proteinuria/necrose

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Ibuprofen-associated renal dysfunction. Pathophysiologic mechanisms of acute renal failure, hyperkalemia, tubular necrosis, and proteinuria.

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Ibuprofen-associated, acute, reversible renal failure with hyperkalemia, tubular necrosis, and proteinuria developed in a patient who had no predisposing underlying disease. A renal biopsy specimen revealed mesangial hypercellularity without glomerular crescent formation. A profound interstitial

Evolution of experimentally induced papillary necrosis to focal segmental glomerulosclerosis and nephrotic proteinuria.

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Bromoethylamine (BEA)-induced papillary necrosis is a reproducible model for analgesic nephropathy. We induced this lesion in groups of male Sprague-Dawley rats and followed the functional and histological changes for 1 year. We found that by 1 month, necrosis of the papilla was complete, glomerular

Successful treatment with anti-tumor necrosis factor (anti-TNF)-alpha of proteinuria in a patient with familial mediterranean fever (FMF) resistant to colchicine: anti-TNF drugs and FMF.

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Familial mediterranean fever (FMF) is an autoinflammatory disease characterized by recurrent attacks of fever, peritonitis, pleuritis, and genetically by autosomal recessive inheritance. The major renal involvement in FMF is the occurrence of amyloidosis that can be prevented by a daily regimen of

Synergism between circulating tumor necrosis factor receptor 2 and HbA(1c) in determining renal decline during 5-18 years of follow-up in patients with type 1 diabetes and proteinuria.

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OBJECTIVE We studied the serum concentration of tumor necrosis factor receptor 2 (TNFR2) and the rate of renal decline, a measure of the intensity of the disease process leading to end-stage renal disease (ESRD). METHODS A cohort of 349 type 1 diabetic patients with proteinuria was followed for 5-18

Late evaluation of glomerular filtration rate, proteinuria, and urinary acidification after acute tubular necrosis.

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Fourteen patients were studied 2 to 36 months after acute tubular necrosis. It was observed that 43% of the patients had decreased glomerular filtration rate. These patients were older and had lower urinary excretion of ammonium and titratable acidity. Proteinuria greater than 150 mg/day, without

Prognostic value of tubular proteinuria and enzymuria in nonoliguric acute tubular necrosis.

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BACKGROUND Acute tubular necrosis (ATN) has high mortality, especially in patients who require renal replacement therapy (RRT). We prospectively studied the diagnostic accuracy of the urinary excretion of low-molecular-weight proteins and enzymes as predictors of a need for RRT in ATN. METHODS In 73

Huaiqihuang Granules () reduce proteinuria by enhancing nephrin expression and regulating necrosis factor κB signaling pathway in adriamycin-induced nephropathy.

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OBJECTIVE To investigate the effects of Huaiqihuang Granules (, HQH), a mixture of Chinese herbs including Trametes robiniophila Murr, Fructus Lycii and Polygonatum sibiricum, on adriamycininduced nephropathy (ADRN) in rats and its underlying mechanisms. METHODS Rats with ADRN were divided into four

D-serine nephrotoxicity. The nature of proteinuria, glucosuria, and aminoaciduria in acute tubular necrosis.

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Administration of D-serine to rats induced acute necrosis of the proximal straight tubules, proteinuria, glucosuria, and aminoaciduria. Proteinuria and glucosuria developed at the onset of tubular necrosis and disappeared when the tubules were completely relined by new epithelium. Our findings

α-asarone reduce proteinuria by restoring antioxidant enzymes activities and regulating necrosis factor κB signaling pathway in doxorubicin-induced nephrotic syndrome.

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α-asarone is natural bioactive compound that has been reported to have many benefits and medicinal properties. The present study aimed to assess the protective effect of α-asarone against doxorubicin (DOX) induced nephrotic syndrome in rats. An experimental nephrotic syndrome was induced by single

Clinical significance of urinary tumor necrosis factor-like weak inducer of apoptosis (TWEAK) in immunoglobulin A nephropathy .

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Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) has been implicated as a mediator of chronic inflammatory processes. Recently, it was reported that TWEAK may play an important role in the pathogenesis of kidney damage. In the present study, we investigated the role of

Long-term follow-up of secondary amyloidosis patients treated with tumor necrosis factor inhibitor therapy: A STROBE-compliant observational study.

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There are no treatment modalities, which were proven to prevent the deposition of amyloid, proteinuria, and loss of renal function due to amyloidosis. Anti-tumor necrosis factor agents (anti-TNFs) were shown to decrease the production of serum amyloid A protein.We aimed to evaluate the long-term

Anti-tumor necrosis factor alpha therapy in fifteen patients with AA amyloidosis secondary to inflammatory arthritides: a followup report of tolerability and efficacy.

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OBJECTIVE Because anti-tumor necrosis factor alpha (anti-TNF) has emerged as a highly effective treatment for numerous inflammatory arthritides, which are a common cause of AA amyloidosis, we retrospectively evaluated the safety and efficacy of anti-TNF in a nationwide study. METHODS The

Long-term Renal Outcome of Biopsy-proven Acute Tubular Necrosis and Acute Interstitial Nephritis

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Background: Although emerging evidence suggest acute kidney injury (AKI) progress to chronic kidney disease (CKD), long-term renal outcome of AKI still remains unclear. Acute tubular necrosis (ATN) is the most common cause of AKI due to

Clinical significance of necrosis in lupus nephritis.

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The significance of necrosis (karyorrhexis), among the most characteristic findings in lupus nephritis, was evaluated by studying the correlation between the existence of necrosis in renal biopsy specimens and laboratory findings. The subjects were 54 patients with diffuse proliferative lupus

[Acute kidney injury by acute tubular necrosis].

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Acute renal failure by acute tubular necrosis. In adults, acute tubular necrosis is the leading cause of acute kidney injury (AKI). Secondary to ischemia and/or tubular toxicity, the commonly found histological lesions are desquamation of tubular epithelial cells and hyaline intra-tubular deposits.

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