Aminoglycosides and renal magnesium homeostasis in humans

Background. The use of aminoglycosides has been linked with hypomagnesaemia in scattered reports. The objective of the study was to measure prospectiv ely the effect of treatment with the aminoglycoside amikacin on renal magne sium homeostasis. Methods. Twenty-four cystic fibrosis patients (aged 9-19 years) admitted be cause of exacerbation of pulmonary symptoms caused by Pseudomonas aeruginos a were treated with the aminoglycoside amikacin and the cephalosporin cefta zidime for 14 days. Renal values and plasma and urinary electrolytes were m easured before and at the end of the systemic antipseudomonal therapy. Results. In the patients with cystic fibrosis, treatment with amikacin and ceftazidime did not modify plasma creatinine or urea and plasma or urinary sodium, potassium and calcium. Treatment with amikacin and ceftazidime sign ificantly decreased both plasma total magnesium (from 0.77 (0.74-0.81) to 0 .73 (0.71-75) mmol/l; median and interquartile range) and ionized magnesium (from 0.53 (0.50-0.55) to 0.50 (0.47-0.52) mmol/l) concentration and incre ased fractional urinary magnesium excretion (from 0.0568 (0.0494-0.0716) to 0.0721 (0.0630-0.111)) and total urinary magnesium excretion (from 30.7 (2 6.5-38.0) to 38.5 (31.5-49.0) mu mol/l glomerular filtration rate). Conclusions. The present study demonstrates that systemic therapy with amik acin plus ceftazidime causes mild hypomagnesaemia secondary to renal magnes ium wasting even in the absence of a significant rise in circulating creati nine and urea.