Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The value of biomarkers of myocardial damage or inflammation in off-pump coronary artery bypass (OPCAB) surgery has not yet been established. In a prospective study of 51 consecutive patients scheduled for elective OPCAB surgery, preoperative levels of troponin T, C-reactive protein, interleukin-6 and tumor necrosis factor-alpha were determined. The primary endpoint was the combination of cardiac death or acute myocardial infarction (AMI) within 30 days. Seven patients (14%) presented with an adverse event: three cardiac deaths and six AMIs. Univariate analysis identified the following adverse event predictors: renal failure (50% vs 11%, P=.028), left ventricular ejection fraction 0.10 ng/dL (43% vs 9%, P=.016), and EuroSCORE rating (7.6 [2.5] VS. 5.2 [2.6], P=.031). A preoperative troponin-T level > 0.10 ng/dL (P=.03) was the only independent adverse event predictor. No significant differences were found with biomarkers of inflammation (P.05). The presence of a preoperative troponin-T level > 0.10 ng/dL is associated with a higher risk of cardiac death or AMI in patients undergoing OPCAB surgery.
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PMID:[Prognostic role of new biomarkers in off-pump coronary artery bypass surgery]. 1671 54

Enhanced chronic systemic inflammation and reduced insulin sensitivity are often associated in patients with chronic renal failure, contributing to cardiovascular morbidity and mortality in these patients. Adipose tissue produces several hormones (adipocytokines including leptin, resistin, tumor necrosis factor-alpha, and adiponectin) that modulate both systemic inflammatory response and insulin action. High leptin, resistin, and tumor necrosis factor-alpha and low adiponectin are associated with proinflammatory conditions, whereas opposite patterns are commonly observed in the presence of increased insulin sensitivity, low inflammation, and reduced cardiovascular risk. Oxidative stress has also been shown recently to modulate adipocytokine production, resulting in a proinflammatory profile. Increments of plasma concentrations of both proinflammatory and anti-inflammatory adipocytokines have been reported in chronic renal failure, possibly caused by both passive accumulation from reduced renal excretion and metabolic abnormalities induced by uremia. The potential role of altered adipose tissue adipocytokine production in the onset of renal failure-associated inflammatory and metabolic derangements remains largely to be elucidated and is discussed in the current report.
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PMID:Inflammation and adipose tissue in uremia. 1682 20

Diabetes mellitus and its complications are a public health problem. Diabetic nephropathy has become the main cause of renal failure, and furthermore is associated with a dramatic increase in cardiovascular risk. Unfortunately, the mechanisms leading to the development and progression of renal injury in diabetes are not yet fully known. There is now evidence that activated innate immunity and inflammation are relevant factors in the pathogenesis of diabetes. Furthermore, different inflammatory molecules, including pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha), play a critical role in the development of microvascular diabetic complications, including nephropathy. This review discusses the role of TNF-alpha as a pathogenic factor in renal injury, focusing on diabetic nephropathy, and describes potential treatment strategies based on modulation of TNF-alpha activity.
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PMID:The role of TNF-alpha in diabetic nephropathy: pathogenic and therapeutic implications. 1711 15

Idiopathic membranous nephropathy (IMN) has a strong association with the major histocompatibility complex HLA B8DR3(17)DQ2 haplotype. The tumor necrosis factor (TNF)A gene is located within the major histocompatibility complex region on chromosome 6. We have studied the influence of two functional polymorphisms; the -308 (promoter region) and the TNFd microsatellites on initiation and/or progression of IMN. This was a case-control study comparing data from 100 Caucasians patients (67 male subjects; 67%) with IMN to 232 Caucasians local controls (171 male subjects; 74%). We have analyzed genotypes and alleles distributions and the role of these polymorphisms in disease progression towards end-stage renal failure or patient death. For -308 TNFA polymorphism, distribution of genotypes was significantly different between IMN and controls (chi(2)=16.25; P=0.0003): the A2 allele frequency was 28.0% in IMN vs 15.3% in controls (chi(2)=14.57; P=0.0001). For TNFd polymorphism, alleles distribution (from d1 to d7) was also significantly different between IMN and controls (chi(2)=56.74; P<0.0001) with both diminished d3 allele frequency (chi(2)=27.30; P<0.0001; Pc=0.001) and increased d2 allele frequency (chi(2)=29.95; P<0.0001; Pc=0.001) in IMN. We could not isolate any significant and independent influence of these different genotypes on IMN disease progression. The TNFA2 and TNFd2 alleles were strongly associated with occurrence/initiation of IMN and should be considered as susceptibility genes for this disease.
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PMID:TNFA2 and d2 alleles of the tumor necrosis factor alpha gene polymorphism are associated with onset/occurrence of idiopathic membranous nephropathy. 1721 76

