C assay generally gave lower values and thereby higher estimated GFRs than the correlated Gentian method. The Abbott enzymatic creatinine assay gave higher values than the correlated Jaffe method. Those results are generally unexpected, but in this study the cause is an automatically applied negative intercept used together with the Jaffe method. Cystatin C showed high stability when stored at room temperature.Conclusions: Estimated GFRs tend to differ depending on the choice of method for analyzing cystatin C or creatinine and this study gives an overview of the range of variation. The study also enlightens the need for an international calibrator for the cystatin C methods presented by different manufacturers.

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21

Tynkevich, Elena. "Muscle Wasting in Non-end Stage Chronic Kidney Disease : Determinants and Outcomes." Thesis, Paris 11, 2014. http://www.theses.fr/2014PA11T086.

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Faible masse musculaire a été peu étudiée chez les patients avant le stade terminal de la maladie rénale chronique (MRC). Nous avons évalué la masse musculaire à partir de la créatininurie des 24h pour étudier ses déterminants, son évolution avec le déclin de la fonction rénale ainsi que ses liens avec les risques de progression vers l’insuffisance rénale terminale traitée (IRTT) et de décès avant IRTT. Dans la cohorte NephroTest incluant 1429 patients avec une MRC stades 1 à 4, le débit de filtration glomérulaire a été mesuré par la clairance du 51Cr-EDTA (DFGm) et estimé par l’équation CKD EPI (DFGe). La créatininurie moyenne à l’inclusion diminuait de 15.3±3.1 à 12.1±3.3 mmol/24 chez les hommes et de 9.6±1.9 à 7.6±2.5 chez les femmes, pour une baisse du DFGm de ≥ 60 à < 15 mL/min/1.73 m2. Être plus âgé, avoir un diabète, un faible IMC ou un niveau faible de protéinurie et d’apports protidiques était associé à un niveau faible de créatininurie. Un déclin annuel du DFGm de 5 mL/min/1.73 m2 était lié à une baisse de créatininurie, indépendamment de ces déterminants. Au cours d’un suivi médian de 3.6 ans, 229 patients ont développé une IRTT, et 113 sont décédés avant IRTT. Après ajustement sur les facteurs de confusion, le hasard ratio (HR) était de 1.6 (0.88-2.9) pour le risque de décès et de 0.60 (0.39-0.91) pour le risque d’IRTT, dans le 1er vs 4ème quartile de créatininurie. La baisse de la créatininurie apparait précocement dans la MRC et est liée au décès avant dialyse. La diminution du risque d’IRTT pourrait s’expliquer par un démarrage plus tardif de la dialyse en raison d’une surestimation du DFGm par le DFGe chez les patients avec une faible créatininurie Mainly described in patients on dialysis, muscle wasting has received little attention in early stage chronic kidney disease (CKD). We used 24-hour creatininuria to assess determinants of low muscle mass and its putative associations with CKD outcomes, using data from the NephroTest cohort, including 1429 non-dialysis patients with CKD stages 1 to 5. Kidney function was assessed with both measured (mGFR, by 51Cr-EDTA renal clearance) and estimated glomerular filtration rate (eGFR, by CKD-EPI equation). End-stage renal disease (ESRD) and pre-ESRD death were the main studied outcomes. The mean baseline creatininuria decreased from 15.3±3.1 to 12.1±3.3 mmol/24 h in men and from 9.6±1.9 to 7.6±2.5 in women, when mGFR fell from ≥ 60 to < 15 mL/min/1.73 m2. Other determinants of low creatininuria were an older age, diabetes, a lower body mass index, a lower level of proteinuria or protein intake. A fast annual decline in mGFR of 5 mL/min/1.73 m2 was linked with a 2-fold decrease in creatininuria, independent of changes in protein intake and other determinants of muscle mass. Over a median follow-up of 3.6 years, 229 patients developed ESRD and 113 patients died before ESRD. After adjustment for confounders, patients with low muscle mass showed a significantly higher risk for pre-ESRD death (HR 1.6, 95% CI 0.88-2.9), but a lower risk for ESRD (HR 0.60, 95% CI 0.39-0.91). The latter was reversed (HR 1.5, 95% CI 1.01-2.4) when mGFR was replaced by eGFR. Decrease in 24-hour creatininuria may appear early in CKD patients, is related to pre-ESRD death. The lower risk for ESRD may reflect later dialysis start due to overestimation of true GFR by eGFR in patients with low muscle mass

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Antunes, Susyane Almeida de Souza. "Efeito do tratamento periodontal em pacientes com doença renal crônica." Universidade do Estado do Rio de Janeiro, 2007. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=6348.

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Fundação de Amparo a Pesquisa do Estado da Bahia O objetivo deste trabalho foi avaliar o efeito do tratamento periodontal sobre marcadores (PCR, albumina, colesterol e triglicerídeos) em indivíduos com Doença Renal Crônica (CRD) bem como sobre o curso da progressão dessa doença. Vinte e seis pacientes, idade média de 60 ( 11,2) anos, com Doença Renal Crônica estágios 3 e 4 com periodontite crônica não severa e severa receberam terapia básica periodontal. Parâmetros clínicos periodontais incluíram Índice de Placa (IP), Sangramento à Sondagem (SS), Profundidade de Bolsa à Sondagem (PBS), Nível de Inserção à Sondagem (NIS). A taxa filtração glomerular estimada (ml/min/1.73 m2) e níveis séricos de proteína C-reativa (mg/dl) (PCR), triglicerídeos (mg/dl), colesterol total (mg/dl) e albumina (g/dl) foram avaliados no dia zero e noventa dias após o tratamento periodontal. No dia zero, os percentuais médios de sítios com PBS ≥ 4mm e NIS ≥ 4mm eram de 23,7 ( 11) e 38,2 ( 16,5), respectivamente. Três meses após, os valores correspondentes diminuíram para 13,3 ( 8,0) e 33,4 ( 16,6). O percentual médio de sítios com PBS ≥ 6mm e NIS ≥ 6 mm diminuiu de 7,8 (8,6) e 24,5 (19,3) para 2,9 (5,1) e 23,8 (20,3). Os valores médios no dia zero de PCR, albumina, triglicerídeos e colesterol total eram de 1,0 mg/dl (1,0), 4,4 g/dl (0,4), 160 mg/dl (61,5), 200,1 mg/dl (36,9), enquanto que 90 dias após o tratamento os valores correspondentes foram de 0,8 mg/dl (0,6), 4,4 g/dl (0,3), 155,8 mg/dl (65,6), 199,5 mg/dl (46), respectivamente. Não havia diferença estatística entre os parâmetros laboratoriais, entre os dias 0 e 90. No dia 0, as taxas da filtração glomerular estimada foram de 41,6 ml/min/1.73m2 (13,1), enquanto no dia 90 esses valores foram de 45 ml/min/1.73m2 (15,7) (p<0.05). Concluiu-se que após o tratamento periodontal os parâmetros clínicos periodontais e a taxa de filtração glomerular estimada melhoraram significantemente e houve uma tendência para diminuição dos níveis de PCR. O significado clínico do aumento da taxa filtração glomerular estimada é discutível. Estudos longitudinais com tempos de observação mais longos são necessários para avaliar se o tratamento periodontal pode oferecer benefício para o paciente renal crônico. The aim of the present study was to evaluate to effect of periodontal treatment in chronic renal disease (CRD) patients. 26 patients with CRD stages 3 and 4 with moderate and severe chronic periodontitis received periodontal basic therapy. Periodontal clinical parameters included plaque index (PI), bleeding on probing (BOP), probing pocket depth (PPD) and probing attachment level (PAL). Estimated glomerular filtration rate (ml/min/1.73m2) and serum levels of C-reactive protein (CRP) (mg/dl), triglicerids (mg/dl), total cholesterol (mg/dl) and albumin (g/dl) were collected on days 0 and 90, after periodontal treatment. On day 0, mean % of sites with PPD ≥ 4mm and PAL ≥ 4mm were 23,7 ( 11) e 38,2 ( 16,5), respectively. On day 90, the corresponding values decreased to 13,3 ( 8,0) e 33,4 (16,6). The mean % of sites with PPD ≥ 6mm and PAL ≥ 6mm decreased from 7,8 (8,6) and 24,5 (19,3) to 2,9 (5,1) e 23,8 (20,3), respectively (P<0,05). On day 0, the mean values of CRP, albumin, triglicerids and total cholesterol was a statistically 1,0 mg/dl (1,0), 4,4 g/dl (0,4), 160 mg/dl (61,5), 200,1 mg/dl (36,9), while the the corresponding values for day 90 were 0,8 mg/dl (0,6), 4,4 g/dl (0,3), 155,8 mg/dl (65,6), 199,5 mg/dl (46), respectively. On day 90, the levels of estimated glomerular filtration rate were 41,6 ml/min/1.73m2 (13,1), and on day 90 the corresponding values were 45 ml/min/1.73m2 (15,7) (p<0.05). The clinical significance of this improvement on estimated glomerular filtration rate is questionable. Further longitudinal studies with longer observation periods are necessary to evaluate if periodontal therapy may be beneficial for CRD patients.

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Antunes, Susyane Almeida de Souza. "Efeito do tratamento periodontal no aumento da taxa de filtração glomerular em pacientes renais crônicos." Universidade do Estado do Rio de Janeiro, 2011. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=6718.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior O objetivo foi avaliar o efeito do tratamento periodontal sobre a progressão da disfunção renal e marcadores sorológicos metabólicos (albumina, colesterol e triglicerídeos) em indivíduos com Doença Renal Crônica (DRC) e periodontite crônica. Cinquenta e sete pacientes com DRC na pré-diálise com periodontite crônica foram avaliados 90 dias e 29 pacientes foram avaliados 180 dias após a terapia básica periodontal. Parâmetros clínicos periodontais incluíram índice de placa (IP), sangramento a sondagem (SS), profundidade de Bolsa à Sondagem (PBS) e nível de Inserção à Sondagem (NIS). Os parâmetros laboratoriais Taxa Filtração Glomerular (TFG) e níveis séricos de creatinina (mg/dl), triglicerídeos (mg/dl), colesterol total (mg/dl) e albumina (g/dl) foram avaliados no dia 0 e 90 e 180 dias após o tratamento periodontal. TFG foi avaliada através da equação Modification of Diet in Renal Disease (MDRD). Noventa dias após o tratamento periodontal (n=57), todos os parâmetros clínicos periodontais apresentaram uma melhora estatisticamente significante (p<0.05). Houve uma melhora estatisticamente significante (p<0.05) nos valores da mediana (intervalo interquartil) da TFG de 36,2 ml/min (24) no dia 0 para 37,5 ml/min (24) aos 90 dias. Após 180 dias do tratamento periodontal (n=29), observou-se melhora dos percentuais médios dos parâmetros clínicos periodontais (p<0.05). A mediana (intervalo interquartil) da TFG foi de 36,2 ml/min (27,3) no dia 0 e 39,4 ml/min (27,9) no dia 180 (p<0.05). Não houve diferença estatisticamente significante nos valores antes e após o tratamento periodontal nos níveis séricos de creatinina, albumina, colesterol, triglicerídeos e colesterol, tanto aos 90 quanto aos 180 dias após o tratamento periodontal. Concluiu-se que após o tratamento periodontal os parâmetros clínicos periodontais e a TFG melhoraram significantemente. Apesar da progressão da função renal ser resultado de fatores multifatoriais, o tratamento periodontal pode ser benéfico no curso da DRC. The aim of this study was to evaluate the effect of periodontal treatment on the progression of renal dysfunction and metabolic markers (albumin, cholesterol and triglycerids) in patients with chronic kidney disease (CKD) and chronic periodontitis. Fifty seven patients with CKD at pre-dyalisis phase and chronic periodontitis were evaluated 90 days, while 29 patients were evaluated 180 days after periodontal therapy. Periodontal clinical parameters included plaque index (PI), bleeding on probing (BOP), probing pocket depth (PPD) and probing attachment level (PAL). The laboratory exams glomerular filtration rate (GFR) and creatinin (mg/dl), triglycerids (mg/dl), total cholesterol (mg/dl) and albumin (g/dl) levels were evaluated at baseline and 90 and 180 days after periodontal therapy. GFR was evaluated with the Modification of Diet in Renal Disease (MDRD) equation. Ninety days after periodontal therapy (n=57), all periodontal clinical parameters significantly improved (p<0.05). There was a significant improvement on the median values (interquartile range) of GFR from 36.2 (24) ml/min on baseline to 37.5 (24) ml/min on day 90. After 180 days of the periodontal therapy (n=29), there was a significant improvement of the periodontal clinical parameters (p<0.05). The median (interquartile range) of the GFR was 36.2 (27.3) on baseline and 39.4 (27.9) ml/min on day 180 (p<0.05). No significant differences were observed at the median values of creatinin, albumin, total cholesterol and triglycerids comparing baseline, 90 and 180 days after periodontal treatment. In conclusion, periodontal clinical parameters and GFR improved significantly 90 and 180 days after periodontal treatment. Although the progression of the renal dysfunction may be related to many factors, periodontal treatment may be beneficial to the course of CKD.

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Nerpin, Elisabet. "The Kidney in Different Stages of the Cardiovascular Continuum." Doctoral thesis, Högskolan Dalarna, Medicinsk vetenskap, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-209644.

