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Journal articles on the topic 'Uremia'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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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 (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 thro

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2

Jawale, Chetan V., Kritika Ramani, De-dong Li, 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 (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. Urem

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3

Peroumal, Doureradjou, Chetan V. Jawale, Dani Antos, et al. "Kidney disease impairs B cells response against infection via inhibiting germinal center formation and antibody titers." Journal of Immunology 210, no. 1_Supplement (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 res

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4

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 (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

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5

Biswas, Partha Sarathi, Chetan V. Jawale, Kritika Ramani, et al. "Metabolic ‘de-programming’ of neutrophils protects against fatal bloodstream fungal infections during kidney disease." Journal of Immunology 204, no. 1_Supplement (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 inc

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6

Kuchma, I. L. "Uremic toxins. Back to the future." KIDNEYS 10, no. 2 (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

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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 (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 f

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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 (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

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9

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 (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

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10

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 co

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11

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 (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

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12

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 r

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13

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 ind

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14

Maciel, Rayana, Regiane Cunha, Valentina Busato, et al. "Uremia Impacts VE-Cadherin and ZO-1 Expression in Human Endothelial Cell-to-Cell Junctions." Toxins 10, no. 10 (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 ur

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15

COMBET, SOPHIE, MARIE-LAURE FERRIER, MIEKE VAN LANDSCHOOT, et al. "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 (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 w

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16

Noris, Marina, Marta Todeschini, Sergio Zappella та ін. "17β-Estradiol corrects hemostasis in uremic rats by limiting vascular expression of nitric oxide synthases". American Journal of Physiology-Renal Physiology 279, № 4 (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

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17

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 (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

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18

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 chron

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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 (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 p

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Akıncı, Tuba, Huzeyfe Köklü, Cenk Murat Ünverdi, and Yılmaz Çetinkaya. "A rare presentiation of uremia: akathisia." Academic Journal of Neurology and Neurosurgery 1, no. 3 (2024): 64–67. http://dx.doi.org/10.51271/ajnn-0015.

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Acute movement disorders associated with bilateral basal ganglia lesions are becoming more common in patients with diabetes and uremia. Pathophysiology is not fully known, although it is believed to be complex, with ischemic/microvascular as well as metabolic/toxic variables influencing lesions and symptoms. We have reported here a uremic diabetic patient who has sudden developed severe akathisia, in magnetic resonance imaging (MRI) showed bilateral symmetric basal ganglia lesions with regression at follow-up. A condition linked with acute bilateral basal ganglia lesions in diabetic uremic ind

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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 (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 pla

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Wei, Mingyu, Xianjing Hu, Min Zhu, et al. "Causal relationships between uremic metabolites or toxins and heart failure: Univariate and multivariate Mendelian randomization." Medicine 103, no. 47 (2024): e40614. http://dx.doi.org/10.1097/md.0000000000040614.

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Studies have shown that uremia, renal failure and heart failure (HF) are closely related. However, whether this association reflects a causal effect is still unclear. The aim of this study was to evaluate the causal effect of uremic metabolites or toxins on HF. Mendelian randomization (MR) analysis was conducted to evaluate the causal effect of 11 uremia-related metabolites on HF risk using single-nucleotide polymorphisms (SNPs) from a genome-wide association study. A protein–protein interaction network was constructed to study the function of SNPs corresponding to HF-related factors. Univaria

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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 (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

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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 (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

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Shin, Jin Ah, Hyerim Park, Hyunsu Choi та ін. "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, № 15 (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 dam

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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 (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 af

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Lu, Jiao, An Na, Yanyun Ren, and Chen Zhang. "Progress in the Diagnosis and Treatment of Itchy Skin in Uremia in Chinese Medicine." Journal of Contemporary Medical Practice 7, no. 6 (2025): 31–35. https://doi.org/10.53469/jcmp.2025.07(06).07.

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Itchy skin in uremia is one of the common complications in the uremic stage of chronic renal failure, which seriously affects the life of patients. Western medical treatment is mostly based on local use of emollient drugs, improving the quality of dialysis and oral antihistamine drugs, but the efficacy is not satisfactory. In recent years, the research on the treatment of itchy skin in uremia by traditional Chinese medicine has become more and more in-depth, and both oral Chinese medicine compound and external Chinese medicine treatments have gained better efficacy in the clinic with fewer adv

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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 (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 (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

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Radbil, O. S. "On the variety of uremic conditions." Kazan medical journal 43, no. 1 (2021): 3–9. http://dx.doi.org/10.17816/kazmj82995.

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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 (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 quantif

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Bergesio, F., R. Ciuti, M. Salvadori, et al. "Are Lipid Abnormalities Reliable Cardiovascular Risk Factors in Dialysis Patients?" International Journal of Artificial Organs 12, no. 11 (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.

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Kocsis, Gabriella F., Márta Sárközy, Péter Bencsik, et al. "Preconditioning protects the heart in a prolonged uremic condition." American Journal of Physiology-Heart and Circulatory Physiology 303, no. 10 (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

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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 (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

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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 (1993): 820–27. http://dx.doi.org/10.1182/blood.v81.3.820.bloodjournal813820.

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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

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Meijers, Björn, Ward Zadora, and Jerome Lowenstein. "A Historical Perspective on Uremia and Uremic Toxins." Toxins 16, no. 5 (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 sensi

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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 (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

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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 (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

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Diaz-Ricart, Maribel, Sergi Torramade-Moix, Georgina Pascual, et al. "Endothelial Damage, Inflammation and Immunity in Chronic Kidney Disease." Toxins 12, no. 6 (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 p

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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 (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 comm

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Andrade, Laila Santos de, Maria Aparecida Dalboni, José Tarcisio Giffoni de Carvalho, et al. "In vitro effect of uremic serum on barrier function and inflammation in human colonocytes." Brazilian Journal of Nephrology 40, no. 3 (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

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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 (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 opera

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Kim, Ji Eun, Hyo-Eun Kim, Ji In Park, et al. "The Association between Gut Microbiota and Uremia of Chronic Kidney Disease." Microorganisms 8, no. 6 (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 f

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Tsai, Han-Mou. "Atypical Hemolytic Uremic Syndrome: Beyond Hemolysis and Uremia." American Journal of Medicine 132, no. 2 (2019): 161–67. http://dx.doi.org/10.1016/j.amjmed.2018.08.011.

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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 (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 ph

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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 (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

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Meyer, Timothy W., and Thomas H. Hostetter. "Uremia." New England Journal of Medicine 357, no. 13 (2007): 1316–25. http://dx.doi.org/10.1056/nejmra071313.

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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 (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 differ

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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 (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

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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 (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

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