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Journal articles on the topic 'Uremia'
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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.
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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.
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Peroumal, Doureradjou, Chetan V. Jawale, Dani Antos, De-dong Li, Shuxia Wang, John F. Alcorn, and Partha Sarathi Biswas. "Kidney disease impairs B cells response against infection via inhibiting germinal center formation and antibody titers." Journal of Immunology 210, no. 1_Supplement (May 1, 2023): 76.01. http://dx.doi.org/10.4049/jimmunol.210.supp.76.01.
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Abstract Immunity to infections is crucial to healthy life. However, recent Covid-19 pandemic has shown that comorbidity such as kidney disease and associated uremia impairs immunity against infections. Uremic patients show high susceptible to infections and also exhibit poor antibody responses to vaccine. The mechanisms by which uremia negatively impacts antibody response is unknown. Using multiple mouse models of uremia, we assessed B cells response to model antigen NP-KLH in alum. We show that uremia inhibits both canonical germinal center (GC) and non-canonical extra-follicular B cells response following NP-KLH immunization. Immunized uremic mice demonstrated compromised affinity maturation, isotype switching, antigen-specific antibody secreting cells, antibody titer and T follicular helper cells response. Consequently, uremic mice exhibited diminished GC and antibody response following prime-boost immunization. B cells showed increased cell cycle arrest, apoptosis and impaired migration between light and dark zone in the uremic GCs. We identified uremic toxin hippuric acid as a major driver of loss of mitochondrial membrane potential leading to increased apoptosis in mouse and human B cells. Finally, we show that GC B cells, T follicular helper cells and antibody response were similarly diminished in uremic mice during influenza virus infection, a major cause of mortality in patients with kidney disease. These results shed light on how uremic toxin(s) suppress antimicrobial immunity and vaccine response in individuals with kidney disease. Knowledge gained from this study may pave the path for developing effective therapeutic and preventive strategies in uremic patients against infections including SARS-CoV-2. R01AI142354, R01AI162616 and R21AI159058
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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
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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.
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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.
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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.
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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.
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Guan, Xi, and 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, no. 4 (July 6, 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.
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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.
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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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Hu, Lanfang, Yanting Ma, Lihong Wang, and Yapping Dai. "Analysis of Nursing Effect of Comprehensive Nursing Intervention on Hemodialysis Patients with Uremia." Contrast Media & Molecular Imaging 2022 (September 26, 2022): 1–14. http://dx.doi.org/10.1155/2022/5820707.
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Uremic pruritus affects 50–90% of hemodialysis patients, making it one of the most frequent medical issues among this group. Pruritus can lead to skin infections, desquamation, pathological skin changes, sleep problems, anxiety, depression, and social problems. The epidemic of uremia pneumonia has put a lot of stress on hemodialysis patients, resulting in negative feelings. As a result, during the prevention and control of uremia, rigorous management and improved nursing intervention are critical. During the uremia disease outbreak, this study will examine and assess the impact of clinically refined nurse intervention on patients receiving maintenance hemodialysis.
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Hofman-Bang, Jacob, Eva Gravesen, Klaus Olgaard, and Ewa Lewin. "Epigenetic Methylation of ParathyroidCaRandVDRPromoters in Experimental Secondary Hyperparathyroidism." International Journal of Nephrology 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/123576.
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Secondary hyperparathyroidism (s-HPT) in uremia is characterized by decreased expression in the parathyroids of calcium sensing (CaR) and vitamin D receptors (VDR). Parathyroid hormone (PTH) is normalized despite low levels ofCaRandVDRafter experimental reversal of uremia. The expression ofCaRin parathyroid cultures decreases rapidly. Methylation of promoter regions is often detected during epigenetic downregulation of gene expression. Therefore, using an experimental rat model, we examined changes in methylation levels of parathyroidCaRandVDRpromotersin vivoandin vitro.Methods. Uremia was induced by 5/6 nephrectomy. Melting temperature profiling ofCaRandVDRPCR products after bisulfite treatment of genomic DNA from rat parathyroids was performed. Real-time PCR measured expression ofPTH, CaR, VDR, andklothogenesin vitro.Results. Parathyroids from uremic rats had similar low levels of methylationin vivoandin vitro. In culture, a significant downregulation ofCaR, VDR, andklothowithin two hours of incubation was observed, while housekeeping genes remained stable for 24 hours.Conclusion. In uremic s-HPT andin vitro, no overall changes in methylation levels in the promoter regions of parathyroidCaRandVDRgenes were found. Thus, epigenetic methylation of these promoters does not explain decreased parathyroid expression ofCaRandVDRgenes in uremic s-HPT.
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Maciel, Rayana, Regiane Cunha, Valentina Busato, Célia Franco, Paulo Gregório, Carla Dolenga, Lia Nakao, et al. "Uremia Impacts VE-Cadherin and ZO-1 Expression in Human Endothelial Cell-to-Cell Junctions." Toxins 10, no. 10 (October 7, 2018): 404. http://dx.doi.org/10.3390/toxins10100404.
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Endothelial dysfunction in uremia can result in cell-to-cell junction loss and increased permeability, contributing to cardiovascular diseases (CVD) development. This study evaluated the impact of the uremic milieu on endothelial morphology and cell junction’s proteins. We evaluated (i) serum levels of inflammatory biomarkers in a cohort of chronic kidney disease (CKD) patients and the expression of VE-cadherin and Zonula Occludens-1 (ZO-1) junction proteins on endothelial cells (ECs) of arteries removed from CKD patients during renal transplant; (ii) ECs morphology in vitro under different uremic conditions, and (iii) the impact of uremic toxins p-cresyl sulfate (PCS), indoxyl sulfate (IS), and inorganic phosphate (Pi) as well as of total uremic serum on VE-cadherin and ZO-1 gene and protein expression in cultured ECs. We found that the uremic arteries had lost their intact and continuous endothelial morphology, with a reduction in VE-cadherin and ZO-1 expression. In cultured ECs, both VE-cadherin and ZO-1 protein expression decreased, mainly after exposure to Pi and uremic serum groups. VE-cadherin mRNA expression was reduced while ZO-1 was increased after exposure to PCS, IS, Pi, and uremic serum. Our findings show that uremia alters cell-to-cell junctions leading to an increased endothelial damage. This gives a new perspective regarding the pathophysiological role of uremia in intercellular junctions and opens new avenues to improve cardiovascular outcomes in CKD patients.
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COMBET, SOPHIE, MARIE-LAURE FERRIER, MIEKE VAN LANDSCHOOT, MARIA STOENOIU, PIERRE MOULIN, TOSHIO MIYATA, NORBERT LAMEIRE, and OLIVIER DEVUYST. "Chronic Uremia Induces Permeability Changes, Increased Nitric Oxide Synthase Expression, and Structural Modifications in the Peritoneum." Journal of the American Society of Nephrology 12, no. 10 (October 2001): 2146–57. http://dx.doi.org/10.1681/asn.v12102146.
