The nephrotoxicity linked to gentamicin exposure commonly manifests as nonoliguric renal failure and tubular dysfunction. The use of gentamicin has been associated with a Bartter-like syndrome in adults but this nephrotoxic syndrome has not been well characterized in children. We describe the clinical course of two patients (41/2 month-old male and 19 year-old female) who developed Bartter-like syndrome following gentamicin therapy. Both demonstrated evidence of renal tubulopathy, primarily affecting the distal nephron and the characteristic electrolyte abnormalities including hypocalcemia, hypomagnesemia, alkalosis, and hypokalemia. Both had complete recovery of renal tubular function after discontinuation of gentamicin therapy. Time of recovery varied from few weeks to a few months. None of the cases needed indomethacin therapy. The transient nature of the metabolic abnormalities and prompt response to appropriate electrolyte replacement therapy is typical of gentamicin induced Bartter-like syndrome. Based on our experience, in addition to following serum creatinine and aminoglycoside levels, patients receiving prolonged gentamicin therapy should be monitored for evidence of renal tubular toxicity, particularly in those where other preexisting risk factors for nephrotoxicity are present.
|Journal||Journal of Investigative Medicine|
|Publication status||Published - 01-01-1999|
All Science Journal Classification (ASJC) codes
- Biochemistry, Genetics and Molecular Biology(all)