Drugs and Nephrotoxicity in the Intensive Care Unit

Abstract

In addition to its role in water and electrolyte homeostasis, the kidney is the primary organ for excretion of drugs and their metabolites from the body. There are three basic processes involved in renal drug excretion: glomerular filtration, tubular secretion, and tubular reabsorption. Most drugs found to cause nephrotoxicity exert toxic effects by one or more common pathogenic mechanisms. These include altered intra glomerular hemodynamics, tubular cell toxicity, inflammation, crystal nephropathy, rhabdomyolysis, and thrombotic micro-angiopathy. Knowledge of offending drugs and their particular pathogenic mechanisms of renal injury is critical to recognizing and preventing drug induced renal impairment. Drugs cause approximately 20 percent of community and hospital acquired episodes of acute renal failure. Among older adults, the incidence of drug-induced nephrotoxicity may be as high as 66 percent. Some patient related risk factors for drug induced nephrotoxicity are age older than 60 years, underlying renal insufficiency (e.g., glomerular filtration rate of less than 60 mL per minute per 1.73 m2), volume depletion, diabetes, heart failure, and sepsis. General preventive measures include using alternative non nephrotoxic drugs whenever possible; correcting risk factors, if possible; assessing baseline renal function before initiation of therapy, followed by adjusting the dosage; monitoring renal function and vital signs during therapy; and avoiding nephrotoxic drug combinations.