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1/6. legionnaires' disease associated with acute renal failure: a report of two cases and review of the literature.

    Renal involvement is a well described complication of legionnaires' disease and is often manifested as mild, transient azotemia, hematuria, proteinuria, pyuria or cylinduria. Acute renal failure complicating legionnaires' disease has also been described, and some patients have required hemodialysis. Renal morphology has only been described in a few cases. We report two cases of legionnaires' disease who developed acute renal failure. The serotype of the legionella pneumophilia isolated from one of the patients had never been isolated from humans before. This patient expired and at autopsy the kidney revealed acute tubular necrosis, but there was no evidence for interstitial or glomerular disease. Renal morphology in six previously reported cases revealed acute tubulointerstitial nephritis in three cases and acute tubular necrosis in the other three. We conclude that acute renal failure may accompany severe legionnaires' disease, and the development of the renal failure is not related to hemodynamic factors, while nephrotoxic antibiotics may be a contributing factor.
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2/6. anorexia nervosa with acute tubular necrosis treated with parenteral nutrition.

    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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3/6. Acute renal failure after acetaminophen overdose: report of two cases.

    Two cases of acute tubular necrosis without hepatic failure following acetaminophen overdose are reported. A 19-year-old Caucasian woman ingested 100 500-mg capsules of acetaminophen. She was admitted to a hospital 68 hours after ingestion, and serum acetaminophen concentration 70 hours after ingestion was 3 microgram/ml. liver-function test results were markedly elevated, and urinalysis was abnormal on admission. liver function improved over the next five days, but the patient's renal function deteriorated. Her condition initially was diagnosed as prerenal azotemia, but was later consistent with acute tubular necrosis. Hemodialysis was begun on the fifth day of hospitalization. On the eleventh hospital day, the patient's renal function began to improve, and she was subsequently discharged. In the second case, a 19-year-old Spanish-American woman ingested 30 500-mg capsules of acetaminophen. She was seen in an emergency room 16 hours after the ingestion; her serum acetaminophen concentration was 32 microgram/ml 19 hours after ingestion. Oral acetylcysteine therapy was begun, and liver-function test results were elevated and peaked on the third hospital day. Renal function began to decline on the fifth hospital day; her condition was consistent with acute tubular necrosis. She was hemodialyzed once, and her renal function improved on the tenth hospital day. She was subsequently discharged. It is concluded that acute renal failure without prior hepatic failure may occur after acetaminophen overdose.
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4/6. Acute nephropathy of organotin compounds.

    Three patients who developed acute nephropathy following ingestion of triphenyltin acetate (TPTA) are described. All of them had significant proteinuria, azotemia, and polyuria. Mild neurological manifestations in all patients were also noted. hematuria and pyuria were noted in 1 severely poisoned patient. Evidence for hepatitis was present in 2 patients, and for pancreatitis in 1. Renal biopsy showed focal fusion of glomerular cell processes and proximal tubular damage with cellular necrosis. Two patients survived with complete recovery of renal functions. One old patient died of aspiration pneumonia. Acute nephropathy following organotin intoxication appears to result mainly from proximal renal tubular damage with a benign and reversible clinical course.
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5/6. rhabdomyolysis and shock after intravenous amphetamine administration.

    Five patients who had injected intravenous (i.v.) phenmetrazine or methamphetamine developed marked prostration resembling septic shock, disseminated intravascular coagulation, rhabdomyolysis with myoglobinuria, and azotemia. Soon after injection, four noted chills, fever, sweats, nausea, and abdominal cramps. Within hours, they developed vomiting, myalgias, paresthesias, headache, and orthostasis. Cardiorespiratory arrest, accelerated bleeding, and noncardiac pulmonary edema were observed in one patient. From 4 to 11 litres of saline were required in the first 24 h to maintain blood pressure and urine output, suggesting that shock resulted from massive loss of intravascular volume into necrotic muscle. Recognition of this syndrome and treatment by aggressive volume replacement led to the recovery of all five patients.
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6/6. The FENa test. Use in the differential diagnosis of acute renal failure.

    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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