Sulbenicillin-induced kaliuresis in man.

Abstract

The mechanism of kaliuresis induced by massive antibiotic administration was studied using a-sulfobenzyl penicillin (SBPC). In experimental group (n=8), urinary electrolytes excretion were compared between following the infusion of 10 g SBPC in 200 ml water at a constant rate and following the infusion of 48 mmol of NaCI (equal to that contained in 10 g SBPC) in 200 ml water. For the control group, 96 mmol NaCI in 400 ml water was infused (n=5). In the experimental group, urinary Na (UNaV) and urinary K excretion (UKV) increased relative to the control period. In the control group, UKV was not increased although UNaV was increased (p <0.05). UKV following SBPC infusion was correlated with UNaV (p<0.05) and urinary SBPC excretion (p <0.05). The ratio of urinary anion gap to urinary cation [1-{urinary Cl concentration/(urinary Na concentrations urinary K concentration)}] was significantly increased following SBPC infusion (p<0.005) but not in the control group. This increase in anion gap is possibly due to urinary SBPC, which will be ionized over 90% as nonreabsorbable anion in maximally acidic urine. We conclude that the kaliuresis induced by massive SBPC administration in man is probably caused by the nonreabsorbable anion effect of SBPC itself.