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Patients with chronic kidney disease are at higher risk of developing cardiovascular disease. The complex, interaction between the kidney and the cardiovascular system is incompletely understood, particularly at the early stages of the cardiovascular continuum. The overall aim of this thesis was to clarify novel aspects of the interplay between the kidney and the cardiovascular system at different stages of the cardiovascular continuum; from risk factors such as insulin resistance, inflammation and oxidative stress, via sub-clinical cardiovascular damage such as endothelial dysfunction and left ventricular dysfunction, to overt cardiovascular death. This thesis is based on two community-based cohorts of elderly, Uppsala Longitudinal Study of Adult Men (ULSAM) and Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS). The first study, show that higher insulin sensitivity, measured with euglycemic-hyperinsulinemic clamp technique was associated to improve estimated glomerular filtration rate (eGFR) in participants with normal fasting plasma glucose, normal glucose tolerance and normal eGFR. In longitudinal analyses, higher insulin sensitivity at baseline was associated with lower risk of impaired renal function during follow-up. In the second study, eGFR was inversely associated with different inflammatory markers (C-reactive protein, interleukin-6, serum amyloid A) and positively associated with a marker of oxidative stress (urinary F2-isoprostanes). In line with this, the urinary albumin/creatinine ratio was positively associated with these inflammatory markers, and negatively associated with oxidative stress. In study three, higher eGFR was associated with better endothelial function as assessed by the invasive forearm model. Further, in study four, higher eGFR was significantly associated with higher left ventricular systolic function (ejection fraction). The 5th study of the thesis shows that higher urinary albumin excretion rate (UAER) and lower eGFR was independently associated with an increased risk for cardiovascular mortality. Analyses of global model fit, discrimination, calibration, and reclassification suggest that UAER and eGFR add relevant prognostic information beyond established cardiovascular risk factors in participants without prevalent cardiovascular disease. Conclusion: this thesis show that the interaction between the kidney and the cardiovascular system plays an important role in the development of cardiovascular disease and that this interplay begins at an early asymptomatic stage of the disease process.

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Paníco, Marilia Duarte Brandão. "Doença da artéria periférica sintomática e assintomática:fatores de risco e associação à filtração glomerular." Universidade do Estado do Rio de Janeiro, 2010. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=1755.

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A Doença da Artéria Periférica (DAP) é o resultado do processo aterosclerótico das artérias dos membros superiores, inferiores, aorta abdominal e seus ramos viscerais. Nosso objetivo foi detectar a DAP correlacionando-a com fatores de risco (FR) e a filtração glomerular estimada (FGe) nos pacientes com ≥30 anos, assistidos na Unidade docente - assistencial de Angiologia (UDA) do Hospital Universitário Pedro Ernesto da Faculdade de Ciências Médicas - UERJ, com o intuito de descrever os FR e associação com doença renal crônica à DAP, a partir da aferição do índice tornozelo-braço (ITB); determinar a alteração da FGe por equações, relacionando-a à progressão da DAP. Foi usado um questionário padrão e o ITB para identificar os pacientes com e sem DAP. Correlacionou-se as variáveis laboratoriais, como os níveis séricos de colesterol, triglicerídeos, HDL-c, LDL-c, glicemia, homocisteína com a FGe e com o ITB. As análises estatísticas foram feitas pelo programa Statistical Package for the Social Sciences (SPSS) 16.0 Os resultados apontaram para a importância do ITB no diagnóstico da DAP, com configuração de graus de obstrução leve, discreta, moderada e grave para os sintomáticos, e a identificação dos assintomáticos, possibilitando intervenção nos fatores de risco demarcados e o controle de suas complicações. O tabagismo mostou-se como o FR com razão de risco mais importante para DAP. A hipertensão sistólica e a diastólica foram variáveis clínicas mais significativas que o diabetes mellitus. Os marcadores séricos tradicionais para DAP: colesterol total, triglicerídeos e glicemia mostraram significância estatística. A homocisteína foi o marcador mais significativo em relação à DAP. Ocorreu associação entre redução do ITB com a elevação dos níveis pressóricos, das glicemias, da homocisteína, assim como diminuição das médias da FGe. Foi conclído que nos pacientes com DAP a hiperhomocisteinemia está associada à diminuição da FGe, ambas passíveis de prevenção, contribuindo na redução da morbimortalidade da DAP. A estreita associação da DAP com a FGe diminuída representou relevante contribuição do estudo. Peripheral Artery (DAP) is the result of the atherosclerotic process involving the arteries of the superior and inferior limbs, abdominal aorta and its visceral branches. The objective was detect PAD, using the ankle brachial index (ABI), in patients ≥ 30 years old attended in the Unidade Docente - Assistencial of Angiology (UDA), correlating it with risk factors (RF) and estimated glomerular filtration rate (eGFR), with intention to describe the RF and association with chronic kidney disease. It was used a standard questionnaire and the ABI to identify patients with and without PAD. Laboratorial tests, as total cholesterol, triglycerides, HDL-c, LDL-c, glycemia, creatinine and homocysteine were correlated to ABI. Statistical analyses were done using the Statistical Package for the Social Sciences (SPSS) 16.0 program. The results had pointed to the importance of the ABI in the diagnosis of PAD, with degrees of mild, discrete, moderate and serious stenosis for the symptomatic patients, and the identification of the asymptomatic ones, making possible intervention in the RF and control of their complications. Tabagism was confirmed as the RF with most important odds ratio for PAD. The systolic and diastolic hypertension showed to be more significant than diabetes mellitus, as diseases associated to PAD. In laboratorial evaluation, the traditional blood markers for PAD: total cholesterol, triglycerides and glucose had shown statistics significance. Homocysteine was the marker most significant in PAD. Association between reduction of ABI with systolic and diastolic hypertension and glycemias occurred, as well as reduction of the averages of the eGFR. The conclusion was, in patients with PAD, hyperhomocysteinemia and decrease of eGFR are possible of prevention, contributing in the reduction of the morbimortality of PAD. The narrow association of decrease eGFR in patients with PAD represented excellent contribution of this study.

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Nagy, I. I. (Irina I. ). "Wnt-11 signaling roles during heart and kidney development." Doctoral thesis, Oulun yliopisto, 2014. http://urn.fi/urn:isbn:9789526204666.

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Abstract Organogenesis involves precursor cells proliferation, differentiation along with their coordinated organization into precise multicellular arrangements by planar cell polarity (PCP) pathways. The beta-catenin independent/non-canonical type of Wnt-11 signaling has been known as a PCP modulator during development. In this thesis were analyzed the roles of Wnt-11 in heart and kidney development by using in vivo functional genomics technologies. We show that the Wnt-11 gene is important for murine ventricular myocardium development, since Wnt-11 deficiency in early cardiogenesis leads to impaired organization and maturation of mouse ventricular cardiomyocytes, causing primary cardiomyopathy with in utero lethality. Wnt-11 coordinates the co-localized expression of the cell adhesion molecules N-cadherin and β-catenin, which are critical for the spatially specific organization of cardiomyocytes. We show that Wnt-11 deficiency causes primary hypertrophic and noncompaction cardiomyopathy in adult mice, with consequences for regional myocardium function. The Wnt family of secreted signals has been implicated in kidney tubule development and tubular cystic diseases such as polycystic kidney disease. We show here that Wnt-11 is expressed in mature nephrons and is involved in late steps of nephrogenesis, since the kidney tubule organization is deregulated in Wnt-11 deficient kidneys, to enlarged lumen with increased convolution. These tubule abnormalities are associated with glomerular microcyst formation and kidney failure. Wnt-11 deficiency reduced significantly Wnt-9b expression, a critical signal for PCP-mediated kidney tubule elongation. In the cortical region this associated with reduced expression of nephron and stromal progenitor cell marker. The results in this thesis point out that Wnt-11 function is required for proper myocardium organization and maturation as well as proper morphogenesis of the kidney tubules during the embryonic and postnatal developmental stages. Wnt-11 knockout phenotypes depend on the genetic background, similarly to human congenital disease. This data may be relevant for human congenital cardiomyopathy and glomerulocystic kidney disease studies Tiivistelmä Alkion sisäelinten kehityksen aikana esisolut lisääntyvät ja erilaistuvat muodostaen tarkoin määriteltyjä monisoluisia rakenteita. Muodostuvan kudosrakenteen määrittelyssä erilaiset solusignaalit ovat keskeisessä asemassa. Yksi näistä on nk. Wnt signaali perhe. Wnt perheeen jäsen Wnt-11 tehtävät on huonosti tunnettu. Wnt-11 viestittää ilmeisesti nk. planaaristen solupolariteettireittien (PCP) avulla, joka on beeta-kateniinista riippumattoman nk. ei-kanonisen Wnt signaali. Väitöskirjatyössä selvitettiin Wnt-11:n vaikutuksia sydämen ja munuaisten kehitykseen in vivo funktionaalisten genomisten menetelmien avulla. Ihmisen synnynnäiset kardiomyopatiat ovat sydänlihaksen ensisijaisia vaurioita, joiden taustalla on sydänlihaksen kehityshäiriö. Tutkimuksessa osoitetaan, että Wnt-11-geenillä on tärkeä merkitys hiiren sydänkammion kehitykselle, koska Wnt-11-geenin puute sydämen varhaisen kehityksen vaiheessa johtaa sydänlihassolujen järjestäytymisen ja kypsymisen häiriintymiseen, jolloin seurauksena on ensisijaisesta kardiomyopatiasta johtuva sikiökuolema. Wnt-11 koordinoi kahden solukiinnitysmolekyylin, N-kadheriinin ja β-kateniinin, samanaikasta ilmentymistä. Kyseiset molekyylit ovat keskeisen tärkeitä sydänlihasssolujen spatiaalisen järjestäytymisen kannalta. Tutkimuksessa osoitetaan, että Wnt-11-puutos aiheuttaa aikuisilla hiirillä ensisijaista sydänlihaksen liikakasvua ja trabekuloivaa kardiomyopatiaa, mikä vaikuttaa sydänlihaksen toimintaan. Tuloksilla voi olla merkitystä tutkittaessa ihmisen synnynnäisiä kardiomyopatioita. Wnt-signaaliperheen on osoitettu olevan yhteydessä munuaisputken kehitykseen ja sen sairauksiin, kuten munuaisten monirakkulatautiin. Väitöstutkimuksessa osoitetaan, että Wnt-11 ilmentyy kypsissä nefroneissa ja että se osallistuu nefrogeneesiin myöhempiin vaiheisiin, koska munuaisputken kehityksen säätely on poikkeavaa niissä munuaisissa, joista Wnt-11 puuttuu. Seurauksena on laajentunut, normaalia poimuttuneempi luumen. Munuaisputken poikkeavuuksilla oli yhteyttä munuaiskerästen mikrokystien muodostumiseen sekä munuaisten vajaatoimintaan. Wnt-11 -puute vähensi huomattavasti Wnt-9b-ilmentymistä, joka on PCP-välitteisen munuaisputken pidentymisen kannalta keskeisen tärkeä signaali. Kortikaalialueella Wnt9b:n vaimennussäätely liittyi poikkeavaan solujen lisääntymiseen, apoptoosiin ja kypsymiseen sekä vähentyneeseen nefroni- ja stroomakantasolujen merkkiaineen ilmentymiseen. Väitöskirjatutkimuksen tulokset viittaavat siihen, että Wnt-11 -toiminto on välttämätön sydänlihaksen normaalin muodostumisen ja kypsymisen sekä munuaisputken normaalin morfogeneesin kannalta sikiövaiheen ja syntymän jälkeisen kehityksen aikana. Wnt-11 -poistogeenisen hiiren fenotyypi riippuu geneettisestä tausta, samaan tapaan kuin ihmisen synnynnäisissä sairauksissa. Väitöstutkimuksesta saatavalla tiedolla voi olla merkitystä tutkittaessa ihmisen synnynnnäistä kardiomyopatiaa ja munuaisten monirakkulatautia

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Contreras, Macazana Roxana Milagros. "Estimación de la tasa de filtración glomerular usando las ecuaciones CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration) y MDRD 4 (Modification of Diet in Renal Disease) en pacientes diabéticos tipo 2 atendidos en HNERM." Bachelor's thesis, Universidad Nacional Mayor de San Marcos, 2014. https://hdl.handle.net/20.500.12672/8961.

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Publicación a texto completo no autorizada por el autor Determina la correlación y el grado de concordancia entre la ecuación de CKD-EPI y MDRD con la depuración de creatinina en orina de 24 horas para la estimación de la tasa de filtrado glomerular en pacientes diabéticos tipo 2, mayores de edad que acuden al servicio de Patología Clínica sección Bioquímica depuración de creatinina del HNERM, en el periodo octubre a diciembre 2013. Es un estudio Analítico comparativo, prospectivo observacional. Se obtuvo una muestra de 152 pacientes diabéticos, se aplicó el test de correlación de spearman, se aplicó el coeficiente de correlación de concordancia, y para determinar el bias respecto a la DCC se utilizó la gráfica de Blant altman. Se evaluó las ecuaciones CKD EPI, MDRD 4 con la DCC respectivamente la ecuación CKD EPI tuvo mejor correlación R 0.86, se evaluó el grado de concordancia con el índice Kappa k 0.69 (muy bueno) IC 0.61-0.78, y la ecuación MDRD 4, 0.63, IC 0.56 y 0.71. Se evalúo el bias entre los métodos y se observa en toda la población que la ecuación CKD EPI y MDRD 4 sobrestiman la TFG en relación a la DCC, en -3.1 y -8.1 respectivamente, siendo la ecuación CKD EPI la que tiene menor error sistemático. Se concluye que la ecuación CKD EPI es comparable con la DCC en orina de 24 horas, tiene un mejor desempeño y correlación que la ecuación MDRD 4. Trabajo académico

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Johnston, Nicklett Johnston. "The Effect of Health Literacy in Low Estimated Glomerular Filtration and Diabetes." ScholarWorks, 2017. https://scholarworks.waldenu.edu/dissertations/3895.