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Abstract. Advanced glycation end products (AGE), growth factors, and nitric oxide contribute to alterations of the peritoneum during peritoneal dialysis (PD). These mediators are also involved in chronic uremia, a condition associated with increased permeability of serosal membranes. It is unknown whether chronic uremiaper semodifies the peritoneum before PD initiation. A rat model of subtotal nephrectomy was used to measure peritoneal permeability after 3, 6, and 9 wk, in parallel with peritoneal nitric oxide synthase (NOS) isoform expression and activity and structural changes. Uremic rats were characterized by a higher peritoneal permeability for small solutes and an increased NOS activity due to the up-regulation of endothelial and neuronal NOS. The permeability changes and increased NOS activities correlated with the degree of renal failure. Focal areas of vascular proliferation and fibrosis were detected in uremic rats, in relation with a transient up-regulation of vascular endothelial growth factor and basic fibroblast growth factor, as well as vascular deposits of the AGE carboxymethyllysine and pentosidine. Correction of anemia with erythropoietin did not prevent the permeability or structural changes in uremic rats. Thus, in this rat model, uremia induces permeability and structural changes in the peritoneum, in parallel with AGE deposits and up-regulation of specific NOS isoforms and growth factors. These data suggest an independent contribution of uremia in the peritoneal changes during PD and offer a paradigm to better understand the modifications of serosal membranes in uremia.
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Noris, Marina, Marta Todeschini, Sergio Zappella, Samantha Bonazzola, Carla Zoja, Daniela Corna, Flavio Gaspari, Franco Marchetti, Sistiana Aiello, and Giuseppe Remuzzi. "17β-Estradiol corrects hemostasis in uremic rats by limiting vascular expression of nitric oxide synthases." American Journal of Physiology-Renal Physiology 279, no. 4 (October 1, 2000): F626—F635. http://dx.doi.org/10.1152/ajprenal.2000.279.4.f626.
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Conjugated estrogens shorten the prolonged bleeding time in uremic patients and are similarly effective in a rat model of uremia. We have previously demonstrated that the shortening effect of a conjugated estrogen mixture or 17β-estradiol on bleeding time was abolished by the nitric oxide (NO) precursor l-arginine, suggesting that the effect of these drugs on hemostasis in uremia might be mediated by changes in the NO synthetic pathway. The present study investigated the biochemical mechanism(s) by which conjugated estrogens limit the excessive formation of NO. 17β-estradiol (0.6 mg/kg), given to rats made uremic by reduction of renal mass, significantly reduced bleeding time within 24 h and completely normalized plasma concentrations of the NO metabolites, nitrites and nitrates, and of NO synthase (NOS) catalytic activity, determined by NADPH-diaphorase staining in the thoracic aorta. Endothelial NOS (ecNOS) and inducible NOS (iNOS) immunoperoxidase staining in the endothelium of uremic aortas of untreated rats was significantly more intense than in control rats, while in uremic rats receiving 17β-estradiol staining was comparable to controls. Thus 17β-estradiol corrected the prolonged bleeding time of uremic rats and fully normalized the formation of NO by reducing the expression of ecNOS and iNOS in vascular endothelium. These results provide a possible biochemical explanation of the well-known effect of estrogens on primary hemostasis in uremia, in experimental animals and humans.
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CRISAN, Corina M., Stanca L. PANDREA, Manuela TOMPA, Teodora MOCAN, Aida PUIA, and Lucian MOCAN. "Escherichia coli infection, a negative prognostic factor on the evolution of patients with surgical diseases." Notulae Scientia Biologicae 14, no. 3 (September 29, 2022): 11344. http://dx.doi.org/10.55779/nsb14311344.
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The bacterium Escherichia coli, one of the most studied bacteria in the world, with the greatest epidemiological impact, includes both commensal and pathogenic strains, with a genome that can be extremely varied both in size and genetic content, and it also can produce numerous diseases with specific symptoms. The vast majority of these strains can cause severe gastrointestinal diseases, hemolytic uremic syndrome, hemorrhagic colitis, renal failure and even death. Hemolytic uremic syndrome can be a consequence of the presence of Escherichia coli infection in gastrointestinal diseases. In this study, uremia in patients with and without the declared renal comorbidity, was negatively correlated with the response to antibiotic treatment. The increase of uremia above 92 mg/dl increases the risk of death. The highest risk categories include people with kidney disease like comorbidities starting with admission in surgical and intensive care wards in IRGH Cluj-Napoca, having as main diagnosis of hospitalization surgical digestive diseases. The occurrence of Coli pathogen infection was associated with increased morbidity and mortality rates in patients included in the study. In these patients, it was noticed the need to introduce therapy with increasingly complex antibiotic formulas, which lead to an increase in the duration and cost of hospitalization. In the studied group, due to E coli infection at admission, uremia had an average value of 23.99mg/dl +/-8.987(SD) in the case of patients without kidney disease, the number of patients with normal uremia values was lower than that of those with increased values of uremia. In the case of patients with confirmed kidney disease, uremia had mean values of 65.76 mg/dl +/-52.41(SD). At discharge, both in the case of patients with renal disease and in the case of those without confirmed renal disease, the number of patients with normal values of uremia was higher than those with pathological values, this proportion being reversed in the case of deceased patients where the number of patients with values pathological urea levels were significantly higher than those with normal values, proving kidney damage.
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Wang, Xi, Yong Dai, Wanfan Zhang, S. SunDonglin, and Xinzhou Zhang. "Microarray based circRNA expression profiles in uremic plasma and PBMCs due to chronic glomerulonephritis." Archives of Biological Sciences 69, no. 3 (2017): 523–34. http://dx.doi.org/10.2298/abs160520128w.
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Circular RNAs (circRNAs) have been identified in many diseases and shown to play important roles in pathological processes. The expression patterns of circRNA in uremia remains unknown. The aim of this study was to screen circRNA in plasma and peripheral blood mononuclear cells (PBMCs)in healthy controls and patients with uremia due to chronic glomerulonephritis, and to provide evidence for further exploration of the pathogenesis, diagnosis and treatment of uremic patients. Twenty individuals were included in this study, of which 10 were healthy and 10 were patients with uremia caused by chronic glomerulonephritis without systemic lupus erythematosus(SLE). Peripheral blood was collected from each individual in the two groups and the PBMCs were separated. The circRNAs expression profile was examined using a human circRNA microarray. The expression of differently expressed circRNAs was further validated by qRT-PCR. Seven hundred ten circRNAs were differentially expressed in the plasma in the two groups, accounting for 27.58% of the total circRNA(710/2578). Three hundred eighty-five up regulated circRNAs accounted for 14.93% and 325 down regulated circRNAs accounted for 12.60% of the total circRNAs. Additionally, 968 circRNAs were differentially expressed in PBMCs in the two groups, accounting for 29.24% of all circRNAs (968/3310).Six hundred seventy upregulated circRNAs accounted for 20.24% and 298 down regulated circRNAs accounted for 9.00% of the total circRNAs. The results of qRT-PCR validation were consistent with the microarray gene expression results. The expression profile of circRNAs was altered in the plasma and PBMCs of patients with uremia, which suggests that the changed circRNAs may be potential diagnostic biomarkers that play an important role in the pathogenesis of uremic patients. We speculate that hsa_circ_0053958, hsa_circ_0103281 may be associated with the pathogenesis of uremia and may be potential biological molecular markers for the diagnosis and prognosis of uremia.
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Thornalley, Paul J. "Measurement of Protein Glycation, Glycated Peptides, and Glycation Free Adducts." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 25, no. 6 (November 2005): 522–33. http://dx.doi.org/10.1177/089686080502500603.
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Protein glycation adducts, early glycation adducts, such as N∊-fructosyl-lysine, and advanced glycation end products (AGEs) are uremic toxins. Glycation adducts are found in plasma and tissue proteins (glycation adduct residues), in peptides (glycation adduct peptide residues), and glycated amino acids (glycation free adducts). The latter two analyte groups arise from proteolysis of glycated proteins and glycation of peptides and amino acids. Quantitation of glycation adducts in uremia is difficult because of the presence of many different AGEs at low concentrations in different forms in the presence of many potential interferences. Application of liquid chromatography with tandem mass spectrometric (LC-MS/MS) detection to plasma, urine, and dialysate samples of uremic patients has provided a comprehensive and quantitative analysis of glycation adducts in uremia. Glycation free adducts accumulate markedly in the plasma of uremic patients and are eliminated in the peritoneal dialysate. Multiple glycation adducts, and also protein oxidation and nitration adducts, may be quantified concurrently. Glycation free adducts are the major form of glycation adduct eliminated in dialysate. LC-MS/MS may now be used to quantify concentrations, extents of protein modification, clearances, and excretion rates of glycation adducts in uremia.
