Готові списки джерел за темами / Uremia

Добірка наукової літератури з теми "Uremia"

Автор: Grafiati
Опубліковано: 4 червня 2021
Оновлено: 9 березня 2023

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Статті в журналах з теми "Uremia":

1

Bakkour, Z., D. Laouari, S. Dautrey, J. P. Yvert, and C. Kleinknecht. "Accelerated glycogenolysis in uremia and under sucrose feeding: role of phosphorylase alpha regulators." American Journal of Physiology-Endocrinology and Metabolism 273, no. 1 (July 1, 1997): E17—E27. http://dx.doi.org/10.1152/ajpendo.1997.273.1.e17.

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To understand the mechanism of hepatic glycogen depletion found in uremia and under sucrose feeding, we examined net hepatic glycogenolysis-associated active enzymes and metabolites during fasting. Liver was taken 2, 7, and 18 h after food removal in uremic and pair-fed control rats fed either a sucrose or cornstarch diet for 21 days. Other uremic and control rats fasted for 18 h were refed a sucrose meal to measure glycogen increment. Glycogen storage in uremia was normal, suggesting effective glycogen synthesis. During a short fast, sucrose feeding and uremia enhanced net glycogenolysis through different but additive mechanisms. Under sucrose feeding, there were high phosphorylase alpha levels associated with hepatic insulin resistance. In uremia, phosphorylase alpha levels were low, but the enzyme was probably activated in vivo by a fall of inhibitors (ATP, alpha-glycerophosphate, fructose-1,6-diphosphate, and glucose) and a rise of Pi, as verified in vitro. Enhanced gluconeogenesis was also suggested, but excessive hepatic glucose production was unlikely in uremia. During fasting, hypoglycemia occurred in uremia due to reduced glycogenolysis, inefficient hepatic gluconeogenesis, and impaired renal gluconeogenesis. This may be relevant to poor fasting tolerance in uremia, which could be aggravated under excessive sucrose intake.
2

Jawale, Chetan V., Kritika Ramani, De-dong Li, Bianca M. Coleman, Rohan S. Oberoi, Saran Kupul, Li Lin, et al. "Restoring glucose uptake rescues neutrophil dysfunction and protects against systemic fungal infection in mouse models of kidney disease." Science Translational Medicine 12, no. 548 (June 17, 2020): eaay5691. http://dx.doi.org/10.1126/scitranslmed.aay5691.

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Disseminated candidiasis caused by the fungus Candida albicans is a major clinical problem in individuals with kidney disease and accompanying uremia; disseminated candidiasis fatality is twice as common in patients with uremia as those with normal kidney function. Many antifungal drugs are nephrotoxic, making treatment of these patients particularly challenging. The underlying basis for this impaired capacity to control infections in uremic individuals is poorly understood. Here, we show in multiple models that uremic mice exhibit an increased susceptibility to systemic fungal infection. Uremia inhibits Glut1-mediated uptake of glucose in neutrophils by causing aberrant activation of GSK3β, resulting in reduced ROS generation and hence impaired killing of C. albicans in mice. Consequently, pharmacological inhibition of GSK3β restored glucose uptake and rescued ROS production and candidacidal function of neutrophils in uremic mice. Similarly, neutrophils isolated from patients with kidney disease and undergoing hemodialysis showed similar defect in the fungal killing activity, a phenotype rescued in the presence of a GSK3β inhibitor. These findings reveal a mechanism of neutrophil dysfunction during uremia and suggest a potentially translatable therapeutic avenue for treatment of disseminated candidiasis.
3

Veldhuis, Johannes D., Ali Iranmanesh, Michael J. Wilkowski, and Eugeniusz Samojlik. "Neuroendocrine alterations in the somatotropic and lactotropic axes in uremic men." European Journal of Endocrinology 131, no. 5 (November 1994): 489–98. http://dx.doi.org/10.1530/eje.0.1310489.

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Veldhuis JD, Iranmanesh A, Wilkowski MJ, Samojlik E. Neuroendocrine alterations in the somatotropic and lactotropic axes in uremic men. Eur J Endocrinol 1994;131:489–98. ISSN 0804–4643 To investigate the pathophysiology of altered growth hormone (GH) and prolactin secretion in endstage renal disease, we sampled blood at 10-min intervals for 24 h and applied deconvolution analysis to calculate hormone half-lives and pulsatile secretion rates. Two-site immunoradiometric assays were employed to quantitate presumptively intact GH and prolactin in nine middle-aged men with chronic renal failure and 14 gender-, age-, body weight- and community-matched controls. We observed that the half-lives of endogenous GH and prolactin were prolonged significantly in uremia: for GH, control 17 ±1.4 versus uremia 21 ±1.3 min (p < 0.05); for prolactin, control 66 ±9.3 versus uremia 112 ± 10 min (p < 0.01). Daily GH secretion rates exceeded sex-, age- and weight-predicted values in eight of nine uremic individuals, while values for prolactin were variable but on average twofold higher in uremia. In both the somatotropic and lactotropic axes, the frequency of secretory bursts was increased significantly (for GH, control 11 ± 1.1 versus uremia 15 ± 0.84 secretory events/24 h; for prolactin, control 20 ± 0.90 versus uremia 27 ± 1.3 pulses/24 h. p < 0.05). Although there were no significant alterations in the mean amplitude, duration or mass of GH secretory bursts, prolactin secretory burst amplitudes were elevated threefold in uremia (p < 0.01). These distinctive mechanisms brought about higher 24-h mean serum concentrations of GH (0.70 ±0.17 control versus 1.22 ± 0.32 μg/l uremia) and prolactin (7.3 ± 2.4 control versus 26 ± 6.1 μg/l uremia, p < 0.05). Lastly, serum concentrations of estradiol were increased but those of unconjugated estriol decreased in uremia. We conclude that hypersomatotropinemia and hyperprolactinemia in uremic men result from prolonged hormone half-lives combined with increased frequencies of secretory events driven by unknown stimuli within the respective axes, and/or by defects in their negative-feedback regulation. We postulate that the latter may arise from partial tissue resistance to hormone action in hemodialyzed men. JD Veldhuis, Division of Endocrinology, Department of Internal Medicine, National Science Foundation Center for Biological Timing, University of Virginia Health Sciences Center, Charlottesville, VA 22908, USA
4

Biswas, Partha Sarathi, Chetan V. Jawale, Kritika Ramani, Bianca Coleman, Rohan S. Oberoi, Saran Kupul, Alexander J. Prokopienko, et al. "Metabolic ‘de-programming’ of neutrophils protects against fatal bloodstream fungal infections during kidney disease." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 82.35. http://dx.doi.org/10.4049/jimmunol.204.supp.82.35.

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Abstract Disseminated candidiasis (DC) is the third most common cause of mortality in hospital acquired infections. Disseminated candidiasis caused by the fungus Candida albicans is a major clinical problem in individuals with kidney disease and accompanying uremia. DC fatality is twice as common in patients with uremia as those without renal impairments. Many antifungal drugs are nephrotoxic, making treatment of these patients challenging. The underlying basis for this impaired capacity to control infections in uremic individuals is poorly understood. Here we show that uremic mice show an increased susceptibility to DC. Uremia inhibits Glucose transporter 1 (Glut1)-mediated uptake of glucose in neutrophils by causing aberrant activation of Glycogen synthase kinase 3 beta (GSK3beta), resulting in reduced ROS generation and hence impaired killing of C. albicans in both mice and human cells. Consequently, pharmacological inhibition of GSK3beta ‘de-programs’ neutrophil function and restores glucose uptake, ROS production and candidacidal activity of neutrophils in uremic mice. These findings reveal a central mechanism of neutrophil dysfunction during uremia and suggest a potentially translatable therapeutic avenue for treatment of DC, with broader implications for other fatal systemic infections.
5

Kuchma, I. L. "Uremic toxins. Back to the future." KIDNEYS 10, no. 2 (July 1, 2021): 78–87. http://dx.doi.org/10.22141/2307-1257.10.2.2021.234323.