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Health literacy is widespread, but its potential is not recognized. By not recognizing health literacy, patients have the burden of coping with diabetes with renal complications without full knowledge of their responsibility to their health. The focus of the project was to assess participants with diabetes with low health literacy and low mean glomerular filtration rate (eGFR). The project goal was achieved by the assessment of the participants' health literacy and eGFR before and after education for their diabetes, then assessed to determine if teaching the participants would improve their health literacy, lab values, and overall health. Participants were recruited by being patients of the designated clinic and screened for diabetes and low eGFR, for a total of 30 participants. The Brief Health Literacy Screen was used to measure health literacy. The health of the participants was appraised by the laboratory values of eGFR and fasting glucose. The project methodology was an observational design using correlation and 2-sample t analysis with the variables eGFR, fasting glucose, and health literacy. The variables were compared before and after the participants' education. Results showed health literacy with patient education was associated with greater patient self-efficacy and improved fasting glucose numbers, eGFR flows, and health literacy scores. The current health climate shows value in different types of health providers. Social change was defined by the project launching a nurse practitioner as the leader for advancing the treatment plans of chronic kidney disease. This project impacts social change by showing patients in the process of improved health and empowering the patients to be advocates of their own health.

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Magacho, Edson José de Carvalho. "Rastreamento da doença renal crônica: validação do questionário “Scored" nomograma para estimativa da taxa de filtração glomerular e avaliação dos marcadores funcional e de lesão do parênquima renal." Universidade Federal de Juiz de Fora (UFJF), 2014. https://repositorio.ufjf.br/jspui/handle/ufjf/5552.

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Submitted by isabela.moljf@hotmail.com (isabela.moljf@hotmail.com) on 2017-08-11T13:00:25Z No. of bitstreams: 1 edsonjosedecarvalhomagacho.pdf: 1270417 bytes, checksum: 31d136c0dff33a402802624129e69c27 (MD5) Approved for entry into archive by Adriana Oliveira (adriana.oliveira@ufjf.edu.br) on 2017-08-11T13:02:58Z (GMT) No. of bitstreams: 1 edsonjosedecarvalhomagacho.pdf: 1270417 bytes, checksum: 31d136c0dff33a402802624129e69c27 (MD5) Made available in DSpace on 2017-08-11T13:02:58Z (GMT). No. of bitstreams: 1 edsonjosedecarvalhomagacho.pdf: 1270417 bytes, checksum: 31d136c0dff33a402802624129e69c27 (MD5) Previous issue date: 2014-04-24 FAPEMIG - Fundação de Amparo à Pesquisa do Estado de Minas Gerais Fatores desencadeantes da Doença Renal Crônica (DRC), como hipertensão e diabetes principalmente, apresentam aumento de prevalência à medida que a população envelhece. Como desconhecemos a prevalência da DRC na pré-diálise na população brasileira e Bang e cols. propuseram um método para rastrear a DRC denominado Tabela Screening For Ocult Renal Disease (Scored), o objetivo do estudo foi validar a tabela Scored no Brasil. Trata-se de um estudo transversal cuja amostra foi de 600 servidores da Universidade Federal de Juiz de Fora (UFJF) preferencialmente. Foram coletados dados sociodemográficos, realizados exames físicos, exames de urina e sangue e os entrevistados responderam à Tabela Scored. Para determinação da presença da DRC, foram considerados os critérios de filtração glomerular (FG) < 60mL/min/1,73m2 e/ou presença de proteinúria/microalbuminúria como marcador de lesão renal identificados em um intervalo mínimo de 90 dias, como proposto pelo grupo de trabalho Kidney Disease Outcomes Quality Iniciative (K/DOQI), apoiado pela National Kidney Foundation (NKF) americana. Para validação do questionário original, foi calculada a sensibilidade, a especificidade, a acurácia, valores preditivos positivo (VPP) e negativo (VPN). O questionário Scored apresentou sensibilidade de 80%, especificidade de 65%, VPP de 14%, VPN de 97% e acurácia de 66%. A DRC foi diagnosticada pelo critério de filtração glomerular estimada < 60mL/min/1,73m2 (8,8%), por relação albumina creatinina alterada (5%) e por presença de hematúria glomerular (16,3%) no primeiro exame, tendo se confirmado no segundo exame por filtração glomerular estimada < 60mL/min/1,73m2 (3,5%), por relação albumina creatinina alterada (3%) e por presença de hematúria glomerular (9,5%). As etapas cumpridas no processo de adaptação transcultural permitiram desenvolver a versão brasileira do questionário Scored, de fácil compreensão, aceitação e de baixíssimo custo, e poderá constituir importante instrumento de rastreio de pessoas com chance de apresentar DRC. Na avaliação laboratorial da DRC, a repetição dos exames para estimativa da FG, pesquisa de proteinúria/microalbuminúria e hematúria glomerular se mostrou fundamental para conclusão diagnóstica, principalmente este último que apresentou percentuais importantes de confirmação. Triggering factors of Chronic Kidney Disease (CKD), such as hypertension and diabetes mostly, present an increase in the prevalence as the population ages. We are unaware of the prevalence of CKD in the pre-dialysis of the Brazilian population and Bang and Cols proposed a method to track the DRC called SCORED system (Screening For Occult Renal Disease). The aim of the study was to validate the Scored table in Brazil. This is a cross-sectional study which sampled 600 employees of the Universidade Federal de Juiz de Fora (UFJF), preferably. Socio-demographic data were collected, physical examinations, urine and blood were performed and those interviewed answered the Scored Table. To determine the presence of CKD were considered the Glomerular Filtration Rates (GFR) 60mL/min/1,73m2 and also the presence of proteinuria / microalbuminuria as a marker of kidney damage identified at a interval of at least 90 days, as proposed by the working group Kidney Disease Outcomes Quality Initiative (K / DOQI), supported by the american National Kidney Foundation (NKF). For the validation of the original questionnaire, the sensitivity, specificity, and accuracy were calculated, as well as the positive predictive values (PPV) and negative predictive values (NPV). The Scored questionnaire showed a sensitivity of 80%, specificity of 65%, PPV 14%, NPV 97% and an accuracy of 66%. CKD was diagnosed according to the criteria of estimate glomerular filtration rate < 60mL/min/1,73m2 (8,8%), by the relation of amended albumin creatinine (5%) and by the presence of glomerular hematuria (16.3%) at the first examination, being confirmed in the second examination by estimate glomerular filtration rate of 60mL/min/1,73m2 (3,5%), by the relation of amended albumin creatinine (3%) and by the presence of glomerular hematuria. The steps taken in the cross-cultural adaptation process allowed the development of the Brazilian version of the Scored questionnaire, easy to understand, with good acceptance and very low cost, this may constitute an important screening tool for people with chance of having CKD. As for the laboratory evaluation of CKD, repeating the exams to estimate the GF, the search for proteinuria / microalbuminuria and glomerular hematuria proved fundamental to the diagnostic conclusion, especially this latter, which showed significant percentage of confirmation.

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Tollendal, Ana Luisa Silveira Vieira. "Avaliação dos níveis séricos de ácido úrico como fator de risco para o declínio da taxa de filtração glomerular em pacientes com doença renal crônica." Universidade Federal de Juiz de Fora (UFJF), 2018. https://repositorio.ufjf.br/jspui/handle/ufjf/6722.

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Submitted by Geandra Rodrigues (geandrar@gmail.com) on 2018-04-27T11:55:53Z No. of bitstreams: 1 analuisasilveiravieiratollendal.pdf: 1031624 bytes, checksum: 2a4a0647b9d22be1da3f719765d6d470 (MD5) Approved for entry into archive by Adriana Oliveira (adriana.oliveira@ufjf.edu.br) on 2018-04-27T12:09:21Z (GMT) No. of bitstreams: 1 analuisasilveiravieiratollendal.pdf: 1031624 bytes, checksum: 2a4a0647b9d22be1da3f719765d6d470 (MD5) Made available in DSpace on 2018-04-27T12:09:21Z (GMT). No. of bitstreams: 1 analuisasilveiravieiratollendal.pdf: 1031624 bytes, checksum: 2a4a0647b9d22be1da3f719765d6d470 (MD5) Previous issue date: 2018-01-19 Introdução: A doença renal crônica (DRC) se tornou uma preocupante questão de saúde pública em todo o mundo devido às suas crescentes incidência e prevalência e ao impacto em morbimortalidade por ela desencadeado. O tratamento da DRC se baseia na intervenção em seus fatores de risco. Entretanto, os fatores atualmente conhecidos e sua abordagem não têm sido suficientes para conter a doença. Por esse motivo, torna-se imprescindível a busca por outros fatores associados à sua patogênese. Nesse sentido, a hiperuricemia tem sido apontada, nas últimas décadas, como uma condição associada à DRC, porém sem que ainda tenha sido estabelecida uma associação causal entre ambas. Objetivos: 1. Avaliar as evidências sobre o impacto da hiperuricemia na incidência e progressão da DRC, através de revisão sistemática da literatura; 2. Avaliar o impacto dos níveis séricos de ácido úrico (AU) sobre o declínio da taxa de filtração glomerular (TFG) em uma população de pacientes com DRC. Métodos: Primeiramente, realizou-se revisão sistemática da literatura com busca por artigos publicados no período entre Janeiro de 2005 e Dezembro de 2016, utilizando-se a combinação de palavraschave “chronic renal insufficiency AND hyperuricemia AND uric acid” nos bancos de dados Lilacs e Pubmed. Os resumos dos artigos foram avaliados por dois pesquisadores, de acordo com os critérios de inclusão e exclusão estabelecidos. Na segunda fase do estudo, 788 pacientes incidentes no ambulatório de DRC do Centro Hiperdia Minas/Juiz de Fora tiveram seus registros eletrônicos analisados e o impacto dos níveis de AU na progressão da DRC foi avaliado. Resultados: Relativamente à revisão sistemática, foram encontrados 150 estudos envolvendo seres humanos, dos quais 22 foram elegíveis, 13 estudos avaliaram incidência e 11 avaliaram progressão da DRC (aumento de creatinina, variação da taxa de filtração glomerular, início de terapia renal substitutiva); dois avaliaram ambos os desfechos. Todos os treze artigos que avaliaram associação entre hiperuricemia e incidência de DRC mostraram associação positiva entre ambas. Uma metanálise avaliou impacto da hiperuricemia em 190.718 indivíduos e encontrou relação causal independente para incidência de DRC. Em relação à progressão da DRC, os estudos longitudinais apresentaram resultados conflitantes e três estudos randomizados controlados foram identificados, comparando um grupo tratado com alopurinol e um grupo controle, todos com melhora dos desfechos renais no grupo tratado. Os resultados da análise do banco de dados do Centro HIPERDIA mostraram que pacientes admitidos com hiperuricemia, ou seja, AU maior do que 6,8mg/dL, apresentaram risco quase duas vezes maior (IRR=1,91 95% IC: 1,21-3,00, p=0,005) de progressão rápida da DRC (TFG>5mL/min/ano). Além disso, para cada 1 mg/dL de aumento nos níveis basais de AU houve risco anual 48% maior de progressão rápida (IRR=1,48 95% IC:1,16-1,88, p=0,001). Conclusão: A revisão sistemática sugeriu que hiperuricemia se associa de forma independente com incidência de DRC, porém seu papel na progressão da doença ainda é controverso. Entre os pacientes com DRC do Centro Hiperdia Minas/Juiz de Fora, os níveis séricos aumentados de AU associaramse a maior risco de progressão rápida da doença renal crônica. Introduction: Chronic kidney disease (CKD) has become a worrisome public health problem worldwide due to its increasing incidence and prevalence as well as its impact on morbidity and mortality. Treatment of CKD is based on risk factor intervention. However, currently known factors and their approach are insufficient to stop the disease. For this reason, it is imperative to search for other factors associated with its pathogenesis. Hyperuricemia has been identified as a condition associated with CKD, but causal association between them has not yet been proved. Objectives: 1. To evaluate the impact of hyperuricemia on the incidence and progression of CKD through a systematic review of the literature; 2. To evaluate the impact of serum uric acid levels on the decline of the glomerular filtration rate (GFR) in a population of chronic renal patients. Methods: Initially a systematic review of the literature was carried out between January 2005 and December 2016. The combination of keywords "chronic renal insufficiency AND hyperuricemia AND uric acid" was used to search in the Lilacs and Pubmed databases. The articles’ abstracts were evaluated by two researchers according to established inclusion and exclusion criteria. Secondly, the electronic records of 788 patients of the CKD outpatient clinic of the Hiperdia Minas/Juiz de Fora Center were analyzed and the impact of uric acid levels on the progression of CKD was evaluated. Results: A total of 150 studies involving humans were found. Twenty two were eligible; 13 studies evaluated incidence and 11 evaluated progression of CKD (increase in creatinine, variation of glomerular filtration rate, initiation of renal replacement therapy); two of the articles evaluated both outcomes. All thirteen articles that assessed the association between hyperuricemia and incidence of CKD showed a positive association between both. A further meta-analysis of 190,718 individuals evaluated the impact of hyperuricemia on the incidence of CKD and found an independent causal relationship. Regarding the progression of CKD, longitudinal studies presented conflicting results; three randomized controlled trials compared a group treated with allopurinol and a control group, all with improvement of the renal outcomes within the treated group. The Hiperdia Center database analysis results showed that patients admitted with hyperuricemia, that is, uric acid higher than 6.8mg/dL, presented almost twice the risk (IRR = 1.91 95% CI: 1, 21-3.00, p = 0.005) of rapid progression of CKD (TFG> 5mL/min/year). In addition, for each 1 mg/dL increase in the uric acid levels baseline, there was an additional 48% annual risk of progression (IRR = 1.48 95% CI: 1.16-1.88, p = 0.001). Conclusion: The systematic review suggested that hyperuricemia is independently related to the incidence of CKD, however, its role in disease progression is still controversial. Among patients with CKD, increased serum uric acid levels were associated with an increased progression of chronic kidney disease.

