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

R. E. Cronin, K. L. Nix, E. R. Ferguson

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Abnormalities of potassium and magnesium homeostasis have been reported following the use of gentamicin, and potassium depletion enhances gentamicin nephrotoxicity. The present study investigates these relationships 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 daily) was administered for 4 or 7 days to potassium-depleted or potassium-supplemented animals. The results show that gentamicin nephrotoxicity was characterized by a significant reduction in renal cortex content of potassium (17%), magnesium (19%), and phosphorus (12%) in all groups of animals given gentamicin. However, only potassium-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 sodium (from 25 ± 0.5 to 27.9 ± 1.7 meq/100 g fat-free dry solid wt) and calcium (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 potassium-depleted animals after 4 days (from 11.5 ± 0.9 to 7.8 ± 0.1 μM P(i) x mg protein-1 x h-1) and 7 days (5.9 ± 0.8 μM P(i) x mg protein-1 x h-1) of gentamicin treatment. Thus, gentamicin nephrotoxicity is characterized by sequential changes in renal cortex ionic composition, sodium pump activity, and renal function.

Original languageEnglish (US)
Title of host publicationAmerican Journal of Physiology - Renal Fluid and Electrolyte Physiology
Volume11
Edition5
StatePublished - 1982

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Gentamicins
Ions
Kidney
Potassium
Magnesium
Creatinine
Fats
sodium-translocating ATPase
Sodium-Potassium-Exchanging ATPase
Phosphorus
Proteins
Homeostasis
Sodium
Dogs
Calcium

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Cronin, R. E., Nix, K. L., & Ferguson, E. R. (1982). Renal cortex ion composition and Na-K-ATPase activity in gentamicin nephrotoxicity. In American Journal of Physiology - Renal Fluid and Electrolyte Physiology (5 ed., Vol. 11)

Renal cortex ion composition and Na-K-ATPase activity in gentamicin nephrotoxicity. / Cronin, R. E.; Nix, K. L.; Ferguson, E. R.

American Journal of Physiology - Renal Fluid and Electrolyte Physiology. Vol. 11 5. ed. 1982.

Research output: Chapter in Book/Report/Conference proceedingChapter

Cronin, RE, Nix, KL & Ferguson, ER 1982, Renal cortex ion composition and Na-K-ATPase activity in gentamicin nephrotoxicity. in American Journal of Physiology - Renal Fluid and Electrolyte Physiology. 5 edn, vol. 11.
Cronin RE, Nix KL, Ferguson ER. Renal cortex ion composition and Na-K-ATPase activity in gentamicin nephrotoxicity. In American Journal of Physiology - Renal Fluid and Electrolyte Physiology. 5 ed. Vol. 11. 1982
Cronin, R. E. ; Nix, K. L. ; Ferguson, E. R. / Renal cortex ion composition and Na-K-ATPase activity in gentamicin nephrotoxicity. American Journal of Physiology - Renal Fluid and Electrolyte Physiology. Vol. 11 5. ed. 1982.
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