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In the review, the author returns to the topic of uremia and uremic toxins, their importance for practitioners in the treatment using renal replacement therapies, gives a modern look at their classification, place during the onset and development of pathological processes in the progression of chronic kidney disease. However, current guidelines and studies for the treatment of chro­nic kidney disease indicate a lack of attention to the role and importance of uremic toxins in the predialysis stages of uremia treatment, in particular to the possible damaging effects of substances retained in the body with reduced glomerular filtration, directly to the renal function. The tables with the list of uremic toxins according to their classification are presented. References are made to the results of clinical and laboratory studies of uremic toxins, their impact on the general clinical picture of uremia and ways of their influence on the progression of chronic kidney disease and the further progression of the clinical picture of uremia. Attention is drawn to the fact that substances recognized as uremic toxins are present in healthy individuals without manifestations of their negative effects, and therefore the opinion is expressed about the need to study the physiological significance of these solvents under normal glomerular filtration. The question arises about the consideration of the factors of uremic toxins impact as a point of application in terms of the progression of chronic kidney disease and the use of this knowledge in renoprotective therapy in the predialysis stages of chronic kidney disease.
6

Popkov, Vasily A., Anastasia A. Zharikova, Evgenia A. Demchenko, Nadezda V. Andrianova, Dmitry B. Zorov, and Egor Y. Plotnikov. "Gut Microbiota as a Source of Uremic Toxins." International Journal of Molecular Sciences 23, no. 1 (January 1, 2022): 483. http://dx.doi.org/10.3390/ijms23010483.

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Uremic retention solutes are the compounds that accumulate in the blood when kidney excretory function is impaired. Some of these compounds are toxic at high concentrations and are usually known as “uremic toxins”. The cumulative detrimental effect of uremic toxins results in numerous health problems and eventually mortality during acute or chronic uremia, especially in end-stage renal disease. More than 100 different solutes increase during uremia; however, the exact origin for most of them is still debatable. There are three main sources for such compounds: exogenous ones are consumed with food, whereas endogenous ones are produced by the host metabolism or by symbiotic microbiota metabolism. In this article, we identify uremic retention solutes presumably of gut microbiota origin. We used database analysis to obtain data on the enzymatic reactions in bacteria and human organisms that potentially yield uremic retention solutes and hence to determine what toxins could be synthesized in bacteria residing in the human gut. We selected biochemical pathways resulting in uremic retention solutes synthesis related to specific bacterial strains and revealed links between toxin concentration in uremia and the proportion of different bacteria species which can synthesize the toxin. The detected bacterial species essential for the synthesis of uremic retention solutes were then verified using the Human Microbiome Project database. Moreover, we defined the relative abundance of human toxin-generating enzymes as well as the possibility of the synthesis of a particular toxin by the human metabolism. Our study presents a novel bioinformatics approach for the elucidation of the origin of both uremic retention solutes and uremic toxins and for searching for the most likely human microbiome producers of toxins that can be targeted and used for the therapy of adverse consequences of uremia.
7

Popkov, Vasily A., Denis N. Silachev, Arthur O. Zalevsky, Dmitry B. Zorov, and Egor Y. Plotnikov. "Mitochondria as a Source and a Target for Uremic Toxins." International Journal of Molecular Sciences 20, no. 12 (June 25, 2019): 3094. http://dx.doi.org/10.3390/ijms20123094.

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Elucidation of molecular and cellular mechanisms of the uremic syndrome is a very challenging task. More than 130 substances are now considered to be “uremic toxins” and represent a very diverse group of molecules. The toxicity of these molecules affects many cellular processes, and expectably, some of them are able to disrupt mitochondrial functioning. However, mitochondria can be the source of uremic toxins as well, as the mitochondrion can be the site of complete synthesis of the toxin, whereas in some scenarios only some enzymes of the pathway of toxin synthesis are localized here. In this review, we discuss the role of mitochondria as both the target and source of pathological processes and toxic compounds during uremia. Our analysis revealed about 30 toxins closely related to mitochondria. Moreover, since mitochondria are key regulators of cellular redox homeostasis, their functioning might directly affect the production of uremic toxins, especially those that are products of oxidation or peroxidation of cellular components, such as aldehydes, advanced glycation end-products, advanced lipoxidation end-products, and reactive carbonyl species. Additionally, as a number of metabolic products can be degraded in the mitochondria, mitochondrial dysfunction would therefore be expected to cause accumulation of such toxins in the organism. Alternatively, many uremic toxins (both made with the participation of mitochondria, and originated from other sources including exogenous) are damaging to mitochondrial components, especially respiratory complexes. As a result, a positive feedback loop emerges, leading to the amplification of the accumulation of uremic solutes. Therefore, uremia leads to the appearance of mitochondria-damaging compounds, and consecutive mitochondrial damage causes a further rise of uremic toxins, whose synthesis is associated with mitochondria. All this makes mitochondrion an important player in the pathogenesis of uremia and draws attention to the possibility of reducing the pathological consequences of uremia by protecting mitochondria and reducing their role in the production of uremic toxins.
8

Guan, Xi, та Shanmai Guo. "Ligustrazine Alleviates Kidney Injury in a Rat Model of Uremia via Attenuation of Wnt/β-Catenin Signaling Pathway". Current Topics in Nutraceutical Research 20, № 4 (6 липня 2022): 698–704. http://dx.doi.org/10.37290/ctnr2641-452x.20:698-704.

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Uremia is associated with kidney injury and contributes to chronic renal failure. Ligustrazine, a bioactive alkaloid from traditional Chinese herb Ligusticum wallichii Franchat, exerts renal-protective effect against acute kidney injury. The role of ligustrazine in uremia-associated kidney injury was investigated. To induce uremia, rats were subjected to 5/6 nephrectomy and intravenously administered with saline. Survival rate of rats was decreased by 5/6 nephrectomy, and levels of blood urea nitrogen, serum creatinine, and 24 h urine protein were elevated. Daily administration of ligustrazine to these rats increased the survival rate and reduced levels of blood urea nitrogen, serum creatinine, and 24 h urine protein output. Moreover, analysis of kidney histology showed that ligustrazine also ameliorated pathological changes in kidney. Finally, ligustrazine reduced levels of proinflammatory cytokines and suppressed renal apoptosis in the kidney tissues of uremic rats. In addition, ligustrazine downregulated protein expression of Wnt1 and β-catenin and inhibited nuclear distribution of β-catenin in uremic rats. In conclusion, ligustrazine protects rats against uremia-associated kidney injury and renal inflammation through inactivation of Wnt1/β-catenin pathway.
9

Zhu, Huiping, Liutong Pan, Yuanting Dai, Dan Zheng, and Shasha Cai. "Role of TLR4/MyD88 Signaling Pathway in the Occurrence and Development of Uremia-Induced Myocardial Hypertrophy and Possible Mechanism." Evidence-Based Complementary and Alternative Medicine 2021 (October 13, 2021): 1–9. http://dx.doi.org/10.1155/2021/7883643.

