Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Proteinuria was studied in ten renal allograft recipients; it was defined as: (a) glomerular--characterized by predominant albumin excretion; (b) tubular--significant excretion of both albumin and low molecular weight (LMW) proteins; and (c) glomerulo-tubular or mixed type, a combination of the two. LMW protein and albumin were quantitated by polyacrylamide gel electrophoresis with sodium dodecyl sulfate. In the immediate posttransplant period, LMW protein and albumin excretion, expressed as a percentage of creatinine clearance, were high, revealing a mixed pattern, and excretion of both protein classes was higher than during both acute tubular necrosis and acute rejection crisis. Tubular proteinuria was observed in acute tubular necrosis; a glomerulo-tubular or mixed pattern of protein excretion in acute rejection crises.
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PMID:Proteinuria following renal transplantation. 32 83

A human proximal renal tubular epithelial antigen (designated HRTE-1) was isolated and purified from a crude tubular preparation (Fx1A) by a process of salt fractionation, DEAE anion-exchange chromatography, and Sephadex G-200 gel filtration. Utilizing 125I-HRTE-1 and a rabbit antiserum specific for the proximal tubular brush border, as determined by immunofluorescent microscopy, a radioimmunoassay by competitive protein-binding was developed. HRTE-1 was demonstrated in serum and urine and in extracts of a variety of body organs. A range of concentrations for normal random urine samples and 24-hr urine excretion rates were determined. Random urine samples from 36 patients with a variety of functional and pathologic renal disorders were assayed for the HRTE-1 antigen. Twenty-three of 24 patients with either chronic nephropathy or pre-renal azotemia had normal urinary antigen concentrations, despite wide differences in urine flow rates, the degree of existing renal function, and the amount of proteinuria. Ten of 12 patients with acute tubular necrosis, however, had statistically abnormal HRTE-1 concentrations (high in eight patients, undetectable in two). These findings suggest that HRTE-1 antigen can be detected in both normal and pathologic urines, that altered antigen concentrations can be documented in at least one renal disorder, and that quantitation of HRTE-1 in urine may have clinical value as a marker of acute rubular injury.
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PMID:Radioimmunoassay for urinary renal tubular antigen: a potential marker of tubular injury. 36 38

Many patients with chronic pancreatitis (CP), even in the absence of intrinsic renal disease, are found to have abnormal urine, with persistent proteinuria, cylindruria, microhematuria and leukocyturia. The kidneys of 12 necropsy cases with CP showed mild to moderate arterial and arteriolar nephrosclerosis and no other significant changes. Renal biopsies were performed in 10 patients with CP without evidence of systemic disease or intrinsic renal disease, but with persistent urinary abnormalities. By light microscopy, mild arterial and arteriolar nephrosclerosis was present in 5 instances. In 1 patient, evidence of the reparative phase of acute tubular necrosis was noted. In 5 biopsies, electron microscopy revealed minimal to mild increase in mesangial matrix. Mild thickening of the glomerular basement membrane (GBM) was found in three instances but there was no clear-cut evidence of diabetic glomerulosclerosis. The presence of subendothelial electron-lucent material in 3 cases suggests the possibility of previous subclinical episodes of intravascular coagulation. The most consistent finding was the presence of lipid material in the cytoplasm of glomerular and tubular cells. The renal lesions associated with CP are mild, nonspecific and nonprogressive. Various pathogenetic factors can be invoked to account for their presence and for the urinary abnormalities found in patients with CP.
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PMID:Renal lesions in chronic pancreatitis. 74 Jan 5

This essay illustrates the spectrum of sonographic findings of various renal manifestations of AIDS. The most common renal abnormality in patients with AIDS is nephropathy, which is manifested by deterioration of renal function and proteinuria. Acute tubular necrosis, intrarenal infections, focal nephrocalcinosis, hydronephrosis, and neoplasms also may occur.
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PMID:Renal diseases in patients with AIDS: sonographic findings. 847 Jun 3

A 21-year-old man developed acute renal failure early in the course of hepatitis A infection and recovered after 17 days. There was no evidence of pre-renal azotemia, the hepato-renal syndrome, ischemic acute tubular necrosis, rhabdomyolysis, or thrombotic microangiopathy. There was, however, transient proteinuria and hypocomplementemia. It would appear that the renal failure resulted from viral-induced injury, either direct or mediated by immune complexes.
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PMID:Acute renal failure in hepatitis A. 151 92

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 reaching a nephrotic level, was found in 92% of the patients. The presence of oliguria, the demand of dialysis, and the acute tubular necrosis etiology were not statistically different among the patients who recovered their glomerular filtration rate either totally or partially.
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PMID:Late evaluation of glomerular filtration rate, proteinuria, and urinary acidification after acute tubular necrosis. 156 89

