TY - CHAP M1 - Book, Section TI - Drug-Induced Kidney Disease A1 - Nolin, Thomas D. A1 - Perazella, Mark A. A2 - DiPiro, Joseph T. A2 - Yee, Gary C. A2 - Posey, L. Michael A2 - Haines, Stuart T. A2 - Nolin, Thomas D. A2 - Ellingrod, Vicki PY - 2020 T2 - Pharmacotherapy: A Pathophysiologic Approach, 11e AB - KEY CONCEPTSThe initial diagnosis of drug-induced kidney disease (DIKD) typically involves detection of elevated serum creatinine (Scr) and blood urea nitrogen, for which there is a temporal relationship between the toxicity and use of a potentially nephrotoxic drug.DIKD is best prevented by avoiding the use of potentially nephrotoxic agents for patients at increased risk for toxicity. However, when exposure to these drugs cannot be avoided, recognition of risk factors and specific techniques, such as hydration, may be used to reduce potential nephrotoxicity.Acute tubular injury/necrosis (ATN) is the most common presentation of DIKD in hospitalized patients. The primary agents implicated are aminoglycosides, radiocontrast media, cisplatin, amphotericin B, and osmotically active agents.Angiotensin-converting enzyme inhibitors (ACEIs) and nonsteroidal anti-inflammatory drugs (NSAIDs) are associated with hemodynamically mediated kidney injury, the pathogenesis of which is a decrease in glomerular capillary hydrostatic pressure.Acute allergic interstitial nephritis (AIN) is observed in up to 27% of kidney biopsies performed for hospitalized patients with unexplained acute kidney injury (AKI). Clinical manifestations of AIN typically (but not always) present approximately 14 days after initiation of therapy and may include fever, maculopapular rash, eosinophilia, arthralgia, as well as pyuria, hematuria, proteinuria, and oliguria. SN - PB - McGraw-Hill Education CY - New York, NY Y2 - 2024/03/28 UR - accesspharmacy.mhmedical.com/content.aspx?aid=1182441904 ER -