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The morbidity and mortality of cardiovascular disease (CVD) are relatively high. Studies have shown that most patients with chronic kidney disease (CKD) die from cardiovascular complications. Clinically, the pathophysiological state in which heart disease and kidney disease are causal and influence each other is called cardiorenal syndrome (CRS). Myocardial hypertrophy is the key stage of the heart structure changing from reversible to irreversible. It is an important pathophysiological basis for heart failure. Therefore, this study intends to start with the end-stage uremic phase of CKD to construct an animal model of uremia in rats to study the relationship between uremia, TLR4/MyD88 signaling pathway, and myocardial hypertrophy. The results showed that the uremic rats showed slow weight gain and were thinner. At 12 weeks (w), the serum creatinine and urea nitrogen of the uremic rats increased, and the global hypertrophy index increased. Detecting the expression of Toll-like receptor 4 (TLR4) and myeloid differentiation factor (MyD88) in blood samples of rats, we found that the expression of TLR4 and MyD88 increased at 12 w in the uremia group; pathological observation showed that at 4 weeks of uremia model rats, renal tissue compensatory hypertrophy, renal fibrous membrane proliferation, renal parenchyma atrophy, a large number of fibrous proliferation and inflammatory cell infiltration in the interstitium, and protein casts in the renal tubules were observed. Myocardial cells were obviously hypertrophy and disordered. At 12 w, renal tubules were obviously expanded, the epithelium was flat, the brush border disappeared, and the interstitial fibrous connective tissue of the myocardial tissue was proliferated. The detection of TLR4 and MyD88 in kidney tissue and myocardial tissue revealed that the positive expression of TLR4 and MyD88 gradually increased over time. Therefore, the final result of the study is that uremia can gradually lead to myocardial hypertrophy and TLR4 and MyD88 are highly expressed in serum, kidney, and myocardial tissues of uremic rats, suggesting that TLR4 and MyD88 may be related to the degree of uremic disease and the myocardium caused by it. Hypertrophy is related.
10

Zager, Richard A., Ali C. M. Johnson, and Steve Lund. "Uremia impacts renal inflammatory cytokine gene expression in the setting of experimental acute kidney injury." American Journal of Physiology-Renal Physiology 297, no. 4 (October 2009): F961—F970. http://dx.doi.org/10.1152/ajprenal.00381.2009.

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Inflammatory cytokines are evoked by acute kidney injury (AKI) and may contribute to evolving renal disease. However, the impact of AKI-induced uremia on proinflammatory (e.g., TNF-α, MCP-1, TGF-β1) and anti-inflammatory (e.g., IL-10) cytokine gene expression remains unknown. This study was undertaken to gain some initial insights into this issue. CD-1 mice were subjected to left renal ischemia-reperfusion (I/R) in the absence or presence of uremia (± right ureteral transection). TNF-α, MCP-1, TGF-β1, and IL-10 mRNAs, cytokine protein levels, and RNA polymerase II (Pol II) recruitment to these genes were assessed. Renal cytokine mRNA levels were also contrasted with unilateral vs. bilateral renal parenchymal damage (I/R or ureteral obstruction). Potential effects of uremia on cytokine mRNAs in the absence of parenchymal renal damage [bilateral ureteral transection (BUTx)] were sought. Finally, the impact of simulated in vitro uremia (HK-2 tubular cells exposed to peritoneal dialysate from uremic vs. normal mice) on cytokine mRNA and microRNA profiles was assessed. Uremia blunted TNF-α, MCP-1, and TGF-β1 mRNA increases in all three in vivo parenchymal acute renal failure models. These results were paralleled by reductions in cytokine protein levels and Pol II recruitment to their respective genes. Conversely, uremia increased IL-10 mRNA, both in the presence and absence (BUTx) of parenchymal renal damage. The uremic milieu also suppressed HK-2 cell proinflammatory cytokine mRNA levels and altered the expression of least 69 microRNAs ( P < 0.0001). We conclude that both pro- and anti-inflammatory cytokine gene expressions are influenced by uremia, with a potential predilection toward an anti-inflammatory state. Changes in gene transcription (as reflected by Pol II recruitment), and possible posttranscriptional modifications (known to be induced by microRNAs), are likely involved.
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Статті в журналах Дисертації Книги

Дисертації з теми "Uremia":

1

Vera, Rivera Manel. "Modulación farmacológica de la disfunción endotelial en la uremia." Doctoral thesis, Universitat de Barcelona, 2020. http://hdl.handle.net/10803/669216.

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La enfermedad cardiovascular (CV) es la principal causa de muerte de los pacientes con enfermedad renal crónica terminal (ERCT). Es especialmente llamativa la diferencia que existe, con respecto la población general, en el grupo de pacientes más jóvenes, siendo ésta de hasta 50 veces superior. A pesar de las mejoras técnicas implementadas en diálisis o de las estrategias farmacológicas disponibles, no se ha conseguido reducir la mortalidad de origen CV en este grupo de pacientes. Esta elevada prevalencia de enfermedad CV (en forma de alteraciones microvasculares o macrovasculares -aterosclerosis o arteriosclerosis-) tiene como nexo común la disfunción endotelial (DE), se encuentra agravada en la enfermedad renal crónica (ERC) y se manifiesta presentando un fenotipo proinflamatorio, prooxidante y protrombótico. Esta Tesis Doctoral (TD) plantea la hipótesis de que es posible mejorar la DE presente en la uremia mediante nuevos enfoques de modulación farmacológica a partir de la identificación de nuevas potenciales dianas terapéuticas. Los objetivos son: explorar los efectos de la modulación de distintos sistemas antioxidantes-antiinflamatorios, y la posibilidad de intervención sobre los cambios epigenéticos asociados a la exposición crónica de las células endoteliales (CE) al medio urémico. La metodología se centra en el estudio de los cambios y capacidad de modulación de la DE. Para ello, se ha utilizado un modelo in vitro de cultivo de CE procedentes de venas de cordón umbilical humano (HUVECs), incubadas con suero de pacientes con ERCT en programa de diálisis (diálisis peritoneal o hemodiálisis) y donantes sanos tras la exposición a los distintos compuestos estudiados. Las técnicas utilizadas en el primer trabajo incluyen: inmunofluorescencia para medir la expresión de ICAM-1, técnicas de fluorescencia para la determinación de la generación de radicales libres de oxígeno (ROS), técnicas de ELISA y Western blot para el estudio de la expresión del factor de transcripción NFкB y de la íva p38MAPK y fl uorimetría para la medición de glutatión (GSH). Las técnicas utilizadas en el segundo trabajo incluyen: análisis proteómico para detectar proteínas expresadas de manera diferencial; Western blot e inmunofluorescencia para la cuantificación de la histona desacetilasa (HDAC) tipo 1 (HDAC1) y tipo 2 (HDAC2), y de la vía PI3-kinasa/AKT; inmunofluorescencia para medir la expresión de ICAM-1, Toll Like Receptor 4 (TLR4), factor von Willebrand (FvW) y técnicas de fluorescencia para la determinación de la generación de (ROS). Los resultados del primer trabajo demuestran que la modulación farmacológica de los sistemas antioxidantes, mediante la potenciación de la vía de la glutatión peroxidasa (GPX) inducen una mayor respuesta antioxidante y antiinflamatoria que las estrategias que potencian la vía de la superóxido dismutasa (SOD) o los distintos flavonoides, que obtienen unos resultados parciales. Los resultados del segundo demuestran que el medio urémico induce cambios en la expresión de proteínas a nivel de las CE. Algunos de estos cambios son revertidos por el fármaco defibrotide (DF), con reconocidas propiedades protectoras del endotelio en otros contextos. De las proteínas sobreexpresadas en las CE expuestas al medio urémico y que son normalizadas por el DF destacamos, por su relevancia biológica, HDAC1 y HDAC2. El DF, regulando la sobreexpresión de HDAC1 y HDAC2, logra una mejoría del fenotipo proinflamatorio, protrombótico y prooxidante, y una disminución de la actividad de la inmunidad innata, de las CE expuestas al medio urémico. Así pues, esta TD permite concluir que es posible mejorar la DE presente en la ERC in vitro mediante un abordaje distinto al disponible hasta la fecha, con estrategias que se centren en contrarrestar el entorno prooxidante, así como algunos de los cambios epigenéticos observados en estas CE, abriendo las expectativas de posibles nuevas dianas terapéuticas.
Cardiovascular disease (CV) is the leading cause of death of patients with terminal chronic kidney disease (ERCT). This high prevalence of CV disease (in the form of microvascular or macrovascular alterations - atherosclerosis or arteriosclerosis) has as a common link endothelial dysfunction (ED), is aggravated in chronic kidney disease (CKD) and manifests itself by presenting a proinflammatory, prooxidant and prothrombotic phenotype. This Doctoral Thesis (TD) hypothesizes that it is possible to improve the ED present in uremia through new pharmacological modulation approaches based on the identification of new potential therapeutic targets. The objectives are: to explore the effects of the modulation of different antioxidant-anti-inflammatory systems, and the possibility of intervention on epigenetic changes associated with chronic exposure of endothelial cells (EC) to the uremic environment. he results of the first work show that the pharmacological modulation of antioxidant systems, through the potentiation of the glutathione peroxidase (GPX) pathway, induces a greater antioxidant and anti-inflammatory response than the strategies that enhance the superoxide dismutase (SOD) pathway or the different flavonoids, which obtain partial results. The results of the second show that the uremic medium induces changes in protein expression at the EC level. Some of these changes are reversed by the drug defibrotide (DF), with recognized endothelial protective properties in other contexts. Of the overexpressed proteins in the EC exposed to the uremic environment and which are normalized by the DF, we highlight, due to their biological relevance, HDAC1 and HDAC2. The DF, regulating the overexpression of HDAC1 and HDAC2, achieves an improvement of the proinflammatory, prothrombotic and prooxidant phenotype, and a decrease in the activity of innate immunity, of the EC exposed to the uremic environment. Thus, this TD allows us to conclude that it is possible to improve the ED present in CKD in vitro through a different approach to that available to date, with strategies that focus on counteracting the prooxidant environment, as well as some of the epigenetic changes observed in these CE, opening the expectations of possible new therapeutic targets.
2

