Renal cortex ion composition and Na-K-ATPase activity in gentamicin nephrotoxicity

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Abstract
Abnormalities of K+ and Mg+ homeostasis follow the use of gentamicin [an antibiotic], and K+ depletion enhances gentamicin nephrotoxicity. These relationships were studied in the dog by assessing changes in renal cortex ion composition and renal cortex Na-K-ATPase activity occurring during gentamicin nephrotoxicity. Gentamicin (15 mg/kg i.m. twice/day) was administered for 4 or 7 days to K+-depleted or K+-supplemented animals. Gentamicin nephrotoxicity was characterized by a significant reduction in renal cortex content of K+ (17%), Mg (19%) and P (12%) in all groups of animals given gentamicin. Only K+-depleted animals exposed to 7 days of gentamicin experienced a significant rise in plasma creatinine (from 1.3 .+-. 0.1 to 4.3 .+-. 1.0 mg/dl). Accompanying this increase in plasma creatinine was a significant rise in the renal cortex content of Na (from 25 .+-. 0.5 to 27.9 .+-. 1.7 meq/100 g fat-free dry solid wt) and Ca (from 1.2 .+-. 0.1 to 2.6 .+-. 0.3 mM/100 g fat-free dry solid wt). Na-K-ATPase activity in the renal cortex fell only in K+-depleted animals after 4 days (from 11.5 .+-. 0.9 to 7.8 .+-. 0.1 .mu.M Pi/mg protein per h) and 7 days (5.9 .+-. 0.8 .mu.M Pi/mg protein per h) of gentamicin treatment. Gentamicin nephrotoxicity is characterized by sequential changes in renal cortex ionic composition, Na pump activity and renal function.