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Li, Ming, Tongling Ma, Guoyuan Lu, Kun Deng, Rong Yan, and Kesheng Dai. "Platelet Apoptosis in Uremic Patients." Blood 120, no. 21 (November 16, 2012): 4647. http://dx.doi.org/10.1182/blood.v120.21.4647.4647.
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Abstract Abstract 4647 Introduction: Apoptosis, which serves for the regulation of cell lifespan and is long attributed exclusively to nucleated cells, has been well-documented in anucleate platelets. Diverse cell-external chemical and physical stimuli have been reported to induce transformation of resting platelets to apoptotic state. Uremia, a clinical syndrome associated with retention of various solutes that would normally be excreted by the kidneys, is frequently accompanied by bleeding tendency, and the mechanism remains unclear. The aim of the present study is to investigate whether platelet apoptosis occurs in uremia patients. Methods: Venous blood was drawed from 13 patients with end stage renal disease (ESRD) who exhibited uremia syndrome and 13 health controls. Platelet-rich plasma (PRP) was prepared and then was detected for apoptotic events including depolarization of mitochondrial inner membrane potential (ΔΨm), phosphatidylserine (PS ) exposure, variations of apoptotic Bcl-2 family proteins, activation of caspases-3 by Flow cytometry or Western-blot. Furthermore, normal washed platelets were incubated with the poor- platelet plasma (PPP) from uremic patients, and then were detected for apoptotic events. The comparisons of the data were made using paired Student's t-test. Results: Compared with controls, ΔΨm significantly depolarizated in platelets from uremic patients (P<0.05). Furthermore, Bax was up-regulated, Bcl-2 and Bcl-XL were down-regulated, and caspase-3 was activated in platelets from uremic patients. However, there was not significant difference in PS exposure and P-selectin expression between the platelets from uremic patients and health contols (P>0.05). Next, PPP from uremic patients was incubated with normal platelets, and the platelets presented ΔΨm depolarization, up-regulation of Bax, down-regulation of Bcl-2 and Bcl-XL, and caspase-3 activation. Conclusion: The data demonstrate that platelets are incurred apoptosis in uremia patients. The finding might suggest a novel pathogenic mechanism for bleeding tendency in uremic patients. Disclosures: No relevant conflicts of interest to declare.
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Mann, J. F., K. H. Jakobs, J. Riedel, and E. Ritz. "Reduced chronotropic responsiveness of the heart in experimental uremia." American Journal of Physiology-Heart and Circulatory Physiology 250, no. 5 (May 1, 1986): H846—H852. http://dx.doi.org/10.1152/ajpheart.1986.250.5.h846.
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Cardiac beta-adrenoceptor responsiveness was evaluated in experimental uremia by in vivo and in vitro techniques. Uremia was induced in rats by bilateral nephrectomy for 48 h. In rats with chronic intra-arterial and intravenous catheters, cardiovascular reflexes and the renin-angiotensin system were blocked with atropine, pentolinium, and a converting-enzyme inhibitor, respectively. Blood pressure (BP) and heart rate (HR) were continuously recorded. Cumulative doses of isoproterenol were injected intravenously. In uremic rats, the dose-response curve for the HR response showed a lower maximal response (P less than 0.01) and no significant difference in 50% effective dose values compared with controls, whereas the BP decrease caused by isoproterenol was similar in control and uremic rats. When forskolin was injected intravenously to stimulate adenylate cyclase in a receptor-independent manner, the maximal HR increase was lower in uremic rats (P less than 0.01). beta-Adrenoceptor density and affinity, measured by 125I-cyanopindolol binding to sarcolemmal membranes, was not different between control and uremic rats. Also binding affinities for the agonist isoproterenol were not different between groups. Basal adenylate cyclase activity, as well as activity after maximal stimulation by isoproterenol and by forskolin were lower in uremic than in control rats (P less than 0.01). The results show that the chronotropic response of the heart is reduced in uremia. Such hyporesponsiveness may be due, at least in part, to a reduced activity of cardiac adenylate cyclase.
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Semple, David J., Sunil Bhandari, and Anne-Marie L. Seymour. "Uremic cardiomyopathy is characterized by loss of the cardioprotective effects of insulin." American Journal of Physiology-Renal Physiology 303, no. 9 (November 1, 2012): F1275—F1286. http://dx.doi.org/10.1152/ajprenal.00048.2012.
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Chronic kidney disease is associated with a unique cardiomyopathy, characterized by a combination of structural and cellular remodeling, and an enhanced susceptibility to ischemia-reperfusion injury. This may represent dysfunction of the reperfusion injury salvage kinase pathway due to insulin resistance. The susceptibility of the uremic heart to ischemia-reperfusion injury and the cardioprotective effects of insulin and rosiglitazone were investigated. Uremia was induced in Sprague-Dawley rats by subtotal nephrectomy. Functional recovery from ischemia was investigated in vitro in control and uremic hearts ± insulin ± rosiglitazone. The response of myocardial oxidative metabolism to insulin was determined by13C-NMR spectroscopy. Activation of reperfusion injury salvage kinase pathway intermediates (Akt and GSK3β) were assessed by SDS-PAGE and immunoprecipitation. Insulin improved postischemic rate pressure product in control but not uremic hearts, [recovered rate pressure product (%), control 59.6 ± 10.7 vs. 88.9 ± 8.5, P < 0.05; uremic 19.3 ± 4.6 vs. 28.5 ± 10.4, P = ns]. Rosiglitazone resensitized uremic hearts to insulin-mediated cardioprotection [recovered rate pressure product (%) 12.7 ± 7.0 vs. 61.8 ± 15.9, P < 0.05]. Myocardial carbohydrate metabolism remained responsive to insulin in uremic hearts. Uremia was associated with increased phosphorylation of Akt (1.00 ± 0.08 vs. 1.31 ± 0.11, P < 0.05) in normoxia, but no change in postischemic phosphorylation of Akt or GSK3β. Akt2 isoform expression was decreased postischemia in uremic hearts ( P < 0.05). Uremia is associated with enhanced susceptibility to ischemia-reperfusion injury and a loss of insulin-mediated cardioprotection, which can be restored by administration of rosiglitazone. Altered Akt2 expression in uremic hearts post-ischemia-reperfusion and impaired activation of the reperfusion injury salvage kinase pathway may underlie these findings.
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Shin, Jin Ah, Hyerim Park, Hyunsu Choi, Yoon-Kyung Chang, Jwa-Jin Kim, Young Rok Ham, Ki Ryang Na, Kang Wook Lee, and Dae Eun Choi. "ω-3 Polyunsaturated Fatty Acids Improve the Blood–Brain-Barrier Integrity in Contrast-Induced Blood–Brain-Barrier Injury in Uremic Mice." International Journal of Molecular Sciences 24, no. 15 (July 29, 2023): 12168. http://dx.doi.org/10.3390/ijms241512168.