Medeiros, Giane Amanda. "Gestação em mulheres em tratamento hemodialítico: repercussões do adoecimento sobre o desejo pela maternidade." Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/5/5148/tde-17022009-110254/.

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A capacidade reprodutiva de mulheres em tratamento dialítico é reduzida devido alterações hormonais, distúrbios de ovulação e menstruais. A gestação neste grupo é considerada rara e de risco. Nas últimas décadas, mudanças no tratamento para insuficiência renal crônica (IRC) resultaram em um aumento da fertilidade. Estudos relatam as possibilidades de sucesso nas gestações neste grupo. Este estudo, de natureza descritiva propôs investigar as informações que as mulheres urêmicas possuem acerca da gestação em mulheres que fazem tratamento hemodialítico, e identificar se a maternidade é desejada por estas mulheres. Utilizou-se como instrumento de coleta de dados: roteiro de entrevista semidirigida; Escala Diagnóstica Adaptativa Operacionalizada EDAO; as pranchas 1, 2, 3MF, 7MF e 16 do Teste de Apercepção Temática TAT. Participaram do estudo 23 mulheres em tratamento hemodialítico, na faixa etária entre 24 e 43 anos. Dezoito entrevistadas têm um ou mais filhos; apenas cinco entrevistadas não têm filhos. Sessenta e cinco por cento das mulheres manifestam desejo em ser mãe novamente. Vimos que há possibilidade de gravidez neste grupo onde 60% das mulheres têm vida sexual ativa, 60% menstruam mensalmente e apenas 52% fazem uso de método contraceptivo. A EDAO revelou que todas as entrevistadas encontram-se com adaptação ineficaz, sendo 18% com adaptação ineficaz leve, 39% com adaptação ineficaz moderada e 43% com adaptação ineficaz severa. As pranchas do TAT revelaram as dificuldades vivenciadas pela dependência à máquina de hemodiálise e quanto o suporte familiar é fundamental para lidar com as limitações pertinentes a condição de doente renal crônico. Os dados da pesquisa indicam que é importante a atenção da equipe de saúde à sexualidade das mulheres em diálise. Também é importante que o diálogo a respeito do planejamento familiar faça parte das intervenções da equipe
The reproductive capacity of women on hemodialysis is reduced because of hormonal changes, ovulation disturbs and menstrual disturbs. Pregnancy to this group is considered rare and risky. In the last two decades, some changes in the treatment to chronic renal disease have resulted in better life quality to patients, including the increase of fertility. Reports have been put on public relating the possibilities of success. This descriptive study has proposed to investigate how much uremic women are informed about pregnancy in their case, and identify if they wish to be pregnant. It was used as data collect: semi directed interview, Operational Adaptative Diagnostic Scale, and the boards 1, 2, 3MF, 7MF and 16 of Thematic Apperception Test TAT. The study included 23 woman with 24 43 age. Eighteen women have at least one child or more, just five of them do not have any children. The results has demonstrated they are not informed about pregnancy and hemodialysis treatment. Most of the women want to be pregnant, including those who have already been. We observed they are able to be pregnant because 60% of them have active sexual life, 60% menstruate monthly and just 52% avoid pregnancy with contraceptive method. Operational Adaptative Diagnostic Scale revealed that every interviewed woman is not adapted to the treatment (all of them considered their adaptation inefficient), 18% light inefficient adaptation, 39% moderated inefficient adaptation, and 43% severe inefficient adaptation. TAT boards revealed difficulties lived by the dependency to the hemodialysis machine, also revealed how much familiar support is important and fundamental to face the pertinent limits to chronic renal disease. The research data indicate it is important to the doctors to be attempted to womens sexuality. And it is also important that dialogue about familiar plan has to happen among the medical group intervention
3

Wolfe, Elizabeth Anne. "The potential applications of microencapsulated urease and zirconium phosphate for the removal of urea in uraemia /." Thesis, McGill University, 1985. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=43587.

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4

Galvão, André Luiz Baptista [UNESP]. "Avaliação clínico-laboratorial de cães com doença renal crônica sob tratamento com o antioxidante N-acetilcisteína." Universidade Estadual Paulista (UNESP), 2010. http://hdl.handle.net/11449/89222.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
O objetivo do presente trabalho foi avaliar os efeitos da n-acetilcisteína (NAC) na função renal, na pressão arterial, no perfil hematológico, hepático e eletrolítico em cães saudáveis e com doença renal crônica. Quatro grupos de cães foram avaliados, grupo normal controle (N-C), grupo normal tratado (N-T), grupo doente renal crônico controle (DRC-C) e grupo doente renal crônico tratado (DRCT). Os grupos N-T e DRC-T foram submetidos ao tratamento com NAC (VO) na dose de 10mg/kg b.i.d, durante 60 dias. Nos grupos N-C e DRC-C não foi realizado qualquer tipo de tratamento. Hemograma, perfil renal, hepático, eletrolítico e pressão arterial sistólica (PAS) foram avaliados previamente, 15, 30, 45 e 60 dias após o tratamento com NAC. A NAC não exerceu qualquer efeito sobre a PAS e o perfil hepático, em nenhum dos grupos estudados (p>0,05). A concentração sérica de uréia e de creatinina do grupo DRC-C (93,42±17,28; 2,52±0,23mg/dL), foi significativamente maior, em relação ao N-C (20,44±3,43; 0,87±0,14mg/dL) e N-T (30,97±1,05; 1,09±0,05mg/dL) (p<0,05). O clereance creatinina do grupo DRC-C (1,13±0,07mL/min/kg) foi significativamente menor, relativamente ao N-C (2,29±0,13mL/min/kg) (p<0.05). O grupo DRC-T apresentou valor de excreção fracionada de sódio (1,19±0,29%) significativamente maior, comparativamente aos grupos N-C (0,25±0,03%) e N-T (0,30±0,08%) (p<0,05). A contagem de hemácias no grupo N-T (7,05±0,48x106/μL) foi significativamente superior, em relação ao grupo DRC-C (5,50±0,11x106/μL) (p<0,05). O grupo N-T apresentou hematócrito (49,44±3,13%) superior ao grupo DRC-C (38,73±1,02%) e DRC-T (43,46±1,42%) (p<0,05). A concentração sérica de sódio no grupo N-T (149±4,99mg/dL) foi superior, em relação ao N-C (141±1,32mg/dL) (p<0,05).
The present study aimed to evaluate the effects of n-acetylcysteine in dogs with chronic kidney disease. To this end, the animals were devided in four groups: healthy control group (H-C), healthy treated group (H-T), control chronic kidney disease (C-CKD), and treated chronic kidney disease (T-CKD). H-T and TCKD groups received 10mg/kg of NAC, PO, q 12h, during 60 days. H-C and TCKD did not receive any treatment. Cell blood count, kidney, hepatic, and electrolytic profile, and systolic blood pressure (SBP) were evaluated previously, 15, 30, 45, and 60 days after treatment with NAC. NAC did not exert any effect on SBP and hepatic profile, in any studied group (P > 0.05). Serum Urea and creatinine values in the group C-CKD (93.42±17.28; 2.52±0.23mg/dL) was significantly higher, in comparison to H-C (20,44±3,43; 0,87±0,14mg/dL) and H-T (30,97±1,05; 1,09±0,05mg/dL) (P < 0.05). Average creatinine clearance of C-CKD group (1.13±0.07 mL/min./kg) was significantly lower than H-C group (2.29±0.13mL/min./kg) (P < 0.05). Excretion fraction of sodium was significantly higher in group T-CKD (1.19±0.29%), than in H-C (0.25±0.03%) and H-T (0.30±0.08%) groups (P < 0.05). Erythrocytes count in the H-T (7.05±0.48x106/μL) increased significantly in comparison to C-CKD (5.50±0.11x106/μL) (P < 0.05). Average hematocrit values changed significantly in the H-T group (49.44±3.13%), when compared to C-CKD (38.73±1.02%) and T-CKD (43.46±1.42%) groups (P < 0.05). Serum sodium concentration in the group H-T (149±4.99mg/dL) increased significantly, when compared to H-C (141±1.32mg/dL) (P < 0.05).
5