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Pinho, Natália Alencar de. "Fatores associados à doença renal crônica em pacientes internados em um hospital universitário na cidade de São Paulo." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/7/7139/tde-19092013-154219/.

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Introdução: a doença renal crônica constitui importante problema de saúde pública mundial. Contudo, pouco se sabe sobre suas características em nosso meio. Objetivo: identificar os fatores associados à doença renal crônica em pacientes internados em um hospital universitário. Método: foram selecionados, aleatoriamente, 386 pacientes que constituíram dois grupos: com e sem doença renal crônica. A doença renal crônica foi definida pela presença de diagnóstico médico ou antecedente pessoal. Os dados foram obtidos do prontuário do paciente. Foram comparados os grupos com e sem doença renal crônica e os hipertensos com e sem doença renal crônica, mediante as variáveis de estudo. Estimou-se a taxa de filtração glomerular (eTFG) dos pacientes sem doença renal a partir das equações Modification of Diet in Renal Disease abreviada (MDRD4) e Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI). Verificou-se a associação da eTFG <90 mL/min/1,73m², pela MDRD4, com dados biossociais e comorbidades. O nível de significância foi de p<0,05. Resultados: a amostra foi 50,5% homens, 64,4% brancos, 50,7% com companheiro e idade de 58,2±18,6 anos. Os pacientes com doença renal crônica se distinguiram daqueles sem a doença (p<0,05) em relação a: viverem com companheiro (59,8% vs 47,3%); idade mais elevada (65,8±15,6 vs 55,3±18,9 anos); menor frequência de fumantes (11,1% vs 29,7%); terem antecedente pessoal de hipertensão arterial (75,2% vs 46,3%), diabetes (49,5% vs 22,4%), dislipidemia (23,8% vs 14,9%), infarto agudo do miocárdio (14,3% vs 6,0%) e insuficiência cardíaca congestiva (18,1% vs 4,3%); evolução a óbito (12,4% vs 1,4%); e maior tempo de internação (11 (818) vs 9 (612) dias); além dos exames laboratoriais, exceto glicemia e perfil lipídico. A análise de regressão logística indicou associação independente da doença renal crônica com as seguintes variáveis (OR, odds ratio; IC, intervalo de confiança de 95%): idade (OR 1,019, IC 1,003-1,036); hipertensão arterial (OR 2,032, IC 1,128-3,660), diabetes (OR 2,097, IC 1,232-3,570) e insuficiência cardíaca congestiva (OR 2,665, IC 1,173-6,056). Os hipertensos com e sem doença renal crônica foram distintos (p<0,05) em relação a: possuíam companheiro (64,3% vs 50,7%); uso de maior número de medicamentos (4,0 (2,05,0) vs 2,0 (0,5 4,0)), não fumantes (9,9% vs 25%); terem antecedentes pessoais para diabetes (53,5% vs 36,4%) e insuficiência cardíaca congestiva (19,8% vs 7,0%); uso de medicamentos anti-hipertensivos (79,1% vs 66,4%,); tratamento com insulina (24,4% vs 7,0%); além dos exames laboratoriais, exceto glicemia, perfil lipídico e ácido úrico. Houve boa concordância da classificação da eTFG de pacientes sem doença renal crônica pelas equações MDRD4 e CKD-EPI (kappa 0,854). De acordo com a equação MDRD4, 54,4% tinham eTFG 90 mL/min/1,73m²; 37,7%, eTFG 60-89 mL/min/1,73m²; e 7,8%, eTFG <60 mL/min/1,73m². Pacientes com eTFG <90 mL/min/1,73m² se destacaram (p<0,05) por apresentar maior frequência de hipertensão arterial (63,3% vs 32,0%), diabetes (29,7% vs 16,3%) e dislipidemia (24,2% vs 7,2%) em relação a pacientes com eTFG 90 mL/min/1,73m². Conclusão: a doença renal crônica esteve associada a fatores de risco cardiovascular, em sua maioria, modificáveis. Introduction: chronic kidney disease is an important public health problem worldwide. Nevertheless, little is known about its features in our setting. Objective: identify factors associated with chronic kidney disease among hospitalized patients in a university hospital. Method: 386 patients were randomly selected and divided in two groups: with and without chronic kidney disease. Chronic kidney disease was defined by the presence of medical diagnosis or personal history. Data was acquired from medical records. Patients with and without chronic kidney disease, as well as hypertensive patients with and without chronic kidney disease, were compared with regard to the variables under study. Glomerular filtration rate (eGFR) of patients without chronic kidney disease was estimated using abbreviated Modification of Diet in Renal Disease (MDRD4) and Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equations. The association between eTFG <90/mL/min/1,73m² and biosocial data and comorbidities was assessed. Significance level was p<0,05. Results: the study sample was 50,5% male, 64,4% white, 50,7% living with partner, and 58,2±18,6 years-old. Patients with chronic kidney disease differed (p<0,05) from patients without, regarding to: living with partner (59,8% vs 47,3%); older age (65,8±15,6 vs 55,3±18,9 years-old); no smokers (11,1% vs 29,7%); personal history of hypertension (75,2% vs 46,3%), diabetes (49,5% vs 22,4%), dyslipidemia (23,8% vs 14,9%), acute myocardial infarction (14,3% vs 6,0%) and congestive heart failure (18,1% vs 4,3%); occurrence of death (12,4% vs 1,4%); and length of hospitalization (11 (818) vs 9 (612) days), as well as laboratory tests, excepted blood glucose level and lipidemic profile. Logistic regression indicated independent association of chronic kidney disease for the following variables (OR, odds ratio; CI, confidence interval at 95%): age (OR 1,019, CI 1,003-1,036); hypertension (OR 2,032, CI 1,128-3,660), diabetes (OR 2,097, CI 1,232-3,570) and congestive heart failure (OR 2,665, CI 1,173-6,056). Hypertensive patients with and without chronic kidney disease were different (p<0,05) regarding to: living with partner (64,3% vs 50,7%); greater number of continuous-use medication (4,0 (2,05,0) vs 2,0 (0,5 4,0)); no smokers (9,9% vs 25%); personal history of diabetes (53,5% vs 36,4%) and congestive heart failure (19,8% vs 7,0%); use of antihypertensive drugs (79,1% vs 66,4%); insulin therapy (24,4% vs 7,0%); as well as laboratory tests, excepted blood glucose level, lipidemic profile and uric acid. Relevant agreement was shown between eGRF classification by MDRD4 and CKD-EPI equations for patients without kidney disease (kappa 0,854). According to MDRD4 equation, 54,4% had eGRF 90 mL/min/1,73m²; 37,7%, eGFR 60-89 mL/min/1,73m²; and 7,8%, eGFR <60 mL/min/1,73m². Patients with eGFR <90 mL/min/1,73m² stood out (p<0,05) from those with eGFR 90 mL/min/1,73m² as presenting higher frequencies of hypertension (63,3% vs 32,0%), diabetes (29,7% vs 16,3%) and dyslipidemia (24,2% vs 7,2%). Conclusion: chronic kidney disease showed association with cardiovascular risk factors, most of which modifiable.

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Singh, Dhruvaraj Kailashnath. "Clinical studies in diabetic vasculopathy to assess interactions between blood, bone and kidney." Thesis, University of Hertfordshire, 2010. http://hdl.handle.net/2299/4186.

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Diabetic vasculopathy (DV) is the most important consequence of chronic hyperglycemia in patients with diabetes mellitus (DM). This thesis explores the interaction of blood, bone and kidney in the pathogenesis of DV by i) reviewing the current understanding of pathogenesis of macrovascular and microvascular diseases in DM to identify gaps in literature and generate hypotheses relating to various facets of DV ii) undertaking a series of prospective studies to examine these hypotheses iii) analysing the findings and integrating any new information obtained from the clinical studies into the current knowledge base and iv) generating hypotheses upon which future work might be based. The literature search was carried out with the aim of understanding current concepts of pathogenesis of DV and its potential modulators. The original reviews resulting from this process are presented in chapters 2 to 4. A series of pilot studies reported in chapters 7 to 11, were then carried out to interrogate hypotheses originating from this process. The first study was carried out in healthy individuals to define the biological variation of potential modulators of DV, namely erythropoietin (EPO), parathyroid hormone, 25 hydroxyvitamin D and 1, 25-dihydroxyvitamin D to facilitate the design and interpretation of subsequent studies. It revealed a wide biological variation of these modulators in the healthy population thus,emphasizing the need to have a control group in the subsequent study population. To examine whether tubulointerstitial dysfunction occurs before the onset of microalbuminuria, a measurement of the above mentioned parameters was carried out along with markers of tubulointerstitial injury in patients with type 1 and type 2 DM without microalbuminuria and in non-diabetic controls. It was found that tubulointerstitial dysfunction with low levels of EPO and 1, 25-dihydroxyvitamin D and higher excretion of tubular injury markers, occurs before the onset of microalbuminuria. Subsequently, diabetic and nondiabetic chronic kidney disease (CKD) patients with EPO deficiency anaemia were examined to study the effects of EPO therapy on the excretion of tubular injury markers. However, in these patient groups, we were unable to demonstrate an effect of EPO therapy on the markers of tubular injury in spite of a beneficial haematological response. To examine whether vascular calcification (VC) and bone mineral density (BMD) were linked in patients with diabetes mellitus and to explore their relationship to modulators of DV, an assessment of VC and BMD was undertaken in patients with type 2 DM with different degrees of proteinuria and normoalbuminuria. VC was assessed by CT scan and BMD by a DEXA scan. Modulators of DV were measured including serum Osteoprotegerin (OPG) and receptor activator of nuclear factor kappa-b-ligand (RANKL). The findings were i) a high prevalence of VC and osteopenia in normoalbuminuric type 2 DM patients with normal serum creatinine ii) a weak inverse relationship between VC and osteopenia iii) proteinuric patients had worse VC but not osteopenia iv) weak relationships between OPG levels and both VC and osteopenia, masked by age in multivariate analysis. The final study examined the relationship between modulators of DV, including OPG and RANKL, and the degree of CKD. It was found that abnormalities of OPG and RANKL occur before the onset of microalbuminuria and progress with deterioration of renal function. Compared to nondiabetics, DM patients have higher OPG levels in the predialysis phase and lower levels in haemodialysis phase, a phenomenon that might indicate endothelial exhaustion in dialysis patients with DM. The derangements associated with DV seem to occur earlier than previously thought. Further work is required to untangle these complexities and to define the contribution of factors such as the adverse blood milieu, the vasculature, abnormal bone and mineral metabolism, and early tubulointerstitial damage. The findings from the studies reported here may help in the formulation of new hypotheses, which might contribute to future work in this area.

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Cheddani, Lynda. "Comparaison du risque cardiovasculaire et de la mortalité entre patients transplantés rénaux et malades rénaux chroniques à fonction rénale équivalente. Uremic Toxins and Clinical Outcomes: The Impact of Kidney Transplantation Higher mortality risk among kidney transplant recipients than among estimated glomerular filtration rate-matched patients with CKD – preliminary results Less arterial stiffness in kidney transplant recipients than chronic kidney disease patients matched for renal function." Thesis, université Paris-Saclay, 2021. http://www.theses.fr/2021UPASR006.

