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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

A patient with nonoliguric acute renal failure secondary to acute tubular necrosis in conjunction with anorexia nervosa is described. Parenteral feeding at a critical time has salutory effects on the biosynthesis of new protein and thereby reduces many of the hazards of azotemia. The technique of estimating endogenous acid production is applied for the first time in a severely malnourished subject and documents the retention of dietary sulfur which presumably is retained in the formation of new tissue in the recovery phase.
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PMID:Anorexia nervosa with acute tubular necrosis treated with parenteral nutrition. 40 63

Review of clinical and pathologic data from ten fatal cases of Rocky Mountain spotted fever (RMSF) revealed the importance of acute renal failure in the clinical course and of multifocal perivascular interstitial nephritis as the principal pathologic lesion. In nine cases, Rickettsia rickettsii were demonstrated by immunofluorescence in the areas of vasculitis. Evidence was lacking for the role of disseminated intravascular coagulation, glomerulonephritis, or myoglobinuria in the pathogenesis of acute renal failure in these cases. Rickettsia-induced vascular injury led to acute renal failure by several mechanisms. Hypovolemia early in the course resulted in reversible, prerenal azotemia. Transient hypotension in midcourse produced acute tubular necrosis. In fulminant cases, preterminal circulatory collapse was associated with coma and oliguria. The interstitial nephritis could not be demonstrated conclusively to contribute to the acute renal failure.
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PMID:Acute renal failure in Rocky Mountain spotted fever. 43 98

A prospective analysis of the value of urinary diagnostic indices in ascertaining the cause of acute renal failure was undertaken. Our results show that in the setting of acute oliguria a diagnosis of potentially reversible prerenal azotemia is likely with urine osmolality greater than 500 mosm/kg H2O, urine sodium concentration less than 20 meq/litre, urine/plasma urea nitrogen ratio greater than 8, and urine/plasma creatinine ratio greater than 40. Conversely, a urine osmolality less than 350 mosm/kg, urine sodium concentration greater than 40 meq/liter, urine/plasma urea nitrogen ratio less than 3, and urine/plasma creatinine ratio less than 20 suggest acute tubular necrosis. A significant number of oliguric patients will not have urinary indices that fall within these guidelines. In this setting, urine sodium concentration divided by the urine-to-plasma creatinine ratio (the renal failure index) and the fractional excretion of filtered sodium provide a reliable means of differentiating reversible prerenal azotemia from acute tubular necrosis.
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PMID:Urinary diagnostic indices in acute renal failure: a prospective study. 66 84

The FENa test, a determination of the excreted fraction of the filtered sodium, was performed in patients in the oliguric phase of acute renal failure. Patients with prerenal azotemia had an FENa of less than 1, and patients with acute tubular necrosis had an FENa of more than 3 (P less than .001). This simple test clearly differentiates between these two conditions and, thus, is of considerable clinical value.
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PMID:The FENa test. Use in the differential diagnosis of acute renal failure. 94 39

The occurrence of rhabdomyolysis and acute renal failure associated with cytomegaloviral infection is rare. A 27-year-old housewife was admitted to our hospital with complaints of thirst, muscle weakness, abdominal pain and oliguria. There was no past history of diabetes, drinking, fever or drug habituation and a negative family history. Laboratory tests revealed myoglobinuria, hyper-pancreatic type amylaseuria, hyperglycemia, azotemia and highly increased creatine phosphokinase in the plasma. She was treated with hemodialysis and insulin therapy. Serological studies showed a 4-fold increase in cytomegalovirus antibody titers 4 weeks after admission. Muscle biopsy specimens showed hyaline degeneration and infiltration of T cell lymphocytes in the muscle. Renal biopsy specimens showed acute tubular necrosis and some myoglobin casts. No cytomegalovirus antigen was found in renal specimens by immunofluorescence study. From these results, it was determined that a systemic cytomegalovirus infection triggered pancreatitis which caused diabetic ketoacidosis, rhabdomyolysis and acute renal failure.
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PMID:Cytomegalovirus infection associated with acute pancreatitis, rhabdomyolysis and renal failure. 131 48

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

Between 1980 and 1988, 12 patients at the Cleveland Clinic had biopsy-proven acute tubulointerstitial nephritis. Etiologies of the disease included drugs, systemic illness, and idiopathic causes. Clinical features were nonspecific, and the diagnosis of acute tubulointerstitial nephritis was seldom entertained in these patients prior to biopsy. Seven patients had unrelated underlying renal disease. Treatment included discontinuation of the offending agent and/or a trial of steroids. All patients had final creatinine levels lower than at diagnosis. Because the condition is potentially reversible, this disease should be considered in all patients with new azotemia who do not exhibit prerenal factors, features typical of acute tubular necrosis, red blood cell casts heralding a glomerular process, or evidence of obstructive uropathy.
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PMID:Acute tubulointerstitial nephritis. 155 Dec 11

The hepatorenal syndrome (HRS) is a well-known complication of liver failure, and medical treatment is usually not successful unless liver function can be improved. The authors review their experience with 130 adults undergoing orthotopic liver transplantation (OLT) over a 20-month period to determine the incidence of HRS and its effects on patient outcome, need for hemodialysis (HD), and the degree of recovery of renal function. The clinical diagnosis of HRS preoperatively was made by using criteria to exclude prerenal azotemia, acute tubular necrosis, and primary renal diseases. Nineteen patients were identified as having the HRS for a preoperative incidence of 15.1 per cent. Overall, 41 of the 126 patients reviewed required postoperative HD, and the mortality in this group was 54 per cent. Fifty-eight per cent of the HRS patients were dialyzed postoperatively vs 28 per cent of non-HRS patients. The mean posttransplant creatinine improved over time in the HRS patients while it worsened slightly in the non-HRS group. At 12 weeks posttransplant, there was a significant difference in the mean creatinine levels (1.8 +/- 0.3 mg/dl vs 1.2 +/- 0.04 mg/dl, P = .001). However, at 24 weeks the small difference was not statistically significant between the two groups (1.6 +/- 0.15 mg/dl vs 1.3 +/- 0.06 mg/dl, P = NS). The current survival of the hepatorenal group is comparable to the nonhepatorenal patients at a follow-up of 6 to 25 months: 68 per cent vs 78 per cent, P = NS. The authors conclude that liver transplantation reverses the HRS, and that hepatorenal patients can undergo liver transplantation with outcomes comparable to nonhepatorenal patients.
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PMID:The hepatorenal syndrome in liver transplant recipients. 174 99

Azotemia and diabetes mellitus are now well-known adverse reactions associated with Pentamidine treatment, especially since its prescription in case of Pneumocystis carinii pneumonia. We report the case of a 2 year-old boy, treated for kala-azar with pentamidine and N-methyl glucamine antimoniate who developed adverse effects, characterized by a nephrotic syndrome associated with the classic acute tubular necrosis, and transient diabetes mellitus.
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PMID:[Transitory acute kidney insufficiency and insulin-dependent after treatment of kala-azar with pentamidine and N-methylglucamine antimony]. 185 38


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