Hypokalemia and potassium wasting occur after gentamicin administration. This study assesses the importance of prior potassium depletion on the development of gentamicin nephrotoxicity in the following three groups of dogs: group I, low-potassium diet for 1 week followed by a sham injection for 10 days; group II, low-potassium diet for 1 week followed by gentamicin (15 mg/kg twice daily) for 10 days; group III, potassium-supplemented diet for 1 week followed by the identical dose of gentamicin for 10 days. Groups I and II also received intramuscular DOCA for the first 5 days. Plasma creatinine (mean ± S.E.M.) changes occurring over the 10 day injection period were as follows: group I, 1.1± 0.1 mg/dl to 1.5 ± 0.2, NS; group II, 1.0 ± 0.1 to 15.8 ± 1.8, p < 0.01; and group III, 1.1 ± 0.1 to 3.5 ± 1.1, p < 0.05. Plasma creatinines differed significantly between groups II and III on days 6, 8, and 10. Urinary potassium loss during the 10-day injection period was greater in group II than in group I (2.9 ± 0.5 mEq/kg vs. 0.6 ± 0.2, p < 0.001). Renal cortical gentamicin levels at the end of the 10-day injection period were higher in group II than in group III (673 ± 54 μg/gm vs. 483 ± 59, p < 0.001). Proximal tubular necrosis occurred only in animals receiving gentamicin (groups II and III), was most prominent in the superficial and outer cortex, and correlated (r = 0.91, p < 0.001) with renal functional impairment. These data indicate that potassium depletion potentiates gentamicin nephrotoxicity and that gentamicin nephrotoxicity itself induces potassium wasting.
|Original language||English (US)|
|Number of pages||10|
|Journal||The Journal of Laboratory and Clinical Medicine|
|State||Published - Aug 1981|
ASJC Scopus subject areas
- Pathology and Forensic Medicine