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Aminoglycosides and renal magnesium homeostasis in humans
R O von Vigier1, A C Truttmann, K Zindler-Schmocker
1Department of Pediatrics, University of Bern, Switzerland.
Background:
The use of aminoglycosides has been linked with hypomagnesaemia in scattered reports. The objective of the study was to measure prospectively the effect of treatment with the aminoglycoside amikacin on renal magnesium homeostasis.
Methods:
Twenty-four cystic fibrosis patients (aged 9-19 years) admitted because of exacerbation of pulmonary symptoms caused by Pseudomonas aeruginosa were treated with the aminoglycoside amikacin and the cephalosporin ceftazidime for 14 days. Renal values and plasma and urinary electrolytes were measured before and at the end of the systemic anti-pseudomonal 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 significantly 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 increased 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 (26.5-38.0) to 38.5 (31. 5-49.0) micromol/l glomerular filtration rate).
Conclusions:
The present study demonstrates that systemic therapy with amikacin plus ceftazidime causes mild hypomagnesaemia secondary to renal magnesium wasting even in the absence of a significant rise in circulating creatinine and urea.
Insights
Aminoglycoside treatment, specifically amikacin, can cause hypomagnesaemia in cystic fibrosis patients. This study shows amikacin plus ceftazidime leads to renal magnesium wasting and lower plasma magnesium levels.
Area of Science:
- Nephrology
- Pharmacology
- Pediatrics
Background:
- Aminoglycosides, including amikacin, have been anecdotally linked to hypomagnesaemia.
- Cystic fibrosis patients often require aggressive antibiotic therapy for pulmonary exacerbations.
Purpose of the Study:
- To prospectively evaluate the effect of amikacin treatment on renal magnesium homeostasis in cystic fibrosis patients.
- To determine if amikacin-based therapy impacts magnesium levels and excretion.
Main Methods:
- Twenty-four cystic fibrosis patients (9-19 years) received amikacin and ceftazidime for 14 days.
- Plasma and urinary electrolytes, including magnesium, were measured before and after treatment.
- Renal function markers (creatinine, urea) were also monitored.
Main Results:
- Amikacin and ceftazidime treatment significantly decreased plasma total and ionized magnesium levels.
- Fractional and total urinary magnesium excretion increased, indicating renal magnesium wasting.
- No significant changes were observed in plasma creatinine, urea, or other electrolytes like sodium, potassium, and calcium.
Conclusions:
- Systemic amikacin plus ceftazidime therapy induces mild hypomagnesaemia in cystic fibrosis patients.
- The hypomagnesaemia is secondary to increased renal magnesium wasting.
- This effect occurs despite the absence of significant changes in renal function markers.