Drug-Induced Acute Kidney Injury

Abstract

Abstract The epidemiology of acute kidney injury (AKI) has changed remarkably over the last few decades. Currently a majority of affected patients are critically ill older individuals hospitalized in an intensive care unit (ICU) with comorbidities and multiple organ failure. In the ICU, either nephrotoxicity alone or, most commonly, associated with ischemia, has been a relevant related factor in the pathogenesis of AKI in almost half of the cases. Virtually all mechanisms or processes potentially leading to renal injury have been associated with drug nephrotoxicity: acute tubular cell injury, changes in renal hemodynamics, intratubular obstruction, acute interstitial nephritis, hypersensitivity vasculitis, thrombotic microangiopathy, osmotic nephrosis, and rhabdomyolysis. Measurement of serum creatinine always should be performed before administration of potentially nephrotoxic drugs, and even small increments in creatinine are an independent risk factor for increased mortality in hospitalized patients. The use of a nonnephrotoxic drug must be considered for patients at higher risk for renal injury. Patients must be adequately hydrated and sodium repleted before receiving a nephrotoxic drug. The concomitant use of two or more different nephrotoxic drugs must be avoided. Drug dosage should be adjusted in accordance with organ functional status, distribution volume, and drug pharmacokinetics. It always should be checked if a nephrotoxic drug had specific measures to prevent or attenuate its potential for renal damage. Currently, numerous drugs have been related to development of AKI. Of the vast array of drugs with potential for nephrotoxicity, those more frequently prescribed for patients in the ICU are discussed in this chapter: antiinfective agents (aminoglycosides, vancomycin, amphotericin B, polymyxins, highly active antiretroviral therapy [HAART]), contrast agents, NSAIDs, and drugs blocking the renin-angiotensin-aldosterone system (ACEI, ARB, and renin inhibitors).