Guimarães, Alexandre Costa. "Avaliação do efeito da uremia em diferentes métodos de determinação da A1c em pacientes com e sem Diabetes mellitus." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2015. http://hdl.handle.net/10183/114966.

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O diabetes mellitus (DM) é definido como um conjunto de doenças metabólicas caracterizadas por hiperglicemia e está associada a complicações, disfunções e insuficiência de múltiplos órgãos, especialmente, rins, coração, cérebro, vasos sanguíneos e olhos. A doença renal do diabetes (DRD) é uma das mais relevantes complicações. Nas últimas décadas, a nefropatia diabética se tornou a principal causa da fase final da doença renal no mundo ocidental. Para auxiliar no monitoramento e controle glicêmico dos pacientes com DM existem técnicas laboratoriais que medem as proteínas glicadas, entre elas a hemoglobina glicada (A1c). Um aumento do nível de A1c tem sido relatado em pacientes sem DM com insuficiência renal, independente da glicemia, e apesar do menor tempo de vida dos eritrócitos nestes pacientes. Várias hipóteses foram formuladas para explicar esse fato e de acordo com alguns investigadores, o aumento na A1c em pacientes sem DM com doença renal foi atribuído principalmente à carbamilação de hemoglobina. O estado urêmico pode afetar a acurácia da determinação de A1c, através da modificação da hemoglobina, formando um composto carbamilado que eleva os resultados de A1c nos métodos com base em separação iônica ou HPLC. No entanto existem controvérsias na literatura sobre o efeito da uremia nos níveis de A1c determinados pelos diferentes métodos disponíveis. Apesar disso, A1c é utilizada para o monitoramento da glicemia em pacientes com DRD. Contudo, há necessidade de uma definição se a uremia interfere ou não nos diferentes métodos para dosagem de A1c, visando garantir a qualidade final e interpretação correta dos resultados de A1c em pacientes uremicos, sendo eles diabéticos ou não diabéticos. Neste trabalho avaliamos quatro métodos diferentes de determinação de A1c: equipamento Variant II Turbo – HPLC por troca iônica, Tosoh A1c 2.2 – HPLC por troca iônica, Advia 1800 – Imunoturbidimetria e Capillarys 2 Flex Piercing - Eletroforese capilar. Nossos resultados mostraram que em amostras de pacientes sem DM não há interferência da uremia ou hemoglobina carbamilada, porem em amostras de pacientes com DM, a uremia interfere nos resultados de A1c principalmente em amostras com níveis de A1c mais elevados. Portanto a utilização do teste de A1c no monitoramento da glicose nos pacientes com DM e com uremia deve ser realizada com cautela, pois os métodos avaliados podem superestimar os valores de A1c nesses pacientes.
6

Silveira, Isadora Pereira da. "Epidemiologia, prevalência e distribuição das lesões extrarrenais de uremia em cães." Universidade Federal de Santa Maria, 2015. http://repositorio.ufsm.br/handle/1/10192.

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The kidneys have vital functions to the organism, such as catabolites excretion, maintenance of salt and water concentrations, hormone production, and acid-basic regulation. Retention of nitrogen products of the protein catabolism occurs, with the severe loss of the renal function, a condition called azotemia. Uremia is understood as a condition resulting from prolonged azotemia and is considered an important cause of death in dogs. Aiming to determine the epidemiology, prevalence, and morphological characteristics (including the anatomic localization) of the extrarenal uremic lesions, as well as to determine the main lesions of the urinary system associated to the occurrence of uremia, the protocols of necropsies performed in dogs between January 1996 and December 2012 (17 years) at the Laboratório de Patologia Veterinária of the Universidade Federal de Santa Maria were analyzed. A total of 4,201 dogs were necropsied and 161 (3,8%) had extrarenal uremic lesions. Clinical signs associated to uremia were reported in 134 dogs (83,2%). The extrarenal lesions more often observed, in descending order of prevalence, were: ulcerative and hemorrhagic gastritis (56,5%), soft-tissue mineralization (55,9%), pulmonary edema (47,2%), ulcerative stomatitis and/or glossitis (30,4%), endocarditis/atrial and aortic thrombosis (28,6%), parathyroid hyperplasia (9,3%), fibrous osteodytrophy (8,1%), anemia (6,2%), ulcerative laryngitis (5%), ulcerative and hemorrhagic enteritis (3,7%), fibrinonecrotic esophagitis (1,9%), and fibrinous pericarditis (1,9%). In most of the cases, the extrarenal lesions of uremia were due to prolonged azotemia secondary to severe renal lesions, such as interstitial nephritis and glomerulonephritis (the most prevalent ones).
Os rins exercem funções vitais para o organismo como a excreção de resíduos, manutenção das concentrações de sal e água, produção de hormônios e regulação do equilíbrio ácido-básico. Com a redução severa da função renal, ocorre a retenção de produtos nitrogenados do catabolismo das proteínas, condição denominada de azotemia. A uremia pode ser entendida como uma condição resultante de azotemia prolongada e é uma importante causa de morte em cães. Com o objetivo de determinar a epidemiologia, a prevalência e as características morfológicas, incluindo a localização anatômica, das lesões extrarrenais de uremia, bem como determinar as principais lesões do sistema urinário associadas à ocorrência de uremia, foram revisados os protocolos de necropsias de cães realizadas no Laboratório de Patologia Veterinária da Universidade Federal de Santa Maria entre janeiro de 1996 e dezembro de 2012 (17 anos). Nesse período foram necropsiados um total de 4.201 cães, sendo que 161 (3,8% ) apresentaram lesões extrarrenais de uremia. Em 134 cães (83,2%) foram descritos sinais clínicos associados à uremia. As lesões extrarrenais mais frequentes, em ordem decrescente foram: a gastrite ulcerativa e hemorrágica (56,5%), mineralização de tecidos moles (55,9%), edema pulmonar (47,2%), estomatite e/ou glossite ulcerativa (30,4%), endocardite/trombose atrial e aórtica (28,6%), hiperplasia da paratireoide (9,3%), osteodistrofia fibrosa (8,1%), anemia (6,2%), laringite ulcerativa (5%), enterite ulcerativa/hemorrágica (3,7%), esofagite fibrinonecrótica (1,9%) e pericardite fibrinosa (1.9%). Na maioria dos casos, as lesões extrarrenais de uremia foram decorrentes de azotemia prolongada por lesões renais graves, sendo as mais prevalentes a nefrite intersticial e a glomerulonefrite.
7

Silva, Margarete Mara da. "Aminoácidos plasmáticos e intracelulares em insuficiência renal crônica : aminoácidos em uremia." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2000. http://hdl.handle.net/10183/5755.

