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)

The relative merits of the automated, fluorimetric assay of urinary enzymes and cell exfoliation were compared with other commonly used tests for renal damage. Two types of nephrotoxic agent were used, causing crystal nephropathy and acute tubular necrosis respectively. Groups of marmosets were given one of two drugs known to cause crystal nephropathy. One agent caused intermittent increases in urinary enzyme excretion and an early increase in cell excretion which was not sustained. The second agent in contrast caused elevated cell and enzyme excretion, increasing throughout the period of administration. A nephrotoxic anti-tumour agent also caused increases in cell and enzyme excretion when given to marmosets. The early changes produced by this agent were studied using catheterised rats. Hourly samples of urine were collected and urinary beta-glycosidase excretion was found to give an early indication of renal damage, which correlated with albuminuria and glycosuria. The fluorimetric assay of urinary enzymes provides a sensitive, non-invasive test of nephrotoxicity.
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PMID:Urinary enzyme assays in toxicological studies in the rat and marmoset. 10 49

Although haematuria is a relatively common symptom of hemophilia A and B, renal disease seemed to be a rarity and it has usually been held that this symptom was benign in nature. However detailed studies of renal function in a series of such patients using radiological and biochemical tests of renal function show significant differences compared to normal. These abnormalities seem to be associated with recurrent haematuria but do not appear to be related directly to replacement therapy with plasma concentrate and do not occur more frequently in patients who have received long term fibrinolytic inhibitors. Other rare renal disorders associated with haemophilia include nephrotic syndrome, trauma, acute tubular necrosis, analgesic nephropathy and chronic pyelonephritis.
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PMID:Renal disorders in haemophilia A and B. 26 97

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

The clinical manifestations of drug-induced renal disease may include all the manifestations attributed to natural or spontaneous renal diseases such as acute renal failure, chronic renal failure, acute nephritic syndrome, renal colic, haematuria, selective tubular defects, obstructive nephropathy, etc. It is therefore vital in any patient with renal disease whatever the clinical manifestations might be, to obtain a meticulous drug and toxin inventory. Withdrawal of the offending drug may result in amelioration or cure of the renal disorder although in the case of severe renal failure it may be necessary to utilise haemodialysis or peritoneal dialysis to tide the patient over the period of acute renal failure. Analgesic nephropathy is an important cause of terminal chronic renal failure and it is therefore vital to make the diagnosis as early as possible. The pathogenesis of some drug-induced renal disorders appears to be immunologically mediated. There are many other pathogenetic mechanisms involved in drug-induced renal disorders and some drugs may under appropriate circumstances be responsible for a variety of different nephrotoxic effects. For example, the sulphonamides have been incriminated in examples of crystalluria, acute interstitial nephritis, acute tubular necrosis, generalised hypersensitivity reactions, polyarteritis nodosa and drug-induced lupus erythematosus.
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PMID:Drug-induced renal disease. 38 1

This review concerns the present state of accomplishments in the study of SEM of human and experimental renal disease. Critical techniques of specimen preparation reviewed include perfusion fixation, razor tissue sectioning, alcohol cryofracture, microtome sectioning of paraffin or styrene embedded tissue, ultraplaning with glass knives of hard carbowax embedded tissues and glomerular isolation. Gold-palladium coating and heavy metal impregnation with osmium, uranium, and silver are discussed. A compendium of SEM observations of human glomerular, vascular and tubular disease is presented. Techniques for SEM of experimental renal disease are reviewed. These include latex vascular injection, freeze drying, x-ray microanalysis and use of backscattered electron imaging. Experimental models previously investigated by SEM are puromycin aminonucleoside nephrosis, daunomycin nephrosis, and N,N1-Diacetylbenzedine glomerulopathy, nephrotoxic serum nephritis, and protamine perfusion glomerulopathy. Reviewed are acute tubular necrosis caused either by angiotensin, hypotension, norepinephrine, glycerol, mercury, and unilateral renal artery occlusion, also potassium depletion nephropathy, alloxan diabetes and diphenylamine-induced polycystic disease.
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PMID:SEM of human and experimental renal disease. 52 33

