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

Three patients having lepromatous leprosy developed acute renal failure. Two patients completely recovered and one was left with a moderate degree of renal insufficiency. Renal tissue obtained by percutaneous biopsy revealed acute tubular necrosis in two and diffuse crescentic glomerulonephritis in the third case.
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PMID:Acute renal failure in leprosy. 56 62

Intravesical instillation of formalin in a patient with transitional cell carcinoma of the bladder and radiation cystitis was followed by acute renal failure due to acute tubular necrosis. Formic acid, which is a metabolic product of formalin, has been postulated as the pathogenetic agent responsible for acute tubular necrosis.
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PMID:Acute tubular necrosis following intravesical instillation of formalin. 56 92

Acute renal failure due to intravascular hemolysis is a common clinical problem in North Indian patients. It constituted 21.5 percent of 325 patients dialyzed for acute renal failure over an 11-year period at Chandigarh. Thirty patients had developed acute intravascular hemolysis in association with erythrocyte glucose-6 phosphate dehydrogenase (G-6PD) deficiency, 17 due to copper sulphate intoxication and 8 due to envenomation by snakes. Less frequent causes were insect stings, incompatible blood transfusion, intake of anti-leprosy drug--dapsone in non-G-6PD-deficient patients, and mercuric chloride toxicity in two patients each; naphthalene poisoning in one; and uncertain causes in six patients. Renal histology was available in 55 patients. Acute tubular necrosis was seen in 54 and bilateral diffuse cortical necrosis in one patient. Fifty patients (71.43 percent) survived and 20(28.6 percent) diet. G-6PD erythrocyte deficiency, which is present in 4.5 percent of the North Indian population, was the most frequent cause of acute renal failure in this group.
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PMID:Acute renal failure due to intravascular hemolysis in the North Indian patients. 60 54

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

An 18-year-old girl developed acute renal failure 24 hr after ingestion of potassium dichromate. Laboratory data revealed associated intravascular haemolysis. Renal histology showed features suggestive of acute tubular necrosis. She went into diuretic phase after 11 days of oliguria and subsequently regained normal renal function. Both direct toxic damage by dichromate and intravascular haemolysis may have contributed to the development of acute tubular necrosis and acute renal failure.
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PMID:Intravascular haemolysis and acute renal failure following potassium dichromate poisoning. 68 12

Acute renal failure even today carries a high mortality, which is related directly to the aetiology of the condition and the age of the patient. Modern radiological techniques have added considerably to the early diagnosis of obstructive factors and acute tubular necrosis. Early treatment and correction of prerenal factors can frequently forestall the development of established acute renal failure but if this is inevitable total patient care and full supportive measures including dialysis should be available.
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PMID:Acute renal failure. 68 29

Fifty-three children, ages one day to 15 years, were treated with hemodialysis for acute renal failure between 1968 and 1977. Twenty-three had acute tubular necrosis. Nine had ATN associated with catastrophic medical illnesses; all died. Fourteen had ATN following major surgical procedures; ten died. Thirty had ARF due to primary nephrologic disorders; 27 survived. Thus it was not the ARF per se but the underlying and concomitant disorders which had the major influences on survival. As prognostic indications of survival in patients with postoperative ATN cannot be clearly defined, these patients almost always deserve aggressive management, including dialysis therapy. Patients with ATN associated with severe medical illness often have fatal underlying conditions which cannot be influenced by presently available technologies.
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PMID:Acute renal failure in infants and children: outcome of 53 patients requiring hemodialysis treatment. 71 76

During the last seven years we encountered 117 cases of acute renal failure after 492 renal transplants. The affected patients fall into two general groups that can be broadly identified by an 131I-Hippuran renogram: Those in whom low or no uptake is evident on the renogram (group 1) and those in whom good uptake is evident on the renogram (group 2). Fifty per cent of the patients in group 1 have renal arterial thrombosis or hyperacute rejection. These patients should have a renal arteriogram, and immediate nephrectomy may be necessary. The prognosis in these patients is very grave. In group 2, 89 per cent of the patients have acute tubular necrosis, and they do not differ prognostically from patients who experience immediate renal function. Invasive diagnostic procedures should be avoided in this group because they may increase the mortality rate. We believe that repeated renograms, a reduction in azathioprine dosage and careful dialysis is the only treatment necessary.
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PMID:Etiology and prognosis in acute post-transplant renal failure. 78 39

We report a case of renal cortical microabscesses which presented as oliguric acute renal failure. Prior to the biopsy the patient was suspected of having acute pyelonephritis with acute tubular necrosis. Biopsy was performed to rule out rapidly progressive glomerulonephritis as a cause of his renal failure. To our surprise, we found multiple small microabscesses in the renal cortiex. Renal cortical microabscesses should be considered as a reversible acute renal failure.
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PMID:Renal cortical microabscesses as cause of reversible acute renal failure. 84 81

Eleven out of a series of twenty-nine patients (37-9%) with acute copper sulphate poisoning developed acute renal failure. Intravascular haemolysis appeared to be the chief factor responsible for renal lesions in these patients. Histological lesions observed in the kidney varied from those of mild shock to well established acute tubular necrosis. In one case, granulomatous lesions were seen in response to tubulorrhexis. Renal failure was the chief indication for dialysis in ten patients, whereas one patient was dialysed primarily for removal of copper. Notwithstanding the adequate control of uraemia by dialysis, only six of the eleven patients recovered. Septicaemia was responsible for death in three, hepatic failure in one and methaemoglobinaemia in another. It is postulated that release of copper from haemolysed red cells during acute haemolytic episodes may initiate, or contribute to, the development of renal damage.
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PMID:Acute renal failure following copper sulphate intoxication. 87 9


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