Viomycin-induced electrolyte abnormalities.
Severe hypokalemia (2.6 mEq/l), hypomagnesemia (0.6 mg/dl), mild hypercalcemia (10.9 mg/dl), and secondary hyperaldosteronism developed in a patient receiving viomycin for pulmonary tuberculosis. Reversible renal wasting of both potassium (K+) and magnesium (Mg++) was documented. Viomycin administered to 40 rats resulted in severe damage to the proximal tubule and mild damage to the distal tubule. THe case report and experimental data suggest viomycin induces proximal tubule dysfunction that results in renal wasting of sodium, K+ and Mg++ and secondary hyperaldosteronism. Hypercalcemia, not previously associated with viomycin therapy, may be secondary to hypomagnesemia-induced hyperparathyroidism.
D000328:Adult; D006801:Humans; D006934:Hypercalcemia / Q000209:etiology; D007668:Kidney / Q000503:physiopathology; D008274:Magnesium / Q000097:blood / Q000502:physiology*; D008297:Male; D011188:Potassium / Q000097:blood / Q000502:physiology*; D014397:Tuberculosis, Pulmonary / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D014756:Viomycin / Q000009:adverse effects*
D008274:Magnesium; D011188:Potassium; D014756:Viomycin