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

Inhalation or ingestion of carbon tetrachloride (CCl4) has been said to result in the nephrotoxic lesion of acute tubular necrosis (ATN). We describe three patients who inhaled toxic quantities of CCl4 and presented with oligoanuria and severe hepatoxicity. All patients developed protracted vomiting and were unable to maintain fluid intake for several days prior to our evaluation. Physical examination, urinalysis, and calculated FENa, FEH2O, and renal failure index (RFI) indicated that the acute oliguric renal failure was "prerenal" due to marked extracellular fluid (ECF) volume contraction. Aggressive volume repletion restored renal function to normal in each patient. It is suggested that the acute renal failure following CCl4 exposure begins as a functional disorder and may progress to ATN if volume depletion is not recognized and corrected. Early and aggressive volume repletion will reverse this prerenal state and may prevent the later onset of ATN following CCl4 exposure.
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PMID:Carbon tetrachloride nephrotoxicity: a reassessment of pathophysiology based upon the urinary diagnostic indices. 670 22

In order to clarify the role of endotoxin in acute tubular necrosis in liver cirrhosis, lipopolysaccharide (LPS) was injected to rats with liver injury with exposure to carbon tetrachloride (CCl4) inhalation. Rats showed liver cirrhosis with ascites retention after 10 weeks' CCl4 treatment and liver fibrosis after 6 weeks' CCl4 treatment. Histopathological grading of kidney injuries after LPS treatment was more severe either in cirrhotic rats or in liver fibrotic rats than in normal rats. All cirrhotic rats had severe acute tubular necrosis after either dose of LPS, but only small necrotic foci of tubuli were seen in a few normal and liver fibrotic rats. The results indicate that endotoxin, which overflows due to disturbance of inactivation in the cirrhotic liver, may contribute to acute tubular necrosis. This effect of endotoxin is supposed to be a direct hemodynamic damage.
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PMID:Endotoxin-induced acute tubular necrosis in cirrhotic rats. 815 14

Relationship between cirrhosis and renal dysfunction is not yet fully understood. A model of cirrhosis with acute hepatic and renal damage (RF), produced by CCl4 in rats, with hemodynamic and renal functional alterations, similar to those observed in decompensated cirrhosis (DC) in man, was used to study chemical nephrotoxicity in animals. We performed in male Wistar rats hepatic and renal functional and hemodynamic studies in control, cirrhotic and decompensated cirrhotic (DC) groups. Cirrhosis was induced with carbon tetrachloride by chronic administration. Association between liver and renal functional alterations was detected in rats with decompensated cirrhosis, showing fall in mean arterial pressure and reduction of glomerular filtration rate and filtration fraction. Renal hemodynamics did not change in cirrhotic rats, similarly to what occurs in compensated cirrhotic patients. However, DC rats exhibited increased sodium, glucose and phosphate urinary excretions and decreased ATP in renal cortex. DC animals had severe hypoglycemia. There was an extensive liver fibrosis. Glomeruli had hypercellularity and tubules showed extensive vacuolization in cirrhotic and DC rats. The present study suggests that in this model, damage typical of acute tubular necrosis ensues in cirrhotic rats. We describe functional and morphological damage in liver and kidney in a model of cirrhosis that might predispose to the development of acute renal failure when an individual with hepatic damage is exposed in acute way to chemical toxicants.
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PMID:Acute renal failure induced by carbon tetrachloride in rats with hepatic cirrhosis. 1903 32