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La maladie rénale chronique(MRC) s’associe à un très haut risque cardiovasculaire(CV), et les maladies CV représentent après greffe une des principales causes de décès avec greffon fonctionnel. Le débit de filtration glomérulaire(DFG) influe sur le risque CV. L’objectif de ce travail était de comparer pour la 1ère fois patients MRC et transplantés rénaux(TR) à même niveau de DFG sur 1) le risque de mortalité; 2) le niveau de rigidité aortique (évaluée par la vitesse de l’onde de pouls carotido-fémorale, CF-VOP). Le 3ème objectif visait à comparer l’évolution de la pression pulsée (PP) selon le devenir rénal (dialyse ou transplantation rénale préemptive, TRP) des patients MRC inscrits préemptivement sur liste de greffe. Méthodes. Ce travail est basé sur l’analyse de plusieurs cohortes. Pour l’objectif 1, les données étaient issues de CKD-REIN et DIVAT. CKD-REIN est une cohorte prospective réalisée dans 40 consultations de néphrologie en France, incluant 3033 patients avec MRC modérée à sévère. Le registre DIVAT recense prospectivement les données de patients transplantés de 8 centres français, notre étude concernait le registre nantais. L’objectif 2 était étudié au sein d’une partie de la cohorte prospective parisienne NephroTEST de patients MRC adressés pour bilan standardisé au service des Explorations Fonctionnelles de l’Hôpital Tenon (Paris), et de la cohorte rétrospective TransplanTEST de patients TR également évalués dans ce service (168 patients TR à l’Hôpital Foch-Suresnes). Pour ces objectifs, les patients TR et MRC étaient appariés sur un score de propension qui incluait notamment le DFG. Le 3ème objectif concernait les patients de CKD-REIN inscrits préemptivement sur liste de greffe: le niveau de PP et son évolution étaient comparés selon le type de suppléance rénale (SR) initié au cours du suivi (dialyse ou TRP). Résultats. Dans notre 1ère étude, la TR était associée à une augmentation du risque de mortalité relativement aux patients MRC appariés (HR: 2,6[1,54- 4,56], p=0,001 après ajustement sur l’âge, le DFG et le ratio protide/creatinine urinaire). L’augmentation du risque apparaissait davantage liée à une fréquence accrue des infections sévères et cancers qu’à une augmentation du risque CV. Il n’a pas été mis en évidence de différence concernant le risque de survenue de ≥ 1 événement CV non létal au cours du suivi (HR : 0,8[0,44-1,50], p=0,501). Dans la 2ème étude, les patients TR présentaient à 12 mois de la greffe une CF-VOP significativement plus basse que les patients MRC appariés (10,1m/s vs 11,0m/s, p=0,008), contrairement à l’évaluation réalisée à 3 mois de greffe (10,5m/s vs 11,0m/s, p=0,242). L’amélioration survenant au cours de la 1ère année de greffe conférait aux patients TR évalués à 12 mois un moindre niveau de rigidité aortique relativement aux patients MRC de même DFG. Après ajustement sur l’âge, la pression artérielle moyenne, le DFG mesuré, l’indice de masse corporelle, le statut diabétique et le niveau de PTH sérique, la TR s’associait à une réduction de 60% du risque de CF-VOP>10,6m/s (médiane) à 12 mois de la greffe (OR: 0,4[0,23-0,68]). Enfin, les résultats (préliminaires) de notre 3ème étude n’ont pas retrouvé d’association entre le type de SR et les modalités d’évolution de la PP au cours des 6 mois suivant l’initiation, chez les patients inscrits préemptivement sur liste de greffe. La dégradation du DFG dans l’année précédant la SR était plus rapide dans le groupe ayant évolué vers la dialyse (à étiologies de MRC comparables). Conclusion. Nos résultats confortent l’idée qu’une remise à zéro du risque de mortalité et d’événement CV des patients MRC n’est pas rendu possible, même après TR, de même qu’un retour au niveau d’un patient MRC comparable. Les complications CV post TR apparaissent différer de celles des patients MRC de même DFG. Les stratégies de prévention et de ralentissement de la progression de la MRC doivent par conséquent constituer une priorité en néphrologie Chronic kidney disease (CKD) is associated with a very high cardiovascular (CV) risk, and CV disease is one of the main causes of death with a functioning transplant after kidney transplantation. Glomerular filtration rate (GFR) influences CV risk. The objective of this work was to compare for the first time CKD-patients and renal transplant recipients (RTR) with similar GFR level: 1) on the risk of overall mortality; 2) on aortic stiffness level (assessed by carotid-femoral pulse wave velocity, CF-PWV), a CV risk biomarker. The third objective was to compare pulse pressure (PP) and its evolution according to renal replacement therapy modality (dialysis or preemptive renal transplantation, PRT) in CKD patients pre-emptively registered on the kidney transplant waiting list.Methods. This work is based on the analysis of several cohorts. For the first objective, data came from CKD-REIN and DIVAT. CKD-REIN is a French prospective cohort performed in 40 nephrology consultations, including 3033 patients with moderate to severe CKD. The DIVAT register prospectively collects data of transplant recipients from 8 French centers, our study focused on the Nantes’ register. The second objective was studied in part of the prospective Parisian NephroTEST cohort of CKD-patients who were referred to the Physiology Unit of Tenon Hospital (Paris) for a one-day standardized evaluation, and of the RTR TransplanTEST cohort (retrospective cohort of 168 TR patients at Foch Hospital-Suresnes) evaluated in the same Physiology Unit. For these two objectives, RTR and CKD-patients were matched on a propensity score which included GFR among others. For the third objective, CKD-REIN patients who were pre-emptively registered on the kidney transplant waiting list were compared on PP level and on its evolution, according to the renal replacement therapy (RRT) modality initiated during the follow-up (dialysis or PRT). Results. In our first study, RTR was associated with an increased risk of overall mortality relative to the matched CKD-patients (HR: 2.6 [1.54-4.56], p=0.001 after adjusting for age, GFR and protide/creatinine urinary ratio). The increased risk appeared to be more related to an increased frequency of severe infections and neoplasms than to an increased CV risk. There was no difference between the two groups concerning the occurrence of at least one non-fatal CV event during the follow-up (HR: 0.8 [0.44-1.50], p=0.501). On the other hand, in the second study, RTR presented a significantly lower CF-PWV at 12-months after kidney transplant than the CKD-matched patients (10.1m/s vs 11.0m/s, p=0.008), unlike the evaluation performed at 3 months post-transplant (10.5m/s vs 11.0m/s, p=0.242). The improvement occurring within the 1st year of RT conferred to RTR assessed at 12 months a lower aortic stiffness level in comparison to the CKD-matched patients with similar GFR. After adjustment for age, mean arterial pressure, measured GFR, body mass index, diabetic status and serum PTH level, RT was associated with a 60% reduction in the risk of CF-VOP > 10.6m/s (median) at 12 months after RT (OR: 0.4 [0.23-0.68]). Finally, our latest (preliminary) results (third study) did not find any association between the RRT modality and PP evolution within the 6 months following RRT initiation in patients who were pre-emptively registered on the kidney transplant waiting list. The GFR decline in the year prior to RRT initiation was faster in-group of patients who initiate dialysis (with comparable CKD etiologies). Conclusion. Our results support the idea that, RT does not offset the excess mortality risk observed in CKD patients. At the same level of GFR, post-TR CV complications appear to be different from CV complications in CKD patients. Therefore, we believe that prevention and slowing CKD progression strategies must remain a priority in nephrology

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Magalhães, Andréa Olivares. "Papel do fósforo e do paratormônio na progressão da doença renal crônica." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/5/5148/tde-04042008-142314/.

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Introdução: Os mecanismos envolvidos na progressão da doença renal crônica (DRC) independentemente de sua etiologia, não estão totalmente esclarecidos. O controle do fósforo(P) sérico é uma meta essencial a ser alcançada no tratamento de pacientes com DRC. Inicialmente, a importância deste controle era atribuída a participação do P na patogênese do hiperparatireoidismo secundário. Atualmente sabe-se que a hiperfosfatemia aumenta a mortalidade desses pacientes. Distúrbios do metabolismo mineral participam da progressão da DRC, porém os mecanismos envolvidos na fisiopatologia, não foram esclarecidos. Objetivo: Avaliar o efeito isolado da sobrecarga de P e de diferentes concentrações de paratormônio (PTH) na progressão da doença renal em ratos urêmicos. Materiais e métodos: Ratos Wistar machos adultos foram submetidos à paratireoidectomia (PTX) e nefrectomia 5/6 (NX), a seguir implantamos mini bombas osmóticas com diferentes concentrações de PTH ou veículo. Realizamos 2 experimentos. Experimento 1: Animais que receberam dietas com diferentes conteúdos de P (1,2% ou 0,2% dieta rica e pobre respectivamente).Estes animais receberam infusão fisiológica de PTH (1-34 rat PTH 0,022/100g/h). No experimento 2, os animais receberam as mesmas dietas porém infusão elevada de PTH (1-34 rat PTH 0,11/100g/h). Os animais controles (grupo controle e sham) foram os mesmos para os dois experimentos. A alimentação dos animais foi controlada por pair feeding e a pressão arterial caudal (PAC) foi aferida semanalmente. Após 8 semanas os animais foram sacrificados.Creatinina corrigida por peso, P, cálcio,PTH e hematócrito foram analisados. No tecido renal quantificamos a fibrose intersticial (FI), esclerose glomerular(EG) e o número de células apoptóticas. Avaliamos, no tecido renal a expressão de ED-1, alfa-actina, angiotensina II e TGF-beta. Resultados: Animais NX que receberam infusão fisiológica de PTH e dieta rica em P desenvolveram mais FI, EG, e maior expressão de ED-1. Os animais que receberam infusão elevada de PTH apresentaram maiores níveis tensionais. Foi demonstrado uma correlação entre os marcadores inflamatórios (TGF-beta e Angio II) confirmando a associação entre estes fatores no processo de fibrogênese. O número de células apoptóticas foi maior nos grupos NX que receberam PTH em concentração elevada. Conclusão: Neste estudo, a sobrecarga de P atuou na progressão da DRC ativando principalmente vias inflamatórias e o excesso de PTH agiu piorando a hipertensão arterial. Introduction: The mechanisms involved in the progression of chronic kidney disease (CKD), regardless of its etiology, have yet to be well elucidated. Serum phosphorus control is an essential target to be achieved in the treatment of patients with CKD. Initially, the importance of this control was attributed to the participation of phosphorus (P) in the pathogenesis of secondary hyperparathyroidism. It is currently known that hyperphosphatemia increases mortality in these patients. Disturbances of the mineral metabolism participate in the progression of CKD; however, the mechanisms involved in pathophysiology remain unclear. Objective: To evaluate the isolated effect of phosphorus overload and different PTH concentrations in the progression of kidney disease in uremic rats. Materials and methods: Adult male Wistar rats were submitted to parathyroidectomy and nephrectomy 5/6; subsequently, we implanted mini osmotic pumps with different concentrations of PTH or vehicle. We carried out 2 experiments. Experiment 1: Animals who received diets with different P contents (1.2% or 0.2% rich and poor diet, respectively). These animals received infusion of PTH solution (1-34 rat PTH 0.022/100g/h). In experiment 2, the animals received the same diets; however, with high PTH infusion (1-34 rat PTH 0.11/100g/h). Control animals (control group and sham) were the same for both experiments. Food intake of the animals was controlled by pair feeding, and caudal artery pressure (CAP) was measured weekly. After 8 weeks, the animals were sacrificed. Creatinine, phosphorus, calcium, PTH and hematocrit were analyzed. Interstitial fibrosis (IF), glomerular sclerosis (GS), and number of apoptotic cells were quantified in the renal tissue. ED-1 expression, alfa-actin, angiotensin II and TGF-beta were evaluated in the renal tissue, as well. Results: NX animals that received infusion of PTH solution and P-rich diet developed more IF and GS, and greater ED-1 expression. The animals that received high PTH infusion presented higher tensional levels. A correlation was demonstrated between inflammatory markers (TGF-beta and Angio II) confirming the association between these factors in the fibrogenesis process. The number of apoptotic cells was higher in NX groups that received PTH in high concentration. Conclusion: In this study, phosphorus overload acted in the progression of CKD activating inflammatory pathways; in addition, excess PTH worsened arterial hypertension.

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Kaboré, Jean. "Hypertension artérielle résistante et maladie rénale chronique : déterminants et risques associés." Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS265/document.

