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Concentrations of gentamicin and amikacin in human kidneys
Abstract:
High kidney concentrations of gentamicin or amikacin, measured by an enzymological assay, were found in 9 of 10 patients who died during therapy with these aminoglycosides. Renal cortical concentrations of gentamicin ranged from 140 to 540 mug/g of tissue, with medullary levels of 128 to 230 mug/g. Concentrations of amikacin ranged from 365 to 1,030 mug/g in the cortex and from 270 to 718 mug/g in the medulla. The only patient with low kidney concentrations was an infant who received a single dose of gentamicin. Tissue levels were high in patients with both normal and abnormal renal function. Our results indicate that gentamicin and amikacin are concentrated in renal cortical and medullary tissue.
Insights
High concentrations of gentamicin and amikacin were found in the kidneys of most patients who died during treatment. These aminoglycoside antibiotics accumulate in renal tissues, regardless of kidney function.
Area of Science:
- Pharmacology
- Nephrology
- Toxicology
Background:
- Aminoglycosides like gentamicin and amikacin are crucial antibiotics.
- Kidney accumulation of these drugs can lead to nephrotoxicity.
- Understanding drug concentration in renal tissue is vital for patient safety.
Purpose of the Study:
- To quantify kidney concentrations of gentamicin and amikacin in patients who died during therapy.
- To determine if renal function affects aminoglycoside accumulation in kidney tissue.
Main Methods:
- Enzymological assay used to measure drug concentrations.
- Analysis of kidney tissue (cortex and medulla) for gentamicin and amikacin levels.
- Correlation of tissue levels with patient renal function and clinical outcome.
Main Results:
- Nine out of ten deceased patients showed high kidney concentrations of gentamicin or amikacin.
- Gentamicin levels ranged from 128-540 µg/g, amikacin from 270-1030 µg/g in renal tissues.
- High tissue levels were observed in patients with both normal and impaired renal function.
Conclusions:
- Gentamicin and amikacin significantly concentrate in renal cortical and medullary tissues.
- Drug accumulation occurs irrespective of the patient's baseline renal function.
- These findings highlight potential mechanisms for aminoglycoside-induced nephrotoxicity.