Drugs cause approximately 20% of community- and hospital-acquired episodes of acute kidney failure (1–3). Among older adults, the incidence of drug-induced nephrotoxicity may be as high as 66% (4). Drug-induced nephrotoxicity may account for 20% of acute kidney injury (AKI), including both acute and chronic kidney disease. Prospective cohort studies of AKI have documented the frequency of drug-induced nephrotoxicity to be approximately 14%−26% in intensive care unit cohorts (5–7).
A growing body of literature highlights the potential for drugs to induce not only AKI but also glomerular diseases, termed drug-induced glomerular diseases. Patients with glomerular involvement generally present with one of five clinical syndromes: recurrent macroscopic hematuria, microscopic hematuria associated with proteinuria, heavy proteinuria or nephritic/nephrotic