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Com o objetivo de investigar o padrão dos aminoácidos plasmáticos e intracelulares em 15 indivíduos normais e em 50 pacientes urêmicos em tratamento conservador, em hemodiálise (HD) e em diálise peritoneal ambulatorial contínua (CAPD) foram obtidas em jejum amostras de sangue venoso e, por biópsia, amostras musculares do músculo quadríceps femoral. Todas as amostras foram analisadas através de cromatografia líquida de alta performance (HPLC). A avaliação nutricional dos indivíduos normais e dos pacientes urêmicos teve por base peso, altura, peso corporal relativo, índice de massa corporal magra e de gordura foram analisadas pela Bioimpedância, albumina sérica, taxa de catabolismo protéico e nitrogênio ureico. Os resultados do estudo demonstraram que, entre os aminoácidos plasmáticos essenciais de cadeia ramificada, a leucina (p=0,006) e a valina (p=0,002) eram baixas nos pacientes urêmicos, principalmente em tratamento conservador. Os outros aminoácidos plasmáticos essenciais: triptofano foi mais baixo nos urêmicos, principalmente em HD (p<0,0001), a tirosina mais baixa nos urêmicos, principalmente, em tratamento conservador (p=0,008) e a metionina mais baixa nos pacientes em HD (p=0,027). Com relação aos aminoácidos plasmáticos não-essenciais, a serina estava mais baixa em todos os pacientes urêmicos, principalmente nos HD (p<0,0001) e a citrulina estava elevada em todos os pacientes urêmicos, principalmente em HD (p=0,036). Quanto aos aminoácidos intracelulares essenciais, a valina (p=0,001) e a leucina (p=0,003) estavam baixas nos pacientes urêmicos, principalmente, em CAPD; já no grupo em tratamento conservador estava baixa a concentração de lisina (p=0,049) e alto a concentração de triptofano (p<0,0001). Com relação aos aminoácidos intracelulares não essenciais, a serina estava baixa em todos os grupos de urêmicos (p=0,008), principalmente em CAPD e a arginina mais elevada, principalmente em HD (p=0,002). mais alta em relação aos demais grupos urêmicos. Em conclusão, nessa população de pacientes urêmicos relativamente bem nutrida, reduções ou elevações significativas de aminoácidos plasmáticos nem sempre foram acompanhados de altos títulos a nível intracelular. Entretanto, valina e leucina estiveram reduzidos nos tres grupos urêmicos tanto a nível plasmático como intracelular. Não foi observada correlação entre o grau de acidose metabólica (concentração de bicarbonato sérico) e as concentrações dos aminoácidos de cadeia ramificada, valina, leucina e isoleucina nos indivíduos urêmicos.
8

Uhlin, Fredrik. "Haemodialysis Treatment Monitored On-line by Ultra Violet Absorbance." Doctoral thesis, Linköping : Linköping University, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-7987.

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9

Coussa, Razek. "Artificial cell live yeast microcapsule formulation for use in renal failure uremia." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111612.

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Renal failure uremia occurs when the kidneys fail to function properly. Despite being the main treatment, dialysis and other therapeutic approaches are not only associated with numerous long-term adverse complications often leading to morbidity and mortality events, but are also not affordable. Orally administrating Alginate-Poly-L-Lysine-Alginate microcapsules entrapping live yeast cells to treat renal failure uremia has not yet been investigated. In this thesis, the growth and microencapsulation of yeast were optimized. The efficacy of these microcapsules in removing unwanted electrolytes was tested in vitro in simulated gastro-intestinal media, in vitro in a column bioreactor and in vivo in an uremic rat model. Results showed that these novel microcapsules can not only maintain morphological stability and membrane integrity under gastro-intestinal environments and mechanical stresses, but also, preserve the viability of yeast. These microcapsules were successful in reducing urea concentrations while not harming the human GI tract's microbial flora.
10

Galvão, André Luiz Baptista. "Avaliação clínico-laboratorial de cães com doença renal crônica sob tratamento com o antioxidante N-acetilcisteína /." Jaboticabal : [s.n.], 2010. http://hdl.handle.net/11449/89222.

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Orientadora: Marileda Bonafim Carvalho
Banca: Luciane Helena Gargaglioni Batalhão
Banca: Angela Akamatsu
Resumo: O objetivo do presente trabalho foi avaliar os efeitos da n-acetilcisteína (NAC) na função renal, na pressão arterial, no perfil hematológico, hepático e eletrolítico em cães saudáveis e com doença renal crônica. Quatro grupos de cães foram avaliados, grupo normal controle (N-C), grupo normal tratado (N-T), grupo doente renal crônico controle (DRC-C) e grupo doente renal crônico tratado (DRCT). Os grupos N-T e DRC-T foram submetidos ao tratamento com NAC (VO) na dose de 10mg/kg b.i.d, durante 60 dias. Nos grupos N-C e DRC-C não foi realizado qualquer tipo de tratamento. Hemograma, perfil renal, hepático, eletrolítico e pressão arterial sistólica (PAS) foram avaliados previamente, 15, 30, 45 e 60 dias após o tratamento com NAC. A NAC não exerceu qualquer efeito sobre a PAS e o perfil hepático, em nenhum dos grupos estudados (p>0,05). A concentração sérica de uréia e de creatinina do grupo DRC-C (93,42±17,28; 2,52±0,23mg/dL), foi significativamente maior, em relação ao N-C (20,44±3,43; 0,87±0,14mg/dL) e N-T (30,97±1,05; 1,09±0,05mg/dL) (p<0,05). O clereance creatinina do grupo DRC-C (1,13±0,07mL/min/kg) foi significativamente menor, relativamente ao N-C (2,29±0,13mL/min/kg) (p<0.05). O grupo DRC-T apresentou valor de excreção fracionada de sódio (1,19±0,29%) significativamente maior, comparativamente aos grupos N-C (0,25±0,03%) e N-T (0,30±0,08%) (p<0,05). A contagem de hemácias no grupo N-T (7,05±0,48x106/μL) foi significativamente superior, em relação ao grupo DRC-C (5,50±0,11x106/μL) (p<0,05). O grupo N-T apresentou hematócrito (49,44±3,13%) superior ao grupo DRC-C (38,73±1,02%) e DRC-T (43,46±1,42%) (p<0,05). A concentração sérica de sódio no grupo N-T (149±4,99mg/dL) foi superior, em relação ao N-C (141±1,32mg/dL) (p<0,05).
Abstract: The present study aimed to evaluate the effects of n-acetylcysteine in dogs with chronic kidney disease. To this end, the animals were devided in four groups: healthy control group (H-C), healthy treated group (H-T), control chronic kidney disease (C-CKD), and treated chronic kidney disease (T-CKD). H-T and TCKD groups received 10mg/kg of NAC, PO, q 12h, during 60 days. H-C and TCKD did not receive any treatment. Cell blood count, kidney, hepatic, and electrolytic profile, and systolic blood pressure (SBP) were evaluated previously, 15, 30, 45, and 60 days after treatment with NAC. NAC did not exert any effect on SBP and hepatic profile, in any studied group (P > 0.05). Serum Urea and creatinine values in the group C-CKD (93.42±17.28; 2.52±0.23mg/dL) was significantly higher, in comparison to H-C (20,44±3,43; 0,87±0,14mg/dL) and H-T (30,97±1,05; 1,09±0,05mg/dL) (P < 0.05). Average creatinine clearance of C-CKD group (1.13±0.07 mL/min./kg) was significantly lower than H-C group (2.29±0.13mL/min./kg) (P < 0.05). Excretion fraction of sodium was significantly higher in group T-CKD (1.19±0.29%), than in H-C (0.25±0.03%) and H-T (0.30±0.08%) groups (P < 0.05). Erythrocytes count in the H-T (7.05±0.48x106/μL) increased significantly in comparison to C-CKD (5.50±0.11x106/μL) (P < 0.05). Average hematocrit values changed significantly in the H-T group (49.44±3.13%), when compared to C-CKD (38.73±1.02%) and T-CKD (43.46±1.42%) groups (P < 0.05). Serum sodium concentration in the group H-T (149±4.99mg/dL) increased significantly, when compared to H-C (141±1.32mg/dL) (P < 0.05).
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Книги з теми "Uremia":

1

Gurland, Hans Jürgen, ed. Uremia Therapy. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-72720-7.