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In patients with chronic kidney disease, the need for examinations using contrast media (CM) increases because of underlying diseases. Although contrast agents can affect brain cells, the blood–brain barrier (BBB) protects against brain-cell damage in vivo. However, uremia can disrupt the BBB, increasing the possibility of contrast-agent-induced brain-cell damage in patients with chronic kidney disease (CKD). ω-3 polyunsaturated fatty acids (PUFAs) have shown protective effects on various neurological disorders, including uremic brain injury. This study examined whether ω-3 PUFAs attenuate damage to the BBB caused by uremia and contrast agents in a uremic mouse model and evaluated its associated mechanisms. C57BL/6 mice (eight weeks old, male) and fat-1 mice (b6 background/eight weeks old, male) were divided into groups according to uremic induction, CM, and ω-3 PUFA administration. Uremia was induced via 24 h ischemia–reperfusion (IR) renal injury. One day after CM treatment, the brain tissue, kidney tissue, and blood were collected. The expression levels of glial fibrillary acidic protein (GFAP), claudin 5, CD31, laminin α4, and laminin α5 increased in ω-3 PUFA + CM-treated uremic mice and the brain of fat-1 + CM-treated uremic mice compared with those in the brains of CM-treated uremic mice. The pro-apoptotic protein expression decreased, whereas the anti-apoptotic proteins increased in ω-3 PUFA + CM-treated uremic mice and fat-1 + CM-treated uremic mice compared with CM-treated uremic mice. In addition, the brain-expression levels of p-JNK, p-P53, and p-P38 decreased in the ω-3 PUFA + CM-treated uremic mice and fat-1 + CM-treated uremic mice compared with those in wild-type uremic mice. Our results confirm that uremic toxin and CM damage the BBB and cause brain-cell death. ω-3 PUFAs play a role in BBB protection caused by CM in uremic mice.
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Cecchin, F., O. Ittoop, M. K. Sinha, and J. F. Caro. "Insulin resistance in uremia: insulin receptor kinase activity in liver and muscle from chronic uremic rats." American Journal of Physiology-Endocrinology and Metabolism 254, no. 4 (April 1, 1988): E394—E401. http://dx.doi.org/10.1152/ajpendo.1988.254.4.e394.
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We have studied the structure and function of the partially purified insulin receptors from liver and skeletal muscle in a rat model of severe chronic uremia. 125I-insulin binding was higher in the liver from uremic rats when compared with ad libitum- and pair-fed controls. Furthermore, the ability of insulin to stimulate the autophosphorylation of the beta-subunit and insulin receptor kinase activity using Glu80, Tyr20 as exogenous phosphoacceptor was increased in the liver of the uremic animals. The structural characteristic of the receptors, as determined by electrophoretic mobilities of affinity labeled alpha-subunit and the phosphorylated beta-subunit, were normal in uremia. 125I-insulin binding and insulin receptor kinase activity were similar in the skeletal muscle from uremic and pair- and ad libitum-fed animals. Thus our data are supportive of the hypothesis that in liver and muscle of chronic uremic rats, insulin resistance is due to a defect(s) distal to the insulin receptor kinase.
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Kazakova, I. A. "Effect of hemodialysis on carbohydrate metabolism in patients with chronic renal failure." Kazan medical journal 68, no. 1 (February 15, 1987): 31–33. http://dx.doi.org/10.17816/kazmj95897.
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Interest in the study of the features of metabolism in chronic renal failure is steadily increasing due to the improvement of methods of treatment of uremia patients. Under conditions of prolonged hemodialysis uremia various metabolic disorders are observed, in particular changes in carbohydrate metabolism. As shown by studies in recent years, the majority of patients with chronic renal failure have reduced glucose tolerance with a frequency of 54 to 100%, which served as the basis for the introduction of the term uremic-azotemic pseudodiabetes.
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Oettinger, C. W., L. A. Bland, J. C. Oliver, M. J. Arduino, S. K. McAllister, and M. S. Favero. "The effect of uremia on tumor necrosis factor-alpha release after an in vitro whole-blood endotoxin challenge." Journal of the American Society of Nephrology 4, no. 11 (May 1994): 1890–95. http://dx.doi.org/10.1681/asn.v4111890.
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Uremia has been associated with immunologic aberrations, including anergy, increased susceptibility to infections, and reduced phagocytic activity of polymorphonuclear leukocytes. In this study, cytokine release in uremic and nonuremic blood after in vitro endotoxin stimulation was studied. Blood from nonuremic controls, chronic renal failure patients not on dialysis, and chronic hemodialysis patients predialysis and postdialysis was spiked with 10 ng/mL of Escherichia coli endotoxin and incubated for 2 and 26 h. Plasma tumor necrosis factor-alpha (TNF alpha) concentrations were determined by ELISA after each incubation period. To further study which uremic blood component may be responsible for enhanced release of TNF alpha, plasma and cellular components of chronic renal failure patients and controls were switched and then given an in vitro endotoxin stimulation (1 ng/mL). It was found that (1) TNF alpha release is enhanced by uremia and is exacerbated with progressive declines in renal function, (2) enhanced TNF alpha release is related to a blood cellular phenomenon induced by uremia, and (3) enhanced TNF alpha release in hemodialysis patients is associated with a prolonged stimulation and/or reduced plasma elimination of TNF alpha.
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CENDOROGLO, MIGUEL, BERTRAND L. JABER, V. S. BALAKRISHNAN, MARY PERIANAYAGAM, ANDREW J. KING, and BRIAN J. G. PEREIRA. "Neutrophil Apoptosis and Dysfunction in Uremia." Journal of the American Society of Nephrology 10, no. 1 (January 1999): 93–100. http://dx.doi.org/10.1681/asn.v10193.
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Abstract. The high prevalence of bacterial infections among patients with end-stage renal disease suggests that “professional” phagocytes such as neutrophils are functionally impaired. This dysfunction has been ascribed to uremic toxins, malnutrition, and dialysis. The aim of this study was to investigate the contribution of apoptosis to neutrophil dysfunction in uremia. Neutrophils harvested from uremic patients (n = 6) and age-/gender-matched healthy control subjects (n = 6) were incubated with either 50% autologous plasma or 10% fetal calf serum. After 24-h incubation, apoptosis was quantified by flow cytometry by using propidium iodide nuclear staining. Neutrophils from healthy volunteers were also incubated with either 50% heterologous normal or uremic plasma. After 24-h incubation, apoptosis was quantified by flow cytometry and transmission electron microscopy. In addition, superoxide production was determined by measuring the capacity to reduce ferri- to ferro-cytochrome C by using 4-β-phorbol 12-β-myristate 13-α-acetate or N-formyl methionyl-leucyl-phenylalanine (fMLP) for stimulus. Phagocytosis was determined by the uptake of 14C-labeled heat-killed Staphylococcus aureus. Compared with normal neutrophils, uremic neutrophils demonstrated greater apoptosis in the presence of autologous plasma (9 ± 4 versus 19 ± 6%, P = 0.01) as well as 10% fetal calf serum (19 ± 7 versus 31 ± 6%, P = 0.03). Furthermore, compared with normal neutrophils exposed to heterologous normal plasma, those exposed to heterologous uremic plasma exhibited higher apoptosis rates (19 ± 3 versus 40 ± 5%, P = 0.002), lower fMLP-stimulated superoxide production (22.6 ± 2.5 versus 15.5 ± 1.1 nmol O2[UNK] /3.12 × 105 cells/30 min, P = 0.01), and a lower phagocytosis index (38 ± 3% versus 27 ± 5%, P = 0.04). Apoptosis correlated inversely with fMLP-stimulated superoxide production (r = -0.60, P = 0.04) and phagocytosis (r = -0.57, P = 0.05). These results suggest that uremic neutrophils undergo accelerated in vitro apoptosis. Furthermore, uremic plasma accelerates apoptosis of normal neutrophils, resulting in a dysfunctional pattern that is similar to that observed in uremia.
