ABSTRACT
Although acute nonoliguric renal failure is a well-known nephrotoxic effect of aminoglycoside
antibiotics, less recognized is acquired Bartter-like syndrome. Herein, we describe
four female patients who presented with marked paresthesia, muscle weakness, and tetany
following gentamicin therapy with total dose ranging from 1.2 g to 2.6 g. All were normotensive. Biochemical abnormalities included hypokalemia (K+ 1.8–2.3 mmol/L), metabolic alkalosis (HCO3− 31.9–34.2 mmol/L), hypomagnesemia (Mg2+ 0.9–1.2 mg/dL), hypermagnesiuria (fractional excretion of Mg 3–6%), hypocalcemia (free Ca2+ 2.0–4.1 mg/dL), and hypercalciuria (molar ratio of Ca2+/creatinine 0.23–0.53), all consistent with Bartter-like syndrome. Serum immuno-reactive
parathyroid hormone concentration was low despite the hypocalcemia. The Bartter-like
syndrome lasted for 2 to 6 weeks after cessation of gentamicin, coupled with supplementation
of K+, Ca2+, and Mg2+. These biochemical abnormalities resembled those seen in patients with gain-of-function
mutations in the calcium-sensing receptor. We hypothesize that gentamicin, a polyvalent
cationic molecule, induces the action of calcium-sensing receptor on the thick ascending
loop of Henle and distal convoluted tubule to cause renal wasting of Na+, K+, Cr, Ca2+, and Mg2+.
KEY INDEXING TERMS
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Article info
Publication history
Accepted:
September 17,
2004
Received:
June 4,
2004
Identification
Copyright
© 2005 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.