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2

Parfrey, Patrick S., and John D. Harnett, eds. Cardiac Dysfunction in Chronic Uremia. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3902-5.

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3

S, Parfrey Patrick, and Harnett John D, eds. Cardiac dysfunction in chronic uremia. Boston: Kluwer Academic Publishers, 1992.

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4

Ghent Symposium on Uremic Toxins (1986). Uremic toxins. New York: Plenum Press, 1987.

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5

Niwa, Toshimitsu. Uremic toxins. Hoboken, N.J: John Wiley & Sons, 2012.

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6

United States. Agency for Health Care and Policy Research. Laboratory tests in end-stage renal disease patients undergoing dialysis. Rockville, Md: U.S. Dept. of Health and Human Services, Public Health Service, Agency for Health Care Policy and Research, 1994.

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7

Bolton, Charles Francis. Neurological complications of renal disease. Boston: Butterworths, 1990.

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8

European Study Group for the Conservative Management of Chronic Renal Failure. Scientific Meeting. Low-protein diets in renal patients: Composition and absorption. Edited by Gretz N. 1954-, Giovannetti S, and Strauch M. Basel: Karger, 1989.

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9

Int. Symp. on the Heart in End-Stage Renal Failure (1985 Giessen, Hesse, Germany). The heart in end-stage renal failure: Etiology, symptoms, and management of uremic heart disease. Edited by Wizemann V, Kramer W, and Schütterle G. Basel: Karger, 1986.

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10

Ringoir, Severin, Raymond Vanholder, and Shaul G. Massry, eds. Uremic Toxins. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5445-1.

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Частини книг з теми "Uremia":

1

Theisler, Charles. "Uremia/Uremic Syndrome." In Adjuvant Medical Care, 349. New York: CRC Press, 2022. http://dx.doi.org/10.1201/b22898-340.

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2

Brunkhorst, Reinhard. "Uremia." In Urology at a Glance, 57–60. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-54859-8_12.

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3

Rappold, Gudrun, John-John B. Schnog, Victor E. A. Gerdes, Yvonne G. Weber, Jose M. Serratosa, Anna-Elina Lehesjoki, Alessandra Baumer, et al. "Uremia." In Encyclopedia of Molecular Mechanisms of Disease, 2142. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_8130.

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Klinkmann, H., and C. M. Kjellstrand. "Professor Nils Alwall — In Memoriam." In Uremia Therapy, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-72720-7_1.

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Klinkmann, H., D. Falkenhagen, and J. M. Courtney. "Clinical Relevance of Biocompatibility — The Material Cannot Be Divorced from the Device." In Uremia Therapy, 125–40. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-72720-7_10.

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6

Farrell, P. C. "Unrealized Impact of Kinetic Modeling." In Uremia Therapy, 141–53. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-72720-7_11.

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Heptinstall, R. H. "Influence of the Renal Biopsy." In Uremia Therapy, 157–63. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-72720-7_12.

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Peters, D. K. "Immunological Aspects of Renal Medicine." In Uremia Therapy, 164–69. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-72720-7_13.

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9

Schreiner, G. E. "Impact of Artificial Organs on Modern Medicine." In Uremia Therapy, 170–84. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-72720-7_14.

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10

Colton, Clark K. "Technical Foundations of Renal Prostheses." In Uremia Therapy, 187–217. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-72720-7_15.

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Тези доповідей конференцій з теми "Uremia":

1

Ware, J. A., B. A. Clark, M. Smith, and E. W. Salzman. "ABNORMALITIES OF CYTOPLASMIC [Ca++] IN PLATELETS FROM UREMIC PATIENTS STUDIED WITH AEQU0RIN AND INDO-1." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644748.

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Анотація:
Uremic patients have a hemorrhagic tendency, often with prolonged bleeding times and abnormalities of platelet function in vitro. Whether these defects result from plasma factors, abnormalities in platelet surface receptors, or intracellular mediators is unknown. Accordingly, blood was obtained from 16 patients with severe uremia (BUN >90), and platelets were washed, loaded with aequorin or indo-1, gel-filtered, and resuspended in either plasma or buffer. Of the 16 patients, 4 had template bleeding times greater than 12 minutes, but platelet aggregation in plasma was not consistently impaired. However, the rise in cytoplasmic [Ca++] in response to the Ca++-ionophore A23187 or ADP in aequorin-loaded platelets from the 4 patients with long bleeding times was much lower than in uremic patients with normal bleejljLng times or in normal volunteers. The reduced [Ca++] response was associated with decreased aggregation of gel-filtered platelets in buffer. Prolonged bleeding time was less consistently correlated with decreased responses to epinephrine or arachidonate. Suspending washed aequorin-loaded uremic platelets in normal plasma for 10-20 min did not reverse the decreased agonist-induced rise in [Ca++]; platelets from a normal donor resuspended in uremic pla^iya responded normally. The agonist-induced rise in [Ca++] shown by indo-1 was not abnormal in patients with prolonged bleeding times; however, uremic patients generally had higher indo-l-indicated basal platelet cytoplasmic [Ca++] than normal. We conclude that the hemorrhagic tendency in some patients with uremia (|s associated with abnormal intracellular platelet [Ca++] regulation marked by elevated resting [Ca++] and a decreased rise in cytoplasmic [Ca++] in response to certain agonists; this latter abnormality appears to be correlated with prolonged bleeding times.
2

Vigano, G., E. Marchesi, G. Remuzzi, and G. Mecca. "CONJUGATED ESTROGENS (CE) TO REDUCE BLEEDING IN UREMICS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643077.

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Bleeding is a major complication of uremia. Both cryoprecipitate and desmopressin favourably infuence clinical bleeding, but the former carries the risk of transmitting blood-borne infectious diseases and both have a short duration of action. We recently demonstrated in a controlled study that CE effectively shortened bleeding time (BT) (the best available marker of clinical bleeding) in uremics. The effect of CE on BT is long lasting. Thus CE might represent an alternative to cryoprecipitate or desmopressin when long-lasting hemostatic” competence is required. In the present study we followed for two years 6 uremic patients on chronic hemodialysis with severe bleeding tendence, often requiring blood transfusion. In the first year each hemorrhagic episode was treated only with a replacement therapy, while the subsequent year CE infusions (Emopremarin, 0.6 mg/Kg/die for 5 consecutive days) were given after each bleeding episode. The incidence of hemorrhagic episodes/year and the number of blood transfusions/year decreased from 39 to 8 and from 26 to 9 respectively. No side effects of CE have been noted. Results of this study indicate that CE are effective and safe in treating hemorrhages of uremics.
3

Callisesi, G., C. Corsi, and S. Severi. "Computational analysis of uremia effects on ventricular action potential." In 2008 35th Annual Computers in Cardiology Conference. IEEE, 2008. http://dx.doi.org/10.1109/cic.2008.4749218.

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4

Moia, M., S. Casati, P. Della Valle, P. Passerini, C. Ponticelli, and P. M. Mannucci. "HUMAN RECOMBINANT ERYTHROPOIETIN (rHuEpo) CORRECTS ANEMIA AND SHORTENS THE BLEEDING TIME (BT) IN UREMIC PATIENTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644749.