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Hypertension artérielle résistante et maladie rénale chronique : Déterminants et risques associésL’hypertension résistante, définie par une pression artérielle au-dessus de la cible en dépit de la prise de trois antihypertenseurs à dose optimale dont un diurétique, est fréquemment associée à la maladie rénale chronique (MRC). Sa prévalence, ses déterminants et l’impact potentiel de la MRC sur son pronostic à long terme sont mal connus, notamment chez le sujet âgé. Dans l’étude des 3 cités, incluant 4262 personnes de plus de 65 ans traitées pour hypertension, la prévalence de l’hypertension apparemment résistante (HTAR) - la notion de traitement à dose optimale étant inconnue - était de 11,8% vs 5,2% chez ceux avec vs sans MRC (définie par une fonction rénale < 60 mL/min/1.73 m2). Nous avons montré que l’apparition d’une HTAR était plus fortement liée à la rapidité du déclin annuel de la fonction rénale qu’à son niveau, indépendamment des autres facteurs de risque : obésité, diabète, sexe masculin, antécédent cardiovasculaire. Comparé au groupe de référence (avec hypertension contrôlée et sans MRC), les personnes avec une HTAR et une MRC n’avaient pas de risque significativement plus élevé de mortalité toute cause, mais avaient deux fois plus de risque d’accident vasculaire cérébral (AVC), létal ou non, et de récurrence d’un AVC ou d’un événement coronaire, et trois fois plus de décès coronaire. Cependant, l’’hypothèse d’un effet aggravant de la MRC sur le pronostic de l’HTAR n’a pas été confirmé (interaction non significative).Dans la cohorte CKD-REIN, incluant plus de 3000 patients avec une MRC modérée ou avancée suivis en néphrologie (âge moyen, 70 ans, 60% d’hommes), nos résultats préliminaires montrent une prévalence élevée d’HTAR, 36,7%, et plusieurs facteurs de risque potentiellement modifiables : adhérence médiocre au traitement, absence de diurétique, consommation de sel en excès, obésité.Dans l’ensemble, ces travaux montrent l’importance de la MRC dans le développement de l’HTAR et des risques cardiovasculaires associés, et suggère des moyens de prévention au-delà des traitements médicamenteux Resistant hypertension and chronic kidney disease: Determinants and outcomesResistant hypertension defined as blood pressure above goal despite simultaneous use of 3 antihypertensive classes at optimal doses including a diuretic, is commonly associated with chronic kidney disease (CKD). Resistant hypertension prevalence and determinants, and the impact of CKD on its long term outcomes are poorly known, particularly in the elderly population.In the 3 Cities cohort, including 4262 community-dwelling elderly individuals, aged 65 years or older treated for hypertension, the prevalence of apparent treatment resistant hypertension (aTRH) – because of lack of information on optimal treatment dose – was 11.8% vs 5.2% in those with vs without CKD (defined as estimated glomerular filtration rate < 60 mL/min/1.73 m2). We showed that new-onset aTRH was more strongly related to the speed of kidney function decline than kidney function level itself, independent of other risk factors: male sex, obesity, diabetes, and history of cardiovascular disease. Compared to the reference group (with controlled hypertension and no CKD), participants with aTRH and CKD had no significantly higher risk of all-cause mortality, but had a risk of fatal or non-fatal stroke and of recurrent stroke or coronary events more than twice as high, and of coronary death more than three times higher. However, the hypothesis that CKD may worsen the prognosis of aTRH was not confirmed (no significant interaction).In the CKDREIN cohort, which included more than 3000 nephrology outpatients with moderate or severe CKD (mean age, 70 years, 60% of men), our preliminary results showed a high prevalence of aTRH, 36,7% and several potentially modifiable risk factors : poor treatment adherence, lack of diuretic use, excess salt intake and obesity.Overall, this work shows the importance of CKD in the development of aTRH and associated cardiovascular outcomes, and suggests means for prevention beyond drug therapy

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Boubred, Farid. "Conséquences vasculaires et rénales à long terme de la restriction de croissance intra-utérine et de la nutrition postnatale chez le rat." Thesis, Aix-Marseille 2, 2010. http://www.theses.fr/2010AIX20693.

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Le faible poids de naissance et/ou une accélération de la croissance pondérale durant l’enfance sont reconnus actuellement comme facteur de risque de maladies cardiovasculaires (hypertension artérielle, en particulier). Leur rôle dans la progression des maladies rénales chroniques de l’adulte est moins évident. Cette association entre un faible poids de naissance et un risque accru d’hypertension artérielle (HTA) à l’âge adulte ferait intervenir une réduction du nombre de néphrons. Ce déficit néphronique, associé au faible poids de naissance, est responsable d’une hyperfiltration glomérulaire au sein de chaque néphron. Ce mécanisme adaptatif entraîne au fil du temps des lésions rénales, une protéinurie, une insuffisance rénale chronique et une véritable hypertension artérielle. Mais l’hypothèse pathogénique du déficit néphronique reste discutable. De plus peu l’influence de la nutrition postnatale précoce a été très peu étudiée chez l’animal. A travers 2 modèles de restriction de croissance intra-utérine (RCIU) chez le rat, nous avons montré que, plus que la RCIU elle-même, le devenir vasculaire et rénal chez le rat RCIU dépend de la sévérité du déficit néphronique. Un déficit néphronique modéré n’est pas suffisant pour affecter à long terme les fonctions/structures vasculaires et rénales chez le rat RCIU obtenu par une restriction protéique maternelle modérée (caséine 9 %)Nous avons également validé un modèle de rattrapage pondéral précoce, chez le rat. Nous avons montré qu’un rattrapage pondéral et/ou une croissance exagérée durant la période néonatale jouent un rôle primordial sur la pression artérielle, les fonctions et la structure rénale à l’âge adulte. Ces paramètres étaient d’autant plus affectés que la suralimentation néonatale était associé à une RCIU. Les maladies vasculaires et rénales résulteraient, en grande partie, d’une inadéquation entre le nombre de néphrons, réduit lors d’un faible poids de naissance, et la nutrition néonatale/postnatale, surabondante.Chez l’homme, la mise en place de nouvelles cohortes est nécessaire afin de mieux comprendre le rôle de la nutrition durant différentes phases de croissance (fœtale, néonatale, enfance et adolescence) dans le développement des maladies chroniques de l’adulte. Ces études devraient évaluer la pertinence de marqueurs précoces, et permettre la mise en œuvre de stratégies préventives précoces nutritionnelles ou médicamenteuses chez les personnes les plus à risques Evidence suggest that low birth weight and/or postnatal catch-up growth increase the risk for long term cardiovascular diseases (hypertension especially). Their role on the progression of chronic kidney disease is less evident. The mechanism is incompletely known. Nephron number deficit, associated with low birth weight, may play an important role. In such a condition, an adaptative single nephron glomerular hyperfiltration to meet excretory demands may lead overtime to renal damages. However this hypothesis is still questionable.In the rat, through two experimental models of intrauterine growth restriction (IUGR), we have shown that adverse long term vascular and renal functions are highly dependent on the severity of nephron number deficit. Moreover, we have demonstrated that a rapid neonatal catch-up growth plays a determinant role. Neonatal overfeeding and a high protein diet following IUGR accelerate the expression of hypertension and the progression of chronic kidney disease. Long term vascular and renal diseases may thus result from a mismatch between adverse fetal environment and postnatal beneficial environment. In human prospective epidemiological studies are needed with the aim to evaluate the effect of postnatal nutrition and to determine early markers for future preventive studies

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Boucquemont, Julie. "Modèles statistiques pour l'étude de la progression de la maladie rénale chronique." Thesis, Bordeaux, 2014. http://www.theses.fr/2014BORD0411/document.

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Cette thèse avait pour but d'illustrer l'intérêt de méthodes statistiques avancées lorsqu'on s'in téresse aux associations entre différents facteurs et la progression de la maladie rénale chronique (MRC). Dans un premier temps, une revue de la littérature a été effectuée alin d'identifier les méthodes classiquement utilisées pour étudier les facteurs de progression de la MRC ; leurs limites et des méthodes permettant de mieux prendre en compte ces limites ont été discutées. Notre second travail s'est concentré sur les analyses de données de survie et la prise en compte de la censure par intervalle, qui survient lorsque l'évènement d'intérêt est la progression vers un stade spécifique de la MRC, et le risque compétitif avec le décès. Une comparaison entre des modèles de survie standards et le modêle illness-death pour données censurées par intervalle nous a permis d'illustrer l'impact de la modélisation choisie sur les estimations à la fois des effets des facteurs de risque et des probabilités d'évènements, à partir des données de la cohorte NephroTest. Les autres travaux ont porté sur les analyses de données longitudinales de la fonction rénale. Nous avons illustré l'intérêt du modèle linéaire mixte dans ce contexte et présenté son extension pour la prise en compte de sous-populations de trajectoires de la fonction rénale différentes. Nous avons ainsi identifier cinq classes, dont une avec un déclin très rapide et une autre avec une amélioration de la fonction rénale au cours du temps. Des perspectives de travaux liés à la prédiction permettent enfin de lier les deux types d'analyses présentées dans la thèse The objective of this thesis was to illustrate the benefit of using advanced statistical methods to study associations between risk factors and chrouic kidney disease (CKD) progression. In a first time, we conducted a literature review of statistical methods used to investigate risk factors of CKD progression, identified important methodological issues, and discussed solutions. In our sec ond work, we focused on survival analyses and issues with interval-censoring, which occurs when the event of interest is the progression to a specifie CKD stage, and competing risk with death. A comparison between standard survival models and the illness-death mode! for interval-censored data allowed us to illustrate the impact of modeling on the estimates of both the effects of risk factors and the probabilities of events, using data from the NephroTest cohort. Other works fo cused on analysis of longitudinal data on renal function. We illustrated the interest of linear mixed mode! in this context and presented its extension to account for sub-populations with different trajectories of renal function. We identified five classes, including one with a strong decline and one with an improvement of renal function over time. Severa! perspectives on predictions bind the two types of analyses presented in this thesis

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Canale, Daniele. "Mecanismos de lesão renal em ratos com deficiência de vitamina D submetidos ao tratamento com Tenofovir." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/5/5148/tde-06062014-100748/.

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A Síndrome da Imunodeficiência Adquirida (AIDS) é um problema de saúde pública. O Tenofovir Disoproxil Fumarato (TDF) foi o primeiro inibidor do nucleotídeo da transcriptase reversa e é a droga mais recomendada para o tratamento da AIDS. Entretanto, o uso prolongado de TDF está associado com a nefrotoxicidade. A deficiência de vitamina D tem alta prevalência em indivíduos infectados com o Vírus da Imunodeficiência Humana (HIV). A vitamina D participa da regulação de atividades fisiológicas de diversos órgãos, incluindo o rim, oferecendo proteção contra as lesões ocasionadas por diferentes causas. Portanto, pacientes com níveis baixos de vitamina D infectados com o HIV podem apresentar complicações renais e cardiovasculares durante a terapia antirretroviral. Sendo assim, a carência desta vitamina pode acelerar a progressão da doença renal. Tendo em vista o aumento da incidência de hipovitaminose D na população mundial, esse trabalho tem o objetivo de verificar os mecanismos que levam ao desenvolvimento da lesão renal em ratos depletados de vitamina D submetidos ao tratamento com TDF. Ratos Wistar foram divididos em quatro grupos: controle, animais que receberam dieta padrão por 60 dias; dVD, animais que receberam dieta depletada em vitamina D por 60 dias; TDF, animais que receberam dieta padrão por 60 dias com a adição de TDF (50 mg/kg de dieta) nos últimos 30 dias; e dVD+TDF, animais que receberam dieta depletada em vitamina D por 60 dias com a adição de TDF nos últimos 30 dias. Ao final dos 60 dias, os animais foram submetidos à eutanásia, amostras de sangue, urina e o tecido renal foram coletados para a análise dos mecanismos de lesão renal. O tratamento com TDF levou a insuficiência renal observada pela queda da filtração glomerular e lesão tubular proximal com aparecimento de fosfatúria ocasionada pela diminuição do cotransportador sódio/fosfato subtipo IIa. Essas alterações foram acompanhadas de hipertensão e modificações no perfil lipídico. A deficiência em vitamina D associada à administração de TDF agravou os efeitos renovasculares e a nefrotoxicidade induzida pelo TDF, pelo menos em parte, devido ao aumento nos marcadores de estresse oxidativo e a participação do sistema renina-angiotensina-aldosterona. Portanto, é essencial monitorar os níveis de vitamina D em pacientes infectados com o HIV tratados com TDF Acquired Immunodeficiency Syndrome (AIDS) has become one of the world\'s most serious health problem. Tenofovir Disoproxil Fumarate (TDF) was the first available nucleotidic reverse transcription inhibitor and is a widely prescribed antiretroviral medication for treatment of Human Immunodeficiency Virus (HIV). However, the long-term use of TDF has been associated with a number of toxicities, including those affecting the kidney. Vitamin D deficiency is prevalent among HIVinfected individuals. Vitamin D not only regulates numerous physiological activities of multiple organ systems, but also protects the kidney from injury from different causes. Thus, HIV-infected subjects with low levels of vitamin D could experience increased complications during antiretroviral therapy, such as cardiovascular disease and renal impairment. In view of the high worldwide incidence of hypovitaminosis D, the aim of this study was to investigate the effects of vitamin D deficiency on TDF-induced nephrotoxicity. Wistar rats were divided into four groups: control, receiving a standard diet for 60 days; dVD, receiving a vitamin D-free diet for 60 days; TDF, receiving a standard diet for 60 days with the addition of TDF (50 mg/kg food) for the last 30 days; and dVD+TDF receiving a vitamin D-free diet for 60 days with the addition of TDF for the last 30 days. At the end of the protocol, animals were euthanized and blood, urine and tissue samples were collected in order to evaluate the mechanisms responsible for renal injury. TDF led to impaired renal function, hyperphosphaturia, hypophosphatemia, hypertension and increased renal vascular resistance due to downregulation of the sodium-phosphorus cotransporter and upregulation of reninangiotensin- aldosterone system (RAAS). TDF also increased oxidative stress, as evidenced by higher TBARS and lower GSH levels, and induced dyslipidemia. Association of TDF and vitamin D deficiency aggravated renovascular effects and TDFinduced nephrotoxicity at least in part by the increase of oxidative stress and the involvement of RAAS. Hence, it is important to monitor vitamin D levels in HIV-infected patients treated with TDF

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"The association of various HLA-A, -B and -DR loci with membranous glomerulonephritis, IgA nephropathy, and focal segmental glomerulosclerosis in KwaZulu-Natal renal patients." Thesis, 2007. http://hdl.handle.net/10413/1789.

