Carbon tetrachloride nephrotoxicity: a reassessment of pathophysiology based upon the urinary diagnostic indices.
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.
D058186:Acute Kidney Injury / Q000209:etiology*; D000328:Adult; D002252:Carbon Tetrachloride Poisoning / Q000097:blood / Q000150:complications / Q000503:physiopathology*; D003404:Creatinine / Q000097:blood; D006801:Humans; D007683:Kidney Tubular Necrosis, Acute / Q000209:etiology*; D008099:Liver / Q000201:enzymology; D008103:Liver Cirrhosis / Q000201:enzymology / Q000209:etiology; D008297:Male; D009846:Oliguria / Q000209:etiology; D012964:Sodium / Q000652:urine
D012964:Sodium; D003404:Creatinine