The role of nitric oxide (NO) in acute renal failure (ARF) is debatable. In the present study, we investigated the effect of acute administration of NO donor, Sodium nitroprusside (SNP), L-Arginine (L-Arg) and NO synthase inhibitor, N(omega)-L-arginine methyl ester (L-NAME) in Fe-NTA induced renal toxicity. Rats were pretreated with SNP (2.5 mg/kg i.p), L-Arg (125 mg/kg, i.p.) and L-NAME (10 mg/kg, i.p.) prior to administration of Fe-NTA (8 mg iron/kg body weight, i.p.) to determine the urea and creatinine levels along with biochemical analysis of oxidative stress. Fe-NTA administration markedly increased the BUN and serum creatinine level which was coupled with a marked lipid peroxidation, decreased levels of reduced glutathione and total nitric oxide levels of rat kidneys coupled with significant morphological alterations. It also resulted in the significant increase in tumor necrosis factor-alpha (TNF-alpha) in serum. Concomitant treatment with SNP and L-Arg significantly reduced the serum creatinine and BUN levels, reduced lipid peroxidation in a significant manner, restored levels of reduced glutathione, increased total nitric oxide levels and restored the normal morphology. Pretreatment with SNP and L-Arg attenuated the levels of TNF-alpha in serum in a significant manner. Prior administration of L-NAME reversed the protective effects produced by SNP and L-Arg. Present findings strongly suggest that nitric oxide plays a significant role in the pathophysiology of iron-induced renal failure and administration of NO donors can be valuable in the treatment of ARF.
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PMID:Sodium nitroprusside and L-arginine attenuates ferric nitrilotriacetate-induced oxidative renal injury in rats. 1728 Jul 60

Carbamylation is a post-translational modification of proteins characterized by the binding of cyanate to amino groups, increased in renal failure. Pathophysiological consequences of carbamylation and adverse effects of carbamylated proteins on cell functions are poorly understood. We studied the influence of carbamylated albumin on polymorphonuclear neutrophil (PMN) O(2)(-) production. Carbamylated albumin significantly decreased O(2)(-) production in PMNs stimulated by type I collagen, but not by phorbol 12-myristate 13-acetate or tumor necrosis factor-alpha. This effect was related to inhibition of p(125)FAK phosphorylation. Such an alteration of neutrophil oxidative functions might explain characteristic complications of renal failure, such as increased occurrence of inflammation or infections.
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PMID:Carbamylated albumin is a potent inhibitor of polymorphonuclear neutrophil respiratory burst. 1737 41

Cisplatin is a chemotherapeutic agent that induces tumor necrosis factor-alpha (TNF-alpha) production in many cell types with unfortunate renal toxicity. We sought to determine the contributions of renal parenchymal cells and bone marrow-derived immune cells to the pathogenesis of cisplatin-induced renal injury in vivo. To do this we created chimeric mice in which the bone marrow was ablated and replaced with donor bone marrow cells from wild-type or from TNF-alpha knockout mice. Six weeks after reconstitution, the chimeric mice were treated with cisplatin and renal structural and functional parameters were measured. Chimeras with kidneys of wild-type animals all developed significant renal failure after 72 h of cisplatin treatment regardless of the immune cell source. Chimeras with kidneys of TNF-alpha knockout mice showed significantly less renal dysfunction (blood urea nitrogen, serum creatinine, and glomerular filtration rate), renal histologic injury, and serum TNF-alpha levels; again regardless of the immune cell source. Urinary excretion of several proinflammatory cytokines was lower in the wild-type bone marrow-knockout kidney chimera mouse than in wild-type background mice. Our results indicate that a substantial portion of circulating and urinary TNF-alpha is derived from nonimmune cells after cisplatin administration. We conclude that the production of TNF-alpha by renal parenchymal cells, rather than by bone marrow-derived infiltrating immune cells, is responsible for cisplatin-induced nephrotoxicity.
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PMID:Cisplatin-induced nephrotoxicity is mediated by tumor necrosis factor-alpha produced by renal parenchymal cells. 1759 86