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This KwaZulu-Natal (KZN) based study investigates hypertension, glomerulonephritides and the rarity of IgA Nephropathy (IgAN) in Africans in association with the Human Leukocyte Antigen (HLA). A retrospective hypertensive study found a positive association with HLA-B40 (P c<0.05) and HLA-B15 (Pc<0.02) in Indians and Africans respectively. No association was found in Whites. A prospective study showed glomerulonephritides to be positively associated with HLA-A33 in Indians (Pc 0.049). No associations were found with glomerulonephritides in Africans and Whites. Combined Race groups show no HLA associations. HLA-A30; HLA-A34; HLA-A29; HLA-B42; HLA-B58; HLA-B70 and HLA-DR11 were extremely significantly higher in Africans compared to Indians and Whites (all P<0.0001). In conclusion, HLA-B40 and I 1LA-B15 are possible disease susceptibility markers in Indian and African hypertensives; HLA-A33 is a possible disease susceptibility marker for glomerulonephritides in Indians and alleles in linkage might be responsible for the rarity of IgAN in Africans but further studies need to be employed. Thesis (M.Med)-University of KwaZulu-Natal, 2007.

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Wootton, Andrew. "The glomerular basement membrane and nephritis." 1986. http://web4.library.adelaide.edu.au/theses/09PH/09phw918.pdf.

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41

Sivaskandarajah, Gavasker. "Role of Vascular Endothelial Growth Factor-A in Diabetic Kidney Disease." Thesis, 2011. http://hdl.handle.net/1807/29625.

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Vascular endothelial growth factor-A (VEGF) is required for endothelial cell differentiation and survival. To investigate the renoprotective properties of VEGF in diabetes an inducible Cre-loxP gene targeting system was used to excise VEGF from podocytes of adult mice (VEGFKO). Diabetes was induced by streptozotocin (STZ) at 2.5 weeks of age and VEGFKO was induced by doxycycline (dox) at 3-4 weeks of age. Blood and urine were collected weekly to monitor for hyperglycaemia and proteinuria, respectively. Mice were dissected 8 weeks after diabetes induction or earlier if morbidly ill; twenty percent of the mice in the DM+VEGFKO group died before the surrogate endpoint. Glomerular VEGF mRNA expression was decreased in VEGFKO mice compared to controls. However, DM+VEGFKO mice had significantly greater proteinuria, degrees of glomerular sclerosis, and glomerular cell apoptosis. These results confirm that VEGF is normally upregulated in diabetes but reducing VEGF expression in diabetes causes severe kidney injury.

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Belghasem, Mostafa. "Pathological and molecular profiling in hypertension-induced glomerular injury." Thesis, 2015. https://hdl.handle.net/2144/13940.

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The increased prevalence of chronic kidney disease (CKD) has become a major global health burden. This increase in CKD burden parallels the increase in hypertension prevalence. In addition, increasing evidence suggest that genetics play a strong role in the susceptibility for renal disease. Inbred mouse strains C57BL/6 and 129S6SvEv differ in their susceptibility to kidney disease when subjected to hypertension using the DOCA/salt uninephrectomy model of hypertension. Similar to others, we found the 129S6SvEv mice to be susceptible to develop severe glomerulosclerosis, whereas the C57BL/6 mice are comparatively resistant. To identify new candidate genes that are involved in the pathogenesis of glomerular disease, we used microarray technology to compare the glomerular transcriptome of both strains and determine changes in glomerular gene expression when subjected to the DOCA/salt uninephrectomy model of systemic hypertension. This approach was accompanied with ultrastructural analysis and glomerular stiffness measurements to identify corresponding structural changes. Here, we have identified novel genes associated with strain differences and hypertension, and we used immunohistochemistry to validate their expression in podocytes and glomerular arterioles in murine and human kidneys. The increased understanding of the molecular mechanisms underlying hypertension-associated podocyte injury and glomerular damage which will result from these studies, will ultimately lead to identification of novel pharmacologic targets or therapeutic strategies for patients with hypertension and renal disease. 2017-11-02T00:00:00Z

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Bondzie, Philip Apraku. "New insights into the molecular regulation of kidney disease: contributions of APOL1 and MYH9." Thesis, 2014. https://hdl.handle.net/2144/15338.

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People of African ancestry (AA) are at greater risk of developing chronic kidney disease than those of non-AA. Much of this risk has been linked to specific genetic haplotypes on chromosome 22, near the genes APOL1, encoding apolipoprotein L1, and MYH9, encoding non-muscle myosin heavy chain IIA (NMHCIIA). The mechanisms by which the disease-associated chromosome 22 haplotypes promote kidney damage are unknown. Apolipoprotein L1 is a circulating protein with no known role in kidney function. However, the kidney disease-associated chromosome 22 haplotypes are protective against trypanosome infection, resulting in positive selective pressure for these haplotypes in western Africa, where trypanosome infection is endemic. In contrast, NMHCIIA may have an important role in glomerular function, and mutations in MYH9 are associated with glomerular disease, yet the disease-associated chromosome 22 haplotypes do not involve coding sequence variations in MYH9. With no clear disease-causing role for genes near the chromosome 22 risk locus, it is plausible that indirect mechanisms of gene regulation may be responsible for the increased disease risk. This study examines several potential pathways for kidney injury, including altered glomerular gene expression in carriers of chromosome 22 risk haplotypes, and the role of altered expression of MYH9 in podocyte cell biology and kidney disease. We found that carriers of chromosome 22 risk variants exhibited differential glomerular gene expression in pathways promoting kidney injury. We also found decreased glomerular NMHCIIA expression in human FSGS kidney biopsies, and altered cell structure and mechanical function when Myh9 is ablated in murine podocytes. Further, Myh9 podocyte deletion predisposed mice to glomerulopathy in response to injury by the DOCA-salt uninephrectomy model of hypertension. Taken together, these findings demonstrate direct and indirect effects of chromosome 22 risk variants on glomerular gene expression which promote kidney injury.

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Naudin, Crystal. "The tetraspanin CD151’s role in the kidney and mapping of genetic modifiers of glomerular disease." Thesis, 2015. http://hdl.handle.net/1959.13/1305765.

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Research Doctorate - Doctor of Philosophy (PhD) Glomerular diseases represent a major burden for both patients and the community. They are responsible for a significant proportion of chronic kidney disease, which can ultimately progress to end stage renal disease, requiring dialysis or transplantation. Glomerular diseases are associated with leakage of proteins across the glomerular filtration barrier into the primary urine (proteinuria or albuminuria – as albumin is the major protein involved). The glomerular filtration barrier is composed of three interconnected layers: podocyte foot processes, the glomerular basement membrane (GBM) and a fenestrated endothelium. The tetraspanin protein CD151 is a crucial component of the glomerular filtration barrier, where it is known to complex with integrins to strengthen podocyte foot process anchorage to the GBM. In addition, previous findings in our laboratory have shown that in FVB/N Cd151-/- mice the disruption and abnormal development of the GBM precedes podocyte foot process abnormalities, suggesting that CD151 also plays a role in the maturation and remodelling of the GBM. In other settings CD151 has been shown to regulate the proteolytic activity of matrix metalloproteinases (MMPs), important players in the homeostasis of basement membranes, and thus CD151 has many potential roles in glomerular homeostasis and disease. Similar to human mutation, Cd151 knockout in the FVB/N mouse strain leads to severe early-onset glomerular disease associated with GBM abnormalities, whereas knockout in the C57Bl/6 mouse strain does not lead to glomerular disease with kidneys presenting healthy. This strong influence of genetic background suggests the action of modifier genes, which may have important roles in human kidney disease where the course of glomerular diseases can vary significantly between patients. It is therefore important to identify the genes modulating progression as they could be used as biomarkers to predict the course of these heterogeneous diseases in patients or as potential therapeutic targets. In order to understand the molecular mechanisms contributing to progression and onset of glomerular disease in FVB/N Cd151-/- mice, whole genome mRNA expression profiles of glomeruli from Cd151+/+ and Cd151-/- mice were investigated on both the C57Bl/6 and FVB/N backgrounds. Analysis was conducted at 3 weeks of age, at this stage in FVB/N Cd151-/- mice changes to the GBM are evident but secondary changes such as glomerulosclerosis are not yet significant or widespread, and therefore allows the identification of genes relevant to early stage disease. The FVB/N Cd151-/- mouse glomeruli showed 24 highly significant transcript changes compared to FVB/N Cd151+/+, including changes in transcription factors, inflammatory factors and extracellular matrix regulators. Many of these changes did not occur in the corresponding comparison in the C57Bl/6 strain (Cd151-/- versus Cd151+/+) and therefore are likely specific to glomerular disease development. Following on from identified changes in transcript expression of MMPs, it was found that the proteolytic activities of pro-MMP-9, MMP-9 and MMP-2 were reduced in FVB/N Cd151-/- glomeruli compared to FVB/N Cd151+/+, C57Bl/6 Cd151+/+ and C57Bl/6 Cd151-/- mice. Furthermore the protein expression of MMP-10 was upregulated specifically in FVB/N Cd151-/- glomeruli. Therefore the GBM defects observed in FVB/N Cd151-/- mice may be due to reduced turnover of basement membrane proteins by MMPs in FVB/N Cd151-/- mice. Eleven pathways were enriched specifically in FVB/N Cd151-/- mice, including robust changes in two cellular signalling gene networks: the T-cell receptor signalling network and the axon guidance network. Firstly, this suggests that the development of glomerular disease in this mouse model may have immune involvement. Secondly this finding supports recent parallels that have been drawn between the signalling molecules involved in elongation and adhesion signalling of podocyte processes and axonal dendrites. Overall the loss of CD151 significantly affects the expression of molecules likely to influence inflammatory signalling in the glomerulus, and cytoskeletal organisation within podocyte foot processes. Mindin, an inflammatory mediator, was significantly and specifically induced in the GBM of FVB/N Cd151-/- mice, as detected by immunofluorescence and was also observed in the urine of these mice by immunoblotting. The functions of mindin have not been investigated in the kidney; however, as it is known to be pro-inflammatory, the potential for mindin to be pathologically contributing to disease progression was investigated. Inflammatory infiltrates including lymphocytes, neutrophils, macrophages and eosinophils, were observed as early as 3 weeks of age in FVB/N Cd151-/- but not in FVB/N Cd151+/+, C57Bl/6 Cd151+/+ and C57Bl/6 Cd151-/- mice. This infiltration was progressive and more pronounced in 12 week old FVB/N Cd151-/- mice, which had developed extensive inflammatory lesions. It can be speculated therefore that mindin is involved in recruiting inflammatory cells into kidneys of FVB/N Cd151-/- mice early in disease, which may then contribute to disease progression. As FVB/N Cd151-/- mice show severe early onset glomerular disease compared to C57Bl/6 Cd151-/- mice, which show a healthy kidney phenotype, this model lends itself to the identification of quantitative trait loci (QTL) influencing glomerular disease development. Therefore, a backcross of the resistant line (C57Bl/6) for two generations onto the permissive line (FVB/N) was carried out. F1 Cd151-/- mice (FVB/N × C57Bl/6) show complete absence of glomerular disease, suggesting that the protective alleles from the C57Bl/6 background are dominant. N2 (F1 x FVB/N) Cd151-/- mice were found to have a highly variable kidney phenotype, with 68% developing albuminuria. Analysis of age at onset of albuminuria in N2 mice showed that there were three statistically distinct groups: no onset (followed up to 12 months of age), early onset (<2 months of age) and late onset (3-4 months of age). Linkage analysis identified 2 regions that account for >50% of the variability in inheritance of the trait. Specifically inheritance of an FVB/N homozygous genotype at a chromosome 14 QTL (45.34cM - 46.34cM) was strongly associated with early onset albuminuria. This region includes only 1 gene, protocadherin 9, which is known to be expressed in human foetal kidney tissue, suggesting a role in kidney development. Taken together, the data suggests that protocadherin 9 represents a modifier gene influencing glomerular phenotype in the absence of CD151. A second linked region on chromosome 1 (40.859cM-44.046cM) also strongly influenced the development of glomerular disease, with susceptibility associating with heterozygosity. Within this region 22 genes, including GBM proteins collagen IV chains α3 and α4 are located. The genetic modifiers responsible for influencing glomerular phenotype in the absence of CD151 in the two QTL regions remain undefined; however, protocadherin 9 and the collagen IV chains α3 and α4 represent likely candidate modifier genes, and require further investigation. To further assess the relationship between genetic background and disease severity and progression, a multiple-trait analysis was performed using albuminuria, GBM defects, creatinine clearance and serum urea as quantitative traits. Using this approach a further 13 QTLs were identified which relate to Cd151-/- glomerular disease progression and severity. Several of the mapped QTLs demonstrated concordance with previously identified QTLs for rodent models of glomerular disease, and concordance with a human locus influencing diabetic nephropathy. In conclusion this is the first reported comprehensive analysis of gene expression changes as well as QTLs in the Cd151-/- model of glomerular disease. The study has identified a number of genes and proteins that likely contribute to disease onset or progression which now require further investigation to determine their function in human kidney diseases.