The cephalosporin antibiotics cephaloridine and cephalothin are known to cause renal damage. Experience with newer congeners is not yet sufficient to predict their potential nephrotoxocity. The renal lesion produced by cephaloridine is primarily due to the intrinsic toxicity of this drug for the cells of the proximal renal tubule and depends upon its peculiar transport characteristics. In contrast, renal injury due to cephalothin resembles that seen with the penicillins. Thus, some instances of cephalothin nephropathy appear to be toxic in nature with a histologic picture of acute tubular necrosis, whereas others exhibit signs of hypersensitivity including rash, eosinophilia, and interstitial nephritis. Among the factors alleged to contribute to the nephrotoxicity of cephalosporins is their administration with aminoglycosides. Although the physician should be aware of the possibility of a potential adverse interaction between these groups of antibiotics, the evidence is not sufficiently conclusive to warrant avoidance of the combination when it appears to be therapeutically useful.
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PMID:The nephrotoxicity of cephalosporins: an overview. 65 5

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

One hundred and seventy-five 67Ga-citrate scans were performed to detect suspected occult inflammatory processes. None of the patients had a known malignancy. Renal activity was noted in 12 patients (6.8%) on the 48-hr image. These patients had either pyelonephritis, acute tubular necrosis, vasculitis, or a renal abscess. Since delayed 67Ga uptake in the kidneys may be the first evidence of renal disease, further investigation, including either arteriography or biopsy, is necessary. In patients with a known malignancy, tumor involvement must be considered.
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PMID:Significance of delayed 67Ga localization in the kidneys. 96 53

131I-labeled autologous fibrinogen was used to detect acute renal allograft rejection in the early postoperative period. Ratios of radioactive counts over transplanted kidneys to those over the heart increased with deposition of radioactive fibrinogen in kidneys undergoing rejection. The test was positive in all instances of acute rejection twelve to twenty-four hours prior to clinical ro biochemical changes. False-positive test results were noted in instances of perinephric hematoma, seroma, and wound abscess and in one patient with urinary tract infection. The test was negative in cases of renal failure secondary to acute tubular necrosis, uric acid nephropathy (in the absence of acute rejection), and chronic rejection. This test is simple, rapid, and practical. It can be performed at the bedside and is free from complications, particularly serum hepatitis.
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PMID:Early detection of acute rejection in renal allografts using radioiodinated autologous fibrinogen. 109 6

Although it has been suggested that cytomegalovirus (CMV) infection of the kidney might facilitate the development of human immunodeficiency virus-associated nephropathy (HIVAN) or other morphologic renal changes in patients with AIDS, no systematic study has been performed on kidneys from AIDS patients. We examined 75 autopsy kidneys, two renal biopsy specimens, and a nephrectomy specimen from 78 HIV-infected patients (five with HIVAN) for the presence of CMV. Immunocytochemistry (ICC) utilizing a monoclonal antibody against the late antigen of CMV and in situ hybridization (ISH) with a biotinylated DNA probe for CMV sequences were used. The detection system for both ICC and ISH was streptavidin-conjugated alkaline phosphatase with Fast Red TR chromogen. CMV was detected in only 10 of the 78 kidneys examined (12.8%): eight by both methods, one by ISH only, and another by ICC only. All 10 positive kidneys were obtained from autopsies of patients with AIDS. The average number of positive cells (in approximately 15 x 10 mm sections) was 22 with ICC and 10 with ISH. Glomerular intracapillary cells (possibly endothelial cells) were the most commonly stained, followed by positive cells in the interstitium and peritubular capillaries. Relatively few tubular epithelial cells were stained. The majority of positive cells by either ICC or ISH did not show nuclear or cytoplasmic inclusions; however, only two of the 10 positive kidneys did not contain cells with typical Cowdry type-A intranuclear CMV inclusions. The most frequent pathologic finding in the kidneys positive for CMV by either ICC or ISH was acute tubular necrosis (in six of 10, 60%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Is cytomegalovirus associated with renal disease in AIDS patients? 132 3


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