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Radbil, O. S. "On the variety of uremic conditions." Kazan medical journal 43, no. 1 (October 17, 2021): 3–9. http://dx.doi.org/10.17816/kazmj82995.
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Bergesio, F., R. Ciuti, M. Salvadori, G. A. Galli, G. Monzani, E. Bertoni, A. Salerno, and V. Frizzi. "Are Lipid Abnormalities Reliable Cardiovascular Risk Factors in Dialysis Patients?" International Journal of Artificial Organs 12, no. 11 (November 1989): 677–82. http://dx.doi.org/10.1177/039139888901201102.
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Patients on chronic hemodialysis often present both hyperlipidemia and a high incidence of cardiovascular disease (CVD). Uremic hyperlipidemia has usually been regarded as one of the most important cardiovascular risk factors (CVRF) in these patients. In order to study whether the “uremia-induced” lipid abnormalities are actually associated with evidence of uremic CVD, and consequently may be considered reliable CVRF, 123 patients on chronic dialysis were reviewed for the presence of CVD and, at the same time, examined for their lipoprotein pattern and other clinical and biochemical variables. Lipids and lipoproteins did not prove helpful in our study in identifying patients with CVD. Despite the fact that they had been on dialysis for a shorter time, CVD patients were significantly older and had higher blood pressure than patients without CVD. Our data suggest that the uremia-induced lipid abnormalities are not reliable markers of CVD in dialysis patients, and support the hypothesis that dialysis per se does not accelerate the atherosclerotic process in uremic patients
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Kocsis, Gabriella F., Márta Sárközy, Péter Bencsik, Márton Pipicz, Zoltán V. Varga, János Pálóczi, Csaba Csonka, Péter Ferdinandy, and Tamás Csont. "Preconditioning protects the heart in a prolonged uremic condition." American Journal of Physiology-Heart and Circulatory Physiology 303, no. 10 (November 15, 2012): H1229—H1236. http://dx.doi.org/10.1152/ajpheart.00379.2012.
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Metabolic diseases such as hyperlipidemia and diabetes attenuate the cardioprotective effect of ischemic preconditioning. In the present study, we examined whether another metabolic disease, prolonged uremia, affects ischemia/reperfusion injury and cardioprotection by ischemic preconditioning. Uremia was induced by partial nephrectomy in male Wistar rats. The development of uremia was verified 29 wk after surgery. Transthoracic echocardiography was performed to monitor cardiac function. At week 30, hearts of nephrectomized and sham-operated rats were isolated and subjected to a 30-min coronary occlusion followed by 120 min reperfusion with or without preceding preconditioning induced by three intermittent cycles of brief ischemia and reperfusion. In nephrectomized rats, plasma uric acid, carbamide, and creatinine as well as urine protein levels were increased as compared with sham-operated controls. Systolic anterior and septal wall thicknesses were increased in nephrectomized rats, suggesting the development of a minimal cardiac hypertrophy. Ejection fraction was decreased and isovolumic relaxation time was shortened in nephrectomized rats demonstrating a mild systolic and diastolic dysfunction. Infarct size was not affected significantly by nephrectomy itself. Ischemic preconditioning significantly decreased infarct size from 24.8 ± 5.2% to 6.6 ± 1.3% in the sham-operated group and also in the uremic group from 35.4 ± 9.5% to 11.9 ± 3.1% of the area at risk. Plasma ANG II and nitrotyrosine were significantly increased in the uremic rats. We conclude that although prolonged experimental uremia leads to severe metabolic changes and the development of a mild myocardial dysfunction, the cardioprotective effect of ischemic preconditioning is still preserved.
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Langsdorf, LJ, and AL Zydney. "Effect of uremia on the membrane transport characteristics of red blood cells." Blood 81, no. 3 (February 1, 1993): 820–27. http://dx.doi.org/10.1182/blood.v81.3.820.820.
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Abstract Even though there is extensive evidence that uremia affects the fragility and deformability of red blood cells (RBCs), essentially all data on the RBC membrane permeability have been obtained with nonuremic blood. Permeability data were obtained for creatinine and uric acid, two metabolites of interest in hemodialysis, using a stirred ultrafiltration device with direct cell- and protein-free sampling. Experiments examined the effects of temperature and suspending phase on solute transport for both normal and uremic blood cells. Creatinine and uric acid transport from normal RBCs at 37 degrees C were characterized by saturation half-times of 40 +/- 10 minutes and 54 +/- 12 minutes, respectively. The corresponding half-times for uremic cells were significantly longer, 94 +/- 26 minutes and 180 +/- 38 minutes. Data indicated that the slower rate of creatinine transport in uremic blood was caused by an alteration in the RBC membrane, while the reduction in uric acid transport was associated with alterations in the uremic plasma. The temperature dependence of the RBC permeability was also much less pronounced for uremic cells for both solutes. These results provide important insights into the effects of uremia on the RBC membrane permeability, and have important implications for dialysis.
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Langsdorf, LJ, and AL Zydney. "Effect of uremia on the membrane transport characteristics of red blood cells." Blood 81, no. 3 (February 1, 1993): 820–27. http://dx.doi.org/10.1182/blood.v81.3.820.bloodjournal813820.
Full textAbstract:
Even though there is extensive evidence that uremia affects the fragility and deformability of red blood cells (RBCs), essentially all data on the RBC membrane permeability have been obtained with nonuremic blood. Permeability data were obtained for creatinine and uric acid, two metabolites of interest in hemodialysis, using a stirred ultrafiltration device with direct cell- and protein-free sampling. Experiments examined the effects of temperature and suspending phase on solute transport for both normal and uremic blood cells. Creatinine and uric acid transport from normal RBCs at 37 degrees C were characterized by saturation half-times of 40 +/- 10 minutes and 54 +/- 12 minutes, respectively. The corresponding half-times for uremic cells were significantly longer, 94 +/- 26 minutes and 180 +/- 38 minutes. Data indicated that the slower rate of creatinine transport in uremic blood was caused by an alteration in the RBC membrane, while the reduction in uric acid transport was associated with alterations in the uremic plasma. The temperature dependence of the RBC permeability was also much less pronounced for uremic cells for both solutes. These results provide important insights into the effects of uremia on the RBC membrane permeability, and have important implications for dialysis.
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Meijers, Björn, Ward Zadora, and Jerome Lowenstein. "A Historical Perspective on Uremia and Uremic Toxins." Toxins 16, no. 5 (May 15, 2024): 227. http://dx.doi.org/10.3390/toxins16050227.
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Uremia, also known as uremic syndrome, refers to the clinical symptoms in the final stage of renal failure. The definition of the term has changed over time due to an improved comprehension of the kidney’s function and the advancement of dialysis technology. Here, we aim to present an overview of the various concepts that have developed regarding uremia throughout the years. We provide a comprehensive review of the historical progression starting from the early days of Kolff and his predecessors, continuing with the initial research conducted by Niwa et al., and culminating in the remote sensing hypothesis of Nigam. Additionally, we explore the subsequent investigation into the function of these toxins as signaling molecules in various somatic cells.
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Park, Jong-Ho, Han-Joon Kim, and Seong-Min Kim. "Acute Chorea with Bilateral Basal Ganglia Lesions in Diabetic Uremia." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 34, no. 2 (May 2007): 248–50. http://dx.doi.org/10.1017/s0317167100006144.
