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

Although acute renal artery obstruction causes cessation of kidney function, the viability of the nephron is often maintained by collateral circulation. When renal artery blood flow is restored, filtration is resumed and the resulting acute tubular necrosis is gradually resolved as renal tubular cells regenerate. We have observed several different mechanisms of acute renal artery obstruction resulting in anuric renal failure: temporary suprarenal placement of an aortic clamp during absominal aneurysmectomy, resulting in bilateral renal artery occlusion; embolus, presumably of cardiac origin, to a solitary kidney; and thrombosis of the distal aorta extending to a level proximal to the renal arteries. There is no correlation between the duration of renal artery occlusion and the viability of kidney parenchyma. Viability of the kidney can only be determined by visual inspection at operation and response to revascularization. When vascular obstruction is a possible cause of acute anuric renal failure, immediate angiography is indicated. If a correctable vascular lesion is identified, operative intervention is mandatory.
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PMID:Revascularization of the ischemic kidney. 62 86

In a series of 183 emergency operations in which intraoperative autotransfusion was used, 14 patients received blood contaminated by intestinal contents. Six of the 14 patients died early in the postoperative period, four of whom had received more than 16 liters of blood. Only two of the eight survivors had received comparable amounts of blood (13 and 17.5 liters). All eight received antibiotics upon admission; four had positive blood cultures within 24 hours of operation. Complications included acute tubular necrosis in three patients and bowel obstruction with intra-abdominal abscess in another. One of the patients with acute tubular necrosis died six weeks later; all others recovered. We believe this procedure may be life-saving in some cases.
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PMID:Autotransfusion of blood contaminated by intestinal contents. 63 87

The courses of 276 acute tubular necrosis patients referred for dialysis were reviewed in search for prognostic indicators. Sixty-three percent survived. Of 28 possible predictor variables, a posttoxic cause and nonoliguria were favorable, whereas myocardial infarction and peritonitis affected survival unfavorably. Total pareneral nutrition influenced survival favorably only in those with multiple complications or peritonitis. No single variable or combination predicted a lethal outcome. Since survivors were frequently restored to complete health, we advocate an aggressive therapeutic approach even in the face of multiple complications.
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PMID:Prevailing patterns and predictor variables in patients with acute tubular necrosis. 64 66

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

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

Hypokalemia is an uncommon cause of rhabdomyolysis with acute tubular necrosis. We recently treated a patient in whom severe hypokalemia attributed to diuretic therapy antedated acute myoglobinuric renal failure by six months. After recovery, hypokalemia persisted and subsequent evaluation disclosed primary aldosteronism. This case is a unique presentation for primary aldosteronism and illustrates the importance of diagnosis before treatment in hypertension as well as the hazards of hypokalemia.
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PMID:Primary aldosteronism presenting as myoglobinuric acute renal failure. 68 40

Twelve patients with otherwise uncomplicated acute viral hepatitis (two were HBsAg-positive) developed renal failure. Apart from dehydration due to repeated vomiting in one patient, no factor responsible for precipitating renal failure could be identified. The clinical course was characterised by renal failure with plasma urea concentrations reaching maximum values of 26-69 mmol/l (175-416 mg/100 ml). Ten patients needed dialysis for up to two weeks. Seven patients recovered completely, while the other five died from sepsis. The types of renal failure were similar to those described in fulminant hepatic failure and cirrhosis--namely, functional renal failure in five patients and acute tubular necrosis in seven. Two of the patients with functional renal failure later developed tubular necrosis. The mechanism responsible for renal failure in acute viral hepatitis is uncertain, though endotoxaemia may contribute.
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PMID:Renal failure in otherwise uncomplicated acute viral hepatitis. 68 5

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


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