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Hsu, Chung-Pang, and 許仲邦. "To evaluate the prediction of cardiovascular diseases hospitalizations, incident dialysis, and mortality by different estimated glomerular filtration rate equations in patients with chronic kidney diseases." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/94028671939221198480.

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碩士 高雄醫學大學 醫學研究所 100 Background: Chronic kidney disease (CKD) has been considered as a global public health problem in the world. The definition of CKD is based on criteria of proteinuria and level of glomerular filtration rate (GFR). Simplified MDRD equation for estimating GFR is most commonly used in clinics. It is not guaranteed that applying the equation to Taiwanese would not result in bias for GFR. Therefore, Taiwanese MDRD equation and Taiwan-intercept equation had been proved more accurate estimation for GFR. However, the performance of predicting risk through estimated GFR (eGFR) by using these equations was not well evaluated. The aim of the study is to compare the performance of models to predict adverse outcomes (cardiovascular disease hospitalization, dialysis and mortality) in different eGFR that were calculated by various equations. Materials and methods: Patients, who had CKD and joined an integrated care program from Dec. 2002 through May. 2008 in one medical center, southern Taiwan, were included to this study. We used simplified MDRD equation, CKD-EPI equation, Taiwanese MDRD equation and Taiwan-intercept equation to estimate various GFR at baseline. We followed up occurrence of cardiovascular diseases hospitalization, dialysis, and mortality to 2008. Cox proportion hazard model was used to estimate the risk of adverse outcomes. We used the statistical value regarding goodness of fit, calibration, and reclassification of models to identify the performance of risk prediction. All statistical analyses were performed by SPSS 19.0 and p<0.005 is considered as statistically significant. Results: Totally, 2,181 patients were included into the study. After excluding the patients joining the integrated care program less than 3 months (n=454), 1,727 patients were followed up regularly. In general, eGFR that were calculated by CKD-EPI equation, Taiwanese MDRD equation and Taiwan-intercept equation respectively provide significant worse risk perdition for dialysis than eGFR that was calculated by simplified MDRD equation. On the contrast, eGFR that was calculated by CKD-EPI equation has significant better reclassification of risk perdition for mortality than simplified MDRD equation. Furthermore, in elderly, female, and diabetes mellitus groups, the eGFR that were calculated by Taiwanese MDRD equation and Taiwan-intercept equation had significant better performance of risk predictions for dialysis than simplified MDRD equation. Conclusion: Taiwanese MDRD equation and Taiwan-intercept equation provide a better risk predicting models for dialysis in old age, female, and diabetes mellitus groups. Our findings need more large-scale studies to further confirm.

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Graça, Ana Beatriz Nunes. "Proteinúria na doença renal crónica: fisiopatologia e valor prognóstico." Master's thesis, 2020. http://hdl.handle.net/10316/97872.

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Trabalho Final do Mestrado Integrado em Medicina apresentado à Faculdade de Medicina A doença renal crónica (DRC) é muito prevalente na população geral e classifica-se de acordo com a sua causa, taxa de filtração glomerular e severidade da proteinúria. O papel da proteinúria no desenvolvimento e progressão da DRC tem sido amplamente estudado e têm-se observado alterações das guidelines internacionais relativas à sua classificação, diagnóstico e tratamento. Vários autores propõem que a proteinúria apresenta mecanismos fisiopatológicos que não só influenciam a progressão da DRC como também têm impacto em comorbilidades intrinsecamente associadas à DRC. O objetivo desta revisão foi reunir dados relevantes e atuais que apoiem o papel da proteinúria na fisiopatologia da DRC, hipertensão, diabetes e patologia cardiovascular, bem como do seu papel como fator de progressão da DRC. Também revimos as mais recentes recomendações de tratamento destas comorbilidades em doentes com proteinúria, com base em guidelines de sociedades internacionais. Tem sido demonstrado que a proteinúria tem um papel relevante na fisiopatologia da DRC e que se associa a progressão mais rápida para DRC-5 e maior risco cardiovascular. Em doentes hipertensos, tem-se verificado que a proteinúria se associa a pior controlo tensional e progressão mais acelerada da DRC. Foi também provado que doentes diabéticos com proteinúria são mais suscetíveis a progredir para DRC-5 e que têm maior risco de eventos cardiovasculares, quando comparados com doentes renais crónicos não diabéticos. A proteinúria é também um fator de risco independente para o desenvolvimento de insuficiência cardíaca, doença coronária e enfarte agudo do miocárdio. Relativamente ao tratamento, o papel de fármacos inibidores do sistema renina-angiotensina-aldosterona é bem aceite e amplamente recomendado, enquanto que outras terapêuticas são mais controversas. Apesar de vastamente estudada, a utilização da proteinúria como fator prognóstico na avaliação do risco para doença coronária na DRC está mais estabelecida para nefrologistas do que para a restante comunidade médica. É importante uma compreensão aprofundada da fisiopatologia e intercomunicação entre a DRC, proteinúria e outcomes relevantes de forma a compreender o seu impacto real na morbimortalidade dos doentes e promover o desenvolvimento de novos fármacos melhorem os resultados clínicos nesta população. Chronic kidney disease (CKD) is very prevalent in the general population and is classified according to its cause, glomerular filtration rate and proteinuria severity. The role of proteinuria in the development and progression of CKD has been largely studied and there have been changes in the classification, diagnosis and treatment guidelines from international societies. It has been proposed that proteinuria has specific pathophysiological mechanisms that influence the progression of CKD as well as a major impact in comorbidities intrinsically associated with CKD. The goal of this review was to gather state of the art data supporting the role of proteinuria in the pathophysiological development of CKD, hypertension, diabetes and cardiovascular disease, in addition to its role as a prognostic factor for the progression of CKD. We have also reviewed the most recent recommendations on the treatment of these comorbidities in patients with proteinuria, regarding international society guidelines. It has been demonstrated that proteinuria plays an important role in the pathophysiology of CKD and it has been associated with faster progression to CKD-5 and increased cardiovascular risk. In hypertensive patients, proteinuria is associated with worst tensional control and progression of the renal disease. It has also been proven that CKD patients with diabetes and proteinuria were more prone to progress to CKD-5 and were at higher risk of cardiovascular events than non-diabetic CKD patients. Proteinuria is also an independent risk factor for the development of heart failure, coronary artery disease and myocardial infarction. Regarding treatment, the role of drugs that inhibit renin angiotensin system is well accepted and widely recommended but other therapies are more controversial. Despite being extensively studied, the use proteinuria as a prognostic factor in the risk evaluation of CKD patients for coronary artery disease is more established for nephrologists than for the rest of the medical community. It is important to deeply understand the pathophysiology and the link between CKD, proteinuria and major outcomes in order to understand the real impact in morbimortality and develop new drugs to improve patients results.

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Lourenço, Rute Sofia Sargaço. "Relatório de Estágio e Monografia intitulada “A influência das fórmulas da TFG no ajuste de dose em doentes com insuficiência renal"." Master's thesis, 2020. http://hdl.handle.net/10316/93016.

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Relatório de Estágio do Mestrado Integrado em Ciências Farmacêuticas apresentado à Faculdade de Farmácia This work is the culmination of the internship report and monograph.I had the opportunity to do two curricular internships, one in Community Pharmacy and the other in Pharmaceutical Industry, which proved to be an asset for my professional training.In the internship reports, a retrospective evaluation is performed, through a SWOT analysis (Strengths; Weaknesses;Opportunities; Theats). This analysis made it possible to identify the internal factors that contributed to my learning, namely, the positive factors that are called Strenghts and the internal factors that proved to be an obstacle or impaired my performance, these are the Weaknesses.This tool also allows the identification of positive external factors, namely, those factors which contribute to my potential professional growth, Opportunities and negative external factors, which can compromise my growth, are therefore called Theats.In the monograph, the topic “The influence of GFR formulas on dose adjustment in patients with renal failure” was addressed.Chronic Kidney pathology is becoming increasingly predominant, being associated with highmorbidity and mortality.In these patients it is necessary estimate glomerular filtration rate (GFR) in order to obtainclinical references and dose adjustments proper to their renal function.There are several formulas (Cockroft and Gault, Modification of Diet in Renal Disease,Chronic Kidney Disease - Epidemiology Collaboration, Berlin Initiative Study) that should beselected taking into account the specific characteristics of each patient.This study aimed to assess the agreement between the different equations and their impactboth on the disease's staging and on dosage adjustment.In this study, were included 50 patients and the TFR was estimated using three equations (CG,MDRD and CKD-EPI). The agreement between the equations, between the patientclassification, and the necessary changes in the dose adjustment of the drugs were analysed.Mainly, different equations lead to different GFR estimates, that lead to different staging of the degree of kidney injury.However, in relation to dose adjustment, the results show high correspondence. Este trabalho é o culminar dos relatórios de estágio e da monografia.Tive a oportunidade de realizar dois estágios curriculares, um em Farmácia Comunitária e outro em Indústria Farmacêutica, o que se revelou uma mais-valia para a minha formação profissional. Pois desta forma contactei com duas realidades bem diferentes o que permitiu um enriquecimento da minha formação.Nos relatórios de estágio é realizada uma avaliação retrospetiva, através de uma análise SWOT (Strengths; Weaknesses;Opportunities; Theats). Esta análise permitiu identificar os fatores internos que contribuíram para a minha aprendizagem, ou seja, os fatores positivos que são designadas de Strenghts (Pontos Fortes) e os fatores internos que se mostraram um obstáculo ou prejudicaram o meu desempenho, são estes as Weaknesses (Pontos Fracos). Esta ferramenta permite também identificar os fatores externos positivos, isto é, os que contribuem para o meu potencial crescimento a nível profissional, as Opportunities (Oportunidades) e os fatores externos negativos, aqueles que podem comprometer o meu crescimento, são por isso designados de Theats (Ameaças).Na monografia foi abordado o tema “A influência das fórmulas da TFG no ajuste de dose em doentes com insuficiência renal”.A Doença Renal Crónica é uma patologia cada vez mais prevalente, estando associada a elevadamorbilidade e mortalidade. Nestes doentes é necessário calcular uma estimativa da taxa defiltração glomerular (TFG) de forma a obter recomendações clínicas e ajustes de doseadequadas à sua função renal. Para isso existem várias fórmulas (Cockroft e Gault, Modificationof Diet in Renal Disease, Chronic Kidney Disease - Epidemiology Collaboration, Berlin Initiative Study) que devem ser selecionadas tendo em conta as características específicas de cada doente.Este trabalho teve como finalidade avaliar a concordância entre as diferentes fórmulas e o seuimpacto tanto no estadiamento da doença como no ajuste de dose.Neste estudo foram incluídos 50 doentes internados e a TFG foi estimada utilizando 3 fórmulas(CG, MDRD e CKD-EPI), foi analisada a concordância entre as fórmulas, entre a classificaçãodo doente, e analisadas as alterações necessárias no ajuste de dose dos medicamentos.Em geral, diferentes fórmulas levam a diferentes estimativas de TFG que conduzem a diferentesestadiamentos do grau de Lesão Renal. No entanto em relação ao ajuste de dose os resultadossugerem elevada concordância.

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Snaith, Beverly, Martine A. Harris, B. Shinkins, M. Jordaan, M. Messenger, and A. Lewington. "Point-of-care creatinine testing for kidney function measurement prior to contrast-enhanced diagnostic imaging: evaluation of the performance of three systems for clinical utility." 2018. http://hdl.handle.net/10454/15685.

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Yes Acute kidney injury (AKI) can occur rarely in patients exposed to iodinated contrast and result in contrast-induced AKI (CI-AKI). A key risk factor is the presence of pre-existing chronic kidney disease (CKD), therefore it is important to assess patient risk and obtain kidney function measurement prior to administration. Point of care (PoC) testing provides an alternative strategy but there remains uncertainty, with respect to diagnostic accuracy and clinical utility. A device study compared three PoC analysers (Nova StatSensor, Abbott i-STAT, Radiometer ABL800 FLEX) with a reference laboratory standard (Roche Cobas 8000 series, enzymatic creatinine). Three hundred adult patients attending a UK hospital phlebotomy department were recruited to have additional blood samples for analysis on the PoC devices. The ABL800 FLEX had the strongest concordance with laboratory measured serum creatinine (mean bias=-0.86, 95% limits of agreement = -9.6 to 7.9) followed by the i-STAT (average bias=3.88, 95% limits of agreement = -8.8 to 16.6) and StatSensor (average bias=3.56, 95% limits of agreement = -27.7 to 34.8). In risk classification, the ABL800 FLEX and i-STAT identified all patients with an eGFR≤30, whereas the StatSensor resulted in a small number of missed high-risk cases (n=4/13) and also operated outside of the established performance goals. The screening of patients at risk of CI-AKI may be feasible with PoC technology. However in this study it was identified that the analyser concordance with the laboratory reference varies. It is proposed that further research exploring PoC implementation in imaging department pathways is needed. Yorkshire and Humber Academic Health Science Network (Grant Number: YHP0318)

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Spieker, Christine. "Die Bedeutung der glomerulären Basalmembrankomponente Nidogen-1 bei podozytären Erkrankungen der Niere." Doctoral thesis, 2017. http://hdl.handle.net/11858/00-1735-0000-0023-3E54-4.

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Tesi sul tema "Kidney glomerulus Diseases"

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