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Uremia is a syndrome of clinical and metabolic abnormalities, which develops in parallel with the deterioration of renal function. Uremic encephalopathy is one of many manifestations of acute or chronic renal failure. It is usually applied to patients with cortical involvement, such as confusion, seizure, tremor, myoclonus, or asterixis. Some cases of acute extrapyramidal movement disorders associated with bilateral basal ganglia lesions, especially parkinsonism have been reported in uremic patients. Here, we report a diabetic uremic patient who developed acute chorea associated with bilateral basal ganglia lesions.
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Kim, Ji Eun, Hyo-Eun Kim, Ji In Park, Hyunjeong Cho, Min-Jung Kwak, Byung-Yong Kim, Seung Hee Yang, et al. "The Association between Gut Microbiota and Uremia of Chronic Kidney Disease." Microorganisms 8, no. 6 (June 16, 2020): 907. http://dx.doi.org/10.3390/microorganisms8060907.
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Chronic kidney disease (CKD)-associated uremia aggravates—and is aggravated by—gut dysbiosis. However, the correlation between CKD severity and gut microbiota and/or their uremic metabolites is unclear. We enrolled 103 CKD patients with stage 1 to 5 and 46 healthy controls. We analyzed patients’ gut microbiota by MiSeq system and measured the serum concentrations of four uremic metabolites (p-cresyl sulfate, indoxyl sulfate, p-cresyl glucuronide, and trimethylamine N-oxide) by liquid chromatography–tandem mass spectrometry. Serum concentrations of the uremic metabolites increased with kidney function deterioration. Gut microbial diversity did not differ among the examined patient and control groups. In moderate or higher stage CKD groups, Oscillibacter showed positive interactions with other microbiota, and the proportions of Oscillibacter were positively correlated with those of the uremic metabolites. The gut microbiota, particularly Oscillibacter, was predicted to contribute to pyruvate metabolism which increased with CKD progression. Relative abundance of Oscillibacter was significantly associated with both serum uremic metabolite levels and kidney function. Predicted functional analysis suggested that kidney-function-associated changes in the contribution of Oscillibacter to pyruvate metabolism in CKD may greatly affect the gut environment according to kidney function, resulting in dysbiosis concomitant with uremic toxin production. The gut microbiota could be associated with uremia progression in CKD. These results may provide basis for further metagenomics analysis of kidney diseases.
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Packard, Gary C., and Mary J. Packard. "Growth of embryonic softshell turtles is unaffected by uremia." Canadian Journal of Zoology 68, no. 5 (May 1, 1990): 841–44. http://dx.doi.org/10.1139/z90-121.
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We injected eggs of softshell turtles (Trionyx spiniferus) with solutions of urea at the midpoint of incubation to induce different levels of uremia in developing embryos. The experiment was undertaken as a test of the hypothesis that urea inhibits intermediary metabolism of embryos and thereby causes a reduction in their rates of growth. The injection protocol elicited a physiologically realistic range of uremias, but we found no evidence that metabolism or growth of embryos was impaired even at the highest levels of uremia. The most likely explanation for our results is that the uremias commonly encountered during natural incubation by embryos of this and other species of turtle are insufficient to inhibit intermediary metabolism. Thus, the influence of the hydric environment on metabolism and growth of embryonic turtles apparently is not mediated by differential rates of increase in the concentration of urea in body fluids.
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Tsai, Han-Mou. "Atypical Hemolytic Uremic Syndrome: Beyond Hemolysis and Uremia." American Journal of Medicine 132, no. 2 (February 2019): 161–67. http://dx.doi.org/10.1016/j.amjmed.2018.08.011.
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Diaz-Ricart, Maribel, Sergi Torramade-Moix, Georgina Pascual, Marta Palomo, Ana Belen Moreno-Castaño, Julia Martinez-Sanchez, Manel Vera, Aleix Cases, and Gines Escolar. "Endothelial Damage, Inflammation and Immunity in Chronic Kidney Disease." Toxins 12, no. 6 (June 1, 2020): 361. http://dx.doi.org/10.3390/toxins12060361.
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Chronic kidney disease (CKD) patients have an accelerated atherosclerosis, increased risk of thrombotic-ischemic complications, and excessive mortality rates when compared with the general population. There is also evidence of an endothelial damage in which the proinflammatory state, the enhanced oxidative stress, or the accumulation of toxins due to their reduced renal clearance in uremia play a role. Further, there is evidence that uremic endothelial cells are both involved in and victims of the activation of the innate immunity. Uremic endothelial cells produce danger associated molecular patterns (DAMPS), which by binding to specific pattern recognition receptors expressed in multiple cells, including endothelial cells, induce the expression of adhesion molecules, the production of proinflammatory cytokines and an enhanced production of reactive oxygen species in endothelial cells, which constitute a link between immunity and inflammation. The connection between endothelial damage, inflammation and defective immunity in uremia will be reviewed here.
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Heunisch, Carol, Daniel J. Resnick, Joseph M. Vitello, and Steven J. Martin. "Conjugated Estrogens for the Management of Gastrointestinal Bleeding Secondary to Uremia of Acute Renal Failure." Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy 18, no. 1 (January 2, 1998): 210–17. http://dx.doi.org/10.1002/j.1875-9114.1998.tb03841.x.
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Bleeding commonly occurs secondary to the uremia of acute and chronic renal failure. Hemodialysis is indicated for the management of uremic bleeding, and administration of red blood cells and cryoprecipitate is also helpful. Desmopressin successfully reduces the bleeding tendency in patients with chronic renal failure for short‐term operations or procedures, but the frequency of tachyphylaxis is high and limits the drug's usefulness for major bleeds. Conjugated estrogens shorten bleeding times in uremia and may provide a more sustained hemostatic effect over desmopressin. A patient with acute renal failure and uncontrolled gastrointestinal bleeding was successfully treated with conjugated estrogens after failing desmopressin and octreotide therapy.
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Andrade, Laila Santos de, Maria Aparecida Dalboni, José Tarcisio Giffoni de Carvalho, Caren Cristina Grabulosa, Natalia Barros Ferreira Pereira, Danilo Takashi Aoike, and Lilian Cuppari. "In vitro effect of uremic serum on barrier function and inflammation in human colonocytes." Brazilian Journal of Nephrology 40, no. 3 (June 18, 2018): 217–24. http://dx.doi.org/10.1590/2175-8239-jbn-3949.
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ABSTRACT Introduction: In chronic kidney disease (CKD), it has been suggested that alterations within the gut are associated with an inflammatory state and uremic toxicity. Studies suggest that uremia may impair the function of the intestinal barrier via the promotion of increased intestinal permeability. To understand the mechanisms that are involved in intestinal barrier damage in the setting of uremia, we evaluated the in vitro effect of uremic serum on transepithelial electrical resistance (TER), inflammation, and apoptosis in intestinal epithelial cells (T84). Methods: Pools of serum from healthy individuals, patients not on dialysis, and patients on hemodialysis (Pre-HD and Post-HD) were prepared. T84 cells were incubated for 24 h in medium, of which 10% consisted of the pooled serum from each group. After incubation, the TER was measured and the following parameters were determined by flow cytometry: expression of toll-like receptors (TLRs), production of reactive oxygen species (ROS), and apoptosis. The level of IL-6 in the culture supernatant was determined by ELISA. Results: No difference was observed among the groups with respect to TER, apoptosis, and ROS or the expression of TLR-2, TLR-4, and TLR-9. IL-6 secretion was higher (p < 0.001) in cells that were incubated with pre- and post-HD serum. Conclusion: The results that were obtained from this model suggest that uremic serum per se does not seem to impair the integrity of intestinal epithelial cells. The increased IL-6 secretion by cells that were incubated with HD serum suggests a potential effect of uremia in the intestinal inflammatory response.