Cytokines play central roles in both innate and adaptive immune responses that lead to renal inflammation. They are involved systemically in cross-talk between antigen-presenting cells, leukocytes, and regulatory cells to initiate and modulate nephritogenic immunity. Within the kidney, cytokines play a central role in signaling between infiltrating leukocytes and intrinsic renal cells and orchestrate the effector responses that lead to renal damage. Glomerulonephritis (GN) is an important cause of renal inflammation leading to renal failure that results from adaptive responses targeted at the kidney. Animal models of GN have shown that cytokines play critical roles in initiation and modulation of renal inflammatory responses through their ability to modulate the T helper 1/T helper 2 balance of nephritogenic immune responses. Evidence from clinical studies is now confirming the importance of this paradigm in directing the inflammatory mechanisms, histologic patterns, and clinical consequences of human GN. Cytokines also have critical intrarenal effector roles in the development, perpetuation, and resolution of GN. The proinflammatory role of intrarenal cytokine production by leukocytes in GN is well recognized, but, more recently, the role of intrinsic renal cell cytokine production in amplifying renal inflammation has been shown in animal models of GN. Studies showing benefits of specific anticytokine therapies directed at tumor necrosis factor in human GN are now appearing.
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PMID:Cytokines in glomerulonephritis. 1753 6

A 30-year-old Japanese woman with falciparum malaria was hospitalized because of fever and renal failure, and prolonged anemia was identified despite the eradication of malaria parasites through anti-malaria therapy. Bone marrow aspiration revealed the presence of macrophages with hemophagocytosis, and serum interleukin (IL)-18 and tumor necrosis factor (TNF)-alpha levels were high in the anemic phase. Hemophagocytosis was confirmed for at least 3 weeks, and prolonged hemophagocytic syndrome is thought to be one of the causes of prolonged anemia in patients with falciparum malaria.
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PMID:CLINICAL case report: falciparum malaria with hemophagocytic syndrome. 1755 3

The pathophysiologic mechanisms leading to acute ischemic renal failure are not completely understood. Melatonin, a compound with well-known antioxidant properties, reduces IR-induced renal injury. The purpose of the present study was to investigate the changes in levels of tumor necrosis factor (TNF)-alpha, IL-beta, and IL-6 in postischemic reperfused renal tissue, and to determine whether the protective effect of melatonin is related the modulation of the production of these inflammatory molecules. Male Wistar albino rats were unilaterally nephrectomized and subjected to 1 hr of renal pedicle occlusion followed by 2 hr or 24 hr of reperfusion. Melatonin (10 mg/kg, i.p.) or vehicle was administrated at 10 min prior to ischemia. After 24 hr of the reperfusion, following decapitation, kidney samples were taken both for histologic examination and for the determination of malondialdehyde (MDA), myeloperoxidase (MPO) activity, total antioxidant capacity (TAC), total oxidative stress (TOS), creatinine, and blood urea nitrogen (BUN). These were measured in serum samples. TNF-alpha, IL-beta, and IL-6 were measured in kidney samples after 2 hr of reperfusion. IR caused a significant increase in renal MDA, MPO, TOS, creatinine, and BUN while decrease TAC without any change in TNF-alpha, IL-beta, and IL-6 levels. Melatonin treatment reduced the biochemical indices without any change in the cytokine levels and ameliorated histopathologic alterations induced by IR. The protective effect of melatonin on IR-induced renal injury is related to its antioxidant properties but not to proinflammatory cytokines.
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PMID:Melatonin protects from ischemia/reperfusion-induced renal injury in rats: this effect is not mediated by proinflammatory cytokines. 1764 95


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