Changes in Tissue Calcium Content during Gentamicin Acute Renal Failure
Aminoglycoside nephrotoxicity is the most important clinical cause of nephrotoxic acute renal failure. The mode of action whereby the aminoglycoside antibiotics kill bacteria and cause nephrotoxicity is probably quite similar. In both cases, drug binding to membrane structures results in death or injury to the cell. In the kidney, aminoglycosides have important effects on plasma, lysozomal, and mitochondrial membranes (1). Studies from this laboratory have investigated the gentamicin model of acute renal failure by evaluating indices of renal cellular integrity that depend in a major way on the integrity of the plasma membrane, i.e. renal cortex ionic composition and renal cortex Na-K ATPase activity (2,3). These studies demonstrated that renal injury was consistently accompanied by a gain in the tissue content of calcium and sodium. Studies in renal and non-renal tissue using ischemic and toxic injuries indicate that accumulation of calcium in the cytosol may play a central role in irreversible cell death (4).
KeywordsAcute Renal Failure Renal Cortex Aminoglycoside Antibiotic Cytosolic Calcium Concentration Aminoglycoside Nephrotoxicity
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