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A hemorrhagic tendency and anemia are two major complications of uremia. There is a significant negative correlation between BT and hematocrit (Ht) in uremic patients. We studied the efficacy of rHuEpo in correcting both these abnormalities in 10 patients on chronic hemodialysis with severe anemia (basal Hb levels 6.2±0.8 g/dL). Seven patients had BT longer than 10 min., 5 had BT longer than 30 min. rHuEpo was given to the patients 3 times a week at increasing doses, from 24 U/Kg to a maximum of 432 U/Kg, aiming to reach Hb levels ⪖12 g/dL. BT was measured (with the template-like disposable device Simplate II) before starting rHuEpo therapy and after reaching the target Hb values. One patient (n° 6) was excluded from the study after 5 weeks of rHuEpo treatment because of development of an arterio-venous fistula thrombosis. The data are shown in the table.Eight of the 9 patients who concluded the study had final BT shorter than 10 min. This demonstrates the efficacy of rHuEpo in correcting both anemia and prolonged BT in uremic patients.
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Lin, Guojian, Qingwei Zeng, Jie Chen, Zefeng Wang, and Jiayuan Tan. "Explanation of uremia from the perspective of traditional Chinese medicine." In 4TH INTERNATIONAL CONFERENCE ON FRONTIERS OF BIOLOGICAL SCIENCES AND ENGINEERING (FBSE 2021). AIP Publishing, 2022. http://dx.doi.org/10.1063/5.0094780.

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Zakaria, El-Rasheid, Magdalini Tsakou, Kirti S. Prabhu, Faheem Sartaj, Asmaa Al-Thani, Shilpa Kuttikrishnan, Ramzi M. Mohammad, Shahab Uddin Khan, and Ashfaq Shuaib. "Molecular and Peritoneal Microvascular Changes Cause Peritoneal Membrane Dysfunction by Uremia-Related Mechanisms." In Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2016. http://dx.doi.org/10.5339/qfarc.2016.hbpp2314.

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7

Lima, Ana Beatriz Marinho Moura, Maria Clara Lino Justino, Graciele Nóbrega Nascimento, Fernando José de Lima Ramos-Júnior, and Deysiane Oliveira Brandão. "ACOMPANHAMENTO DOS MARCADORES UREIA E CREATININIA EM PACIENTES PRÉ E PÓS DIALISE." In I Congresso Brasileiro de Bioquímica Humana On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/667.

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Introdução: Os pacientes que sofrem de insuficiência renal aguda, perdem a capacidade dos seus rins de filtrarem resíduos, sais e líquidos do sangue, trazendo assim desequilíbrio ao organismo. Sendo necessárias sessões de hemodiálise para ajudar o organismo a entrar em equilíbrio fazendo assim a filtragem necessária. É importante a monitorização do paciente em relação a eficiência do tratamento, com acompanhamento nutricional, níveis de ureia e creatinina e demais marcadores. Objetivo: O presente estudo busca realizar um comparativo dos níveis de ureia e creatinina pré e pós diálise em pacientes com insuficiência renal. Material e métodos: Trata-se de uma pesquisa de caráter descritivo, retrospectivo, documental, exploratório, realizado em um laboratório de análises clínicas referência no atendimento a diabéticos na cidade de Campina Grande, Paraíba. Para a pesquisa, foi utilizado o sistema de dados do próprio laboratório, sem possibilidade de identificação individual, onde foram extraídas informações relacionadas a níveis de ureia e creatinina pré e pós diálise durante o período de Janeiro a Dezembro de 2020. Para o tratamento estatístico, foi utilizado o programa Microsoft Office Excel 2016. Resultados: Foram analisados 58 laudos onde a média dos valores de uréia pré dialise foi de 115 mg/dl e pós diálise de 24 mg/dl, observando uma diminuição dos valores característicos dos processos de hemodiálise. Pacientes crônicos com uremia tratada por hemodiálise melhoraram, apesar da manutenção da concentração sanguínea de ureia na faixa de 100 a 200mg/dL. Em relação a média da creatinina pré dialise essa mostrou ser de 9 mg/dl e não houve alteração em relação ao processo pós diálise. Níveis elevados de creatinina se correlacionam com uma baixa mortalidade em pacientes submetidos à hemodiálise, isso porque a taxa de geração de creatinina reflete o tamanho da massa muscular, não sofrendo alteração significativa no processo de diálise. Conclusão: A comparação dos exames de rotina dos pacientes em hemodiálise mostrou que os níveis plasmáticos da creatinina não sofreram alteração após o processo de diálise enquanto os níveis de ureia pré e pós hemodiálise, foram diferentes.
8

Bi, Qingbo, and Shih-Mo Yang. "Detection of Interleukin-6 in the Serum of Uremia Patients Based on Fluorescence Image." In 2022 2nd International Conference on Consumer Electronics and Computer Engineering (ICCECE). IEEE, 2022. http://dx.doi.org/10.1109/iccece54139.2022.9712782.

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Khanal, S., C. Robince, and O. Okorie. "What Hiding Under the Uremia? A Rare Case Presentation and Miraculous Recovery with Clevidipine." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a4263.

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"An Investigation about Level of Awareness of Civil Rights: Case Study Citizens in Uremia- Iran." In Sept. 8-10, 2017 Istanbul (Turkey). URST, 2017. http://dx.doi.org/10.17758/urst.u0917310.

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Звіти організацій з теми "Uremia":

1

Wang, Maohong, and Shifan Yan. Effectiveness and safety of different medicines for Uremia pruritus：A systematic review and network meta-analysis protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2020. http://dx.doi.org/10.37766/inplasy2020.9.0103.

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2

Yang, Xue, Xu Zhang, Ziru Yu, Jin Xian, Changyun Zhang, Xin Zhang, and Huijuan Yu. Effectiveness and safety of acupuncture as a complementary therapy for skin pruritus after uremia hemodialysis: A protocol of systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2021. http://dx.doi.org/10.37766/inplasy2021.11.0112.

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3

Gao, Chao-qing, Jia-jun Zhou, Ya-yin Tan, and Chang-jun Tong. Effectiveness of montelukast for uremic pruritus in hemodialysis patients: A protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2020. http://dx.doi.org/10.37766/inplasy2020.10.0043.

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4

Rossiter, Walter J. Urea-formaldehyde foam insulations :. Gaithersburg, MD: National Bureau of Standards, 1985. http://dx.doi.org/10.6028/nbs.tn.1210.

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5

Wala, Kamila, and Jacek Szepietowski. Difelikefalin in the treatment of chronic kidney disease-associated pruritus: a systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0154.

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Review question / Objective: The objective of this study is to evaluate the clinical efficacy and safety as well as to summarize the current knowledge of difelikefalin in treatment of patients with CKD-aP based on the available clinical trials. Condition being studied: Chronic kidney disease-associated pruritus (CKD-aP), also known as uremic pruritus, is a condition that significantly reduces the quality of life of patients with end-stage renal disease. There were unmet needs in the treatment of this condition. Difelikefalin is a novel opioid agonist with high selectivity for kappa opioid re-ceptors (KOR) that has been shown to be effective in the treatment of this type of chronic pruritus.
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Strey, Daniel J., and Nick E. Christians. Comparison of Polymer-coated Urea Fertilizers. Ames: Iowa State University, Digital Repository, 2014. http://dx.doi.org/10.31274/farmprogressreports-180814-883.

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Ah Mew, Nicholas, Robert McCarter, Rima Izem, Anne Markus, Maya Gerstein, Katie Rice, Jacqueline Sanz, Cynthia Le Mons, Janice Bartos, and Mendel Tuchman. Comparing Treatment Options for Urea Cycle Disorders. Patient-Centered Outcomes Research Institute (PCORI), December 2020. http://dx.doi.org/10.25302/12.20.cer.150227816.

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TRUONG, THANH-TAM. TWO-STEP SYNTHESIS OF POLY (UREA FORMALDEHYDE) MICROCAPSULES. Office of Scientific and Technical Information (OSTI), July 2022. http://dx.doi.org/10.2172/1878530.

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Glass, Robert, and Anh Nguyen-Huu. Urea Sensor Final Report CRADA No. TSB-987-94. Office of Scientific and Technical Information (OSTI), March 2018. http://dx.doi.org/10.2172/1431006.

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Sonder, E., T. C. Quinby, and D. L. Kinser. ZnO varistors made from powders produced utilizing a urea process. Office of Scientific and Technical Information (OSTI), September 1985. http://dx.doi.org/10.2172/5331308.

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