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aminoglycoside nephrotoxicity

Epidemiology: 1) common cause of hospital-acquired acute renal failure 2) risk increases with patient's age, volume-depletion & pre-existing renal disease 3) relatively low mortality 4) increases cost of hospitalization Pathology: 1) aminoglycosides accumulate in proximal tubular epithelial cells 2) oncosis of proximal tubular epithelial cells (ATN) 3) reversible abnormalities herald nephrotoxicity a) glycosuria b) enzymuria c) aminoaciduria d) tubular proteinuria (beta-2 microglobulin) 4) renal K+ & Mg+2 wasting, polyuria & nephrogenic diabetes insipidus may occur Clinical manifestations: 1) generally manifests as non-oliguric acute tubular necrosis when the sole cause of renal dysfunction 2) decreased GFR may not become apparent for 1-2 weeks Laboratory: 1) urine Na+ is generally > 40 meq/L 2) fractional excretion of Na+ (FENA) is > 1.5% Management: 1) therapeutic levels of aminoglycosides should be monitored daily 2) dosage should be adjusted for creatinine clearance 3) discontinue aminoglycoside at 1st sign of nephrotoxicity

Related

acute tubular necrosis; tubulorrhexis (ATN) aminoglycoside antibiotic oncosis (ischemic cell death)

References

Medical Knowledge Self Assessment Program (MKSAP) 11, American College of Physicians, Philadelphia 1998