Kidney disease is often cited as one of the adverse effects of chromium, yet chronic renal disease due to occupational or environmental exposure to chromium has not yet been reported. Occasional cases of acute tubular necrosis (ATN) following massive absorption of chromate have been described. Chromate-induced ATN has been extensively studied in experimental animals following parenteral administration of large doses of potassium chromate (hexavalent) (15 mg/kg body weight). The chromate is selectively accumulated in the convoluted proximal tubule where necrosis occurs. An adverse long-term effect of low-dose chromium exposure on the kidneys is suggested by reports of low molecular weight (LMW) proteinuria in chromium workers. Excessive urinary excretion of beta 2-microglobulin, a specific proximal tubule brush border protein, and retinol-binding protein has been reported among chrome platers and welders. However, LMW proteinuria occurs after a variety of physiologic stresses, is usually reversible, and cannot by itself be considered evidence of chronic renal disease. Chromate-induced ATN and LMW proteinuria in chromium workers, nevertheless, raise the possibility that low-level, long-term exposure may produce persistent renal injury. The absence of evidence of chromate-induced exposure may produce persistent renal injury. The absence of evidence of chromate-induced chronic renal disease cannot be interpreted as evidence of the absence of such injury. Rather, it must be recognized that no prospective cohort or case-control study of the delayed renal effects of low-level, long-term exposure to chromium has been published.
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PMID:Chromium-induced kidney disease. 193 54

The resistive index (RI), calculated from the duplex Doppler waveform, was compared with clinical and laboratory findings and the results of renal biopsy in 41 patients with nonobstructive (medical) renal disease. Kidneys with active disease in the tubulointerstitial compartment had a mean RI of 0.75 +/- 0.07. This was statistically significantly different (p less than .01) from the RI in kidneys with disease limited to the glomeruli (mean RI of 0.58 +/- 0.05). Acute tubular necrosis resulted in an elevated RI (mean RI = 0.78 +/- 0.03) as did vasculitis/vasculopathy (mean RI = 0.82 +/- 0.05). Patients with hypertension, proteinuria, or hematuria did not have kidneys with a significantly higher RI than did patients without these clinical factors. Kidneys found to be abnormally echogenic did not have an RI significantly different from kidneys of normal echogenicity. There was a weak correlation between creatinine level and RI value, reflected by a linear correlation coefficient of 0.34. In patients with normal renal RIs, the mean creatinine level was 1.7 +/- 1.7, whereas in those with abnormal RI values (greater than or equal to 0.70), the mean creatinine level was 3.7 +/- 3.6. We conclude that some forms of nonobstructive renal disease can produce changes in the Doppler waveform detectable by RI measurement. The production of Doppler waveform changes is strongly influenced by the site of the main disease within the kidneys. Active disease within the tubulointerstitial compartment (acute tubular necrosis, interstitial nephritis) or vasculitis/vasculopathy generally resulted in an elevated RI, whereas disease limited to the glomeruli, no matter how severe, did not significantly elevate the RI. Degree of renal dysfunction as indicated by serum creatinine level probably affects the Doppler waveform to some degree, but the relationship is weak.
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PMID:Intrarenal arterial Doppler sonography in patients with nonobstructive renal disease: correlation of resistive index with biopsy findings. 211 Jul 32

Fifteen (34.8%) of 43 patients of falciparum malaria screened for urinary abnormalities showed significant proteinuria (greater than 150 mg/24 h), haematuria (greater than 1/HPF) and casts, with or without azotaemia. Light microscopic examination of renal biopsy tissue from 12 patients revealed mesangial and endothelial proliferative change in 8, and acute tubular necrosis in one patient. Immunofluorescence showed IgM alone, or IgG and IgM along with C3, in 7 patients within the mesangium or along the capillary walls. Repeat kidney biopsy after 6 wk in 5 patients revealed no residual pathology indicating the reversible nature of the lesions.
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PMID:Immunopathological changes in kidney in Plasmodium falciparum malaria. 218 4

Reported was an aged woman (80-year-old) of minimal change nephrotic syndrome which was complicated with reversible oliguric acute renal failure. The patient presented massive proteinuria, anasarca, and severe azotemia. She recovered conservatively from the acute renal failure and subsequently remitted from the nephrotic syndrome after the treatment which comprised albumin infusion, diuretics, adrenocorticosteroid hormones (including the pulse therapy), antiplatelet drug, and anticoagulants. The histopathologic findings of renal biopsy were compatible with minor glomerular abnormalities and acute tubular necrosis with many tubular casts. The previously reported cases older than 80-year-old which remitted from minimal change nephrotic syndrome complicated with reversible acute renal failure, were very rare. The present case was the second case among the literatures.
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PMID:[An aged woman with minimal change nephrotic syndrome complicated with reversible acute renal failure]. 219 Nov 62


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