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Oreopoulos, Antigone K., Elias V. Balaskas, Helen Rodela, G. Harvey Anderson, and Dimitrios G. Oreopoulos. "An Animal Model for the Study of Amino Acid Metabolism in Uremia and during Peritoneal Dialysis." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 13, no. 2_suppl (January 1993): 499–508. http://dx.doi.org/10.1177/089686089301302s123.
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We tried to determine the suitability of the rabbit as an animal model to study amino acid (AA) metabolism in continuous ambulatory peritoneal dialysis. We also measured the effect of intraperitoneal (ip) infusion of AA on blood AA changes and food consumption. Plasma AA levels were measured in 10 normal rabbits after an overnight fasting and 30, 60, and 120 minutes after a meal. Following these baseline observations, rabbits were randomly divided into two groups. One group of five rabbits was made uremic after surgical partial nephrectomy, whereas the remaining (controls) underwent sham operations. Two weeks after the induction of uremia we measured the effect of chronic renal failure on fasting and postprandial (30,60,120 minutes) plasma AA levels. Upon the completion of the second experiment (4 weeks after the induction of uremia) we studied the effect of an ip AA on plasma AA profile 1, 2, 4, and 6 hours after the infusion in both uremic and control rabbits. We also measured the food intake in all experiments. The results of our experiments showed the following: 1. plasma AA in the rabbits decreased after induction of chronic renal failure and increased after food ingestion and ip infusion of AA solution; 2. neither induction of uremia nor ip AA infusion have an effect on food consumption; 3. the majority of the alterations in plasma AA levels we observed in the uremic rabbits were similar to those observed in humans, indicating that the rabbit may be a suitable model for the study of AA metabolism in chronic renal failure and during peritoneal dialysis.
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Meyer, Timothy W., and Thomas H. Hostetter. "Uremia." New England Journal of Medicine 357, no. 13 (September 27, 2007): 1316–25. http://dx.doi.org/10.1056/nejmra071313.
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Jablonski, Greg, Knut H. Klem, Carl Ch Danielsen, Lis Mosekilde, and Jan O. Gordeladze. "Aluminium-induced bone disease in uremic Rats: Effect of deferoxamine." Bioscience Reports 16, no. 1 (February 1, 1996): 49–63. http://dx.doi.org/10.1007/bf01201001.
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We have previously established a rat model of chronic uremia, which is suitable to investigate the effect of various treatment modalities on renal osteodystrophy [1]. After four months subsequent to 5/6 nephrectomy, some animals were treated by gavage for 9 weeks with tap water (controls), or with aluminium (Al-citrate) 3 × 25 mg/week/kg b.wt ± subsequent deferoxamine (DFO) 3 × 50 mg/ week/kg b.wt. for 4 weeks. At termination of the study, serum clinical chemistry, femoral chemical composition and mechanical properties, calvarial parathyroid hormone (PTH)-elicited adenylate cyclase (AC) and phospholipase C (PLC) activities, cross-sectional femoral area, as well as bone histomorphometry, were analyzed. Animals given Al displayed moderately enhanced serum Al and bone Al accumulation, however, DFO-treatment did not fully alleviate bone Al retainment. A small increase in serum PTH was seen in all animals rendered uremic. Furthermore, a marked fall in serum alkaline phosphatase (ALP) below normal controls was observed in Al ± DFO-treated animals compared with uremic controls. The uremic condition led to reduced femoral ratios of hydroxyproline (HYP) over Ca2+ and phosphate (Pi), while Al-intoxication alone enhanced femoral Hyp contents above values seen for normal controls. The protracted ureamia caused a deterioration of long bone resilience and brittleness, however, Al ± DFO-treatment seemed to normalize the latter. Contrastingly, Al ± DFO-gavage enhanced time to fracture. Uremic rats intoxicated with Al showed a complete loss of calvarial PTH-sensitive AC and PLC activities. DFO-treatment normalized PTH-elicited PLC, while PTH-susceptible AC remained super-normal. Al apparently exerts a long term down-regulation of both PTH-sensitive signaling systems as evidenced by studies of rat UMR 106 osteosarcoma cells in culture. The uremic condition enhanced endosteal bone resorption as shown by femoral shaft dimension analysis, while AI ± DFO-treatment insignificantly reversed the condition. Finally, histomorphometrical analyses showed that DFO-administration tended to normalize aberrant trabecular bone volume, while rectifying both bone resorption and degree of mineralization. In conclusion, we assert that Al-intoxication hampers both processes (i.e. formation and resorption) of bone turnover, and that DFO-treatment to a certain extent prevents the uremia- and Al-induced bone disease in rats.
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Jawale, Chetan, Kritika Ramani, and Partha Sarathi Biswas. "Defect in neutrophil function accounts for impaired anti-fungal immunity in kidney dysfunction." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 50.9. http://dx.doi.org/10.4049/jimmunol.200.supp.50.9.
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Abstract Chronic kidney disease is increasingly recognized as a major public health problem, and has a prevalence of 10% in the general population. Accumulation of uremic toxins results in systemic immunosuppression. Sepsis due to microbial infections accounts for 20% of deaths in patients with kidney diseases. Increased susceptibility of uremic patients to invasive fungal infections may attribute to impairment of innate immune defense. However, the molecular mechanisms of impaired anti-fungal immunity in kidney dysfunction are poorly understood. In this study, we have used the mouse model of aristolochic acid nephropathy to investigate the effect of uremia on antifungal immunity. A single IP injection of aristolochic acid I resulted in severe tubulointerstitial injuries accompanied by increased level blood urea nitrogen. Uremic mice showed increased Candida albicans burden in the internal organs following systemic infection. Increased fungal load was not attributed to defect in migration of neutrophils in the infected organs. Uremic condition impaired the ROS production and fungicidal activity of neutrophils. Interestingly, incubation of neutrophils with uremic serum led to impairment of their energy metabolism, indicated by reduced ATP content and lactate production. Neutrophils incubated with uremic serum showed reduced Glut1 protein expression and impaired glucose uptake capacity. Surprisingly, uremic serum inhibited PI3K/AKT pathway leading to aberrant activation of GSK3β in neutrophils. Furthermore, inhibition of GSK3β restored the glucose uptake in neutrophils incubated with uremic serum. These results indicate that uremia suppresses the anti-fungal activity of neutrophils by inhibiting their immunometabolism.
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Kwan, J. T., E. C. Carr, M. R. Bending, and J. L. Barron. "Determination of carbamylated hemoglobin by high-performance liquid chromatography." Clinical Chemistry 36, no. 4 (April 1, 1990): 607–10. http://dx.doi.org/10.1093/clinchem/36.4.607.
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Abstract We have developed an HPLC method for measuring carbamylated hemoglobin (CarHb), based on the quantification of valine hydantoin formed from the released NH2-terminal carbamyl valine residue after acid hydrolysis of hemoglobin. In uremia, CarHb is produced by nonenzymatic post-translational modification of the terminal amino group of hemoglobin monomers by isocyanic acid, derived from the spontaneous dissociation of urea. We measured CarHb in 25 nonuremic control subjects, 24 nonuremic diabetic subjects, and 30 patients with stable chronic renal failure. There was no significant difference between the controls and diabetic patients, their mean (SD) CarHb values being 41 (11.5) and 38 (10.8) micrograms of carbamyl valine per gram of hemoglobin (microgram CV/gHb), respectively. Mean (SD) CarHb values in the uremic patients were much greater, 164 (87.7) microgram CV/gHb. There was significant correlation between the concentrations of CarHb and plasma urea in the uremic subjects. Thus CarHb provides a urea-derived index of chronic uremia.
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Fernández-Moreno, M. D., E. Arilla, and J. C. Prieto. "The effects of experimental uremia in rats on duodenal VIP levels and the interaction of VIP with duodenal epithelial cells." Bioscience Reports 9, no. 2 (April 1, 1989): 207–12. http://dx.doi.org/10.1007/bf01115997.
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The effects of experimental uremia on the concentration of vasoactive intestinal peptide (VIP) in duodenum as well as on the interaction of this neuropeptide with the corresponding epithelial cells were studied in rats. Duodenal VIP concentration was significantly decreased in uremic rats as compared to control animals. The specific binding of VIP to duodenal epithelial cells increased in rats with uremia due to an increase in the number of VIP receptors rather than a change in the binding affinity or in the extent of VIP degradation. On the other hand, the efficacy but not the potency of VIP upon cyclic AMP generation varied in parallel to that observed at the receptor level.
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Chen, Yan, Jie Ding, Chunqing Li, Ting Wu, Qingya Li, Rujing Chen, and Jingfen Zhou. "Study on Nursing Effect of Psychological Intervention on Uremic Hemodialysis Patients." Computational and Mathematical Methods in Medicine 2022 (July 13, 2022): 1–7. http://dx.doi.org/10.1155/2022/8040656.
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Aim. Patients in the hemodialysis stage are prone to psychological pressure of depression and anxiety and have resistance, which affects the clinical treatment effect. Effective psychological intervention plays a very important role in improving patients’ psychological pressure and patients’ compliance. The aim of this study is to explore the nursing effect of psychological intervention on uremic hemodialysis patients. Methods. There were 126 uremic hemodialysis patients admitted to the hospital from August 2020 to December 2021. The patients were randomly divided into the routine nursing care group ( n = 63 ) and psychological intervention group ( n = 63 ). The routine nursing care group received routine nursing care for uremia hemodialysis patients. The psychological intervention group implemented psychological intervention on uremia hemodialysis patients. The methods of psychological intervention mainly include establishing a good nurse-patient relationship, popularizing hemodialysis knowledge, timely psychological counseling for patients, and organizing patient communication meetings. The treatment compliance, Self-rating Anxiety Scale (SAS) and Self-rating Depression Scale (SDS) of the two groups were compared before and after nursing. SF-36 scale was used to evaluate the quality of life of patients. The incidence of complications and nursing satisfaction were compared between the two groups. Results. The treatment compliance rate and nursing satisfaction of hemodialysis uremic patients in the psychological intervention group were significantly higher than the routine nursing care group. The SAS and SDS of hemodialysis uremia patients in the psychological intervention group were significantly lower than the routine nursing care group after psychological intervention, and SF-36 scale was significantly higher than the routine nursing group. The main complications of uremic hemodialysis patients are hypotension, hyperkalemia, internal fistula occlusion, and infection. Compared with the routine nursing care group, the incidence of complications in the psychological intervention group was significantly reduced. Conclusion. The implementation of psychological nursing intervention for uremic hemodialysis patients have a very significant effect on reducing the incidence of complications and improving anxiety, depression, treatment compliance, and the quality of life and the nursing satisfaction.
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Hassan, Alia, Karina Durlacher, Justin Silver, Tally Naveh-Many, and Ronen Levi. "The fibroblast growth factor receptor mediates the increased FGF23 expression in acute and chronic uremia." American Journal of Physiology-Renal Physiology 310, no. 3 (February 1, 2016): F217—F221. http://dx.doi.org/10.1152/ajprenal.00332.2015.
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Serum FGF23 is markedly elevated in chronic kidney disease and has been associated with poor long-term outcomes. FGF23 expression is increased by activation of the FGF receptor 1 (FGFR1) in rats with normal renal function and in vitro in bone-derived osteoblast-like cells. We studied the regulation of FGF23 by FGFR1 in vivo in acute and chronic uremia in mice and rats. Folic acid-induced acute kidney injury increased calvaria FGF23 mRNA and serum FGF23 and parathyroid hormone (PTH) levels at 6 h. The FGFR1 receptor inhibitor PD173074 prevented the folic acid-induced increase in both FGF23 mRNA and serum levels but had no effect on serum PTH levels. A more prolonged uremia due to an adenine high-phosphorus diet for 14 days resulted in high levels of FGF23 mRNA and serum FGF23 and PTH. PD173074 decreased serum FGF23 and mRNA levels with no effect on PTH in the adenine high phosphorus-induced uremic rats. Therefore, a derangement in FGF23 regulation starts early in the course of acute kidney injury, is in part independent of the increase in serum PTH, and involves activation of FGFR1. It is possible that FGFR1 in the osteocyte is activated by locally produced canonical FGFs, which are increased in uremia. This is the first demonstration that activation of FGFR1 is essential for the high levels of FGF23 in acute and chronic experimental uremia.
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Davis, T. A., I. E. Karl, E. D. Tegtmeyer, D. F. Osborne, S. Klahr, and H. R. Harter. "Muscle protein turnover: effects of exercise training and renal insufficiency." American Journal of Physiology-Endocrinology and Metabolism 248, no. 3 (March 1, 1985): E337—E345. http://dx.doi.org/10.1152/ajpendo.1985.248.3.e337.
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Chronic renal failure is associated with an enhanced catabolism of muscle protein. To determine the effect of exercise training and moderate renal insufficiency on net protein catabolism and protein synthesis in isolated epitrochlearis muscles, three-fourth nephrectomized and control rats were exercise trained or remained sedentary. Net muscle protein degradation was determined by measuring the rates of release of phenylalanine and tyrosine. Protein synthesis was determined by measuring the incorporation of [U-14C]phenylalanine into muscle protein. Exercise training reduced the elevated protein degradation of uremia to control levels. In control rats, exercise training had no effect on protein degradation. Exercise training increased alanine release in control rats but did not further increase the elevated alanine release of uremia. Protein synthesis was unaffected by both uremia and exercise training. Exercise training in control and uremic rats moderately increased the responsiveness of muscle to insulin by reducing net protein degradation but did not further enhance the insulin-stimulated increase in protein synthesis. Thus exercise training ameliorates the enhanced muscle protein degradation of moderate renal insufficiency.
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Prabhakar, Sharma S., Guillermo A. Zeballos, Martin Montoya-Zavala, and Claire Leonard. "Urea inhibits inducible nitric oxide synthase in macrophage cell line." American Journal of Physiology-Cell Physiology 273, no. 6 (December 1, 1997): C1882—C1888. http://dx.doi.org/10.1152/ajpcell.1997.273.6.c1882.
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Macrophage dysfunction is considered an important contributory factor for increased propensity of infections in uremia. Because nitric oxide (NO) is believed to be an effector molecule of macrophage cytotoxicity, we propose that the dysfunction may be related to impaired NO synthesis. To verify this hypothesis, we evaluated macrophage NO synthesis in the presence of urea, a compound that accumulates in renal failure and is believed by some to be a uremic toxin. Macrophages (RAW 264.7 cells) were incubated with bacterial lipopolysaccharide to induce NO synthesis, whereas the test groups had various concentrations of urea in addition. NO synthesis was measured by assaying the supernatant for nitrites and nitrates by chemiluminescence. We observed that urea consistently produced a dose-dependent reversible inhibition of inducible NO production in macrophages, whereas parathormone, another toxin retained in uremia, had no such inhibitory effects. Further studies revealed that mRNA for inducible NO synthase was not inhibited by urea. We thus conclude that urea inhibits inducible NO synthesis in macrophages by a posttranscriptional mechanism and that this may be important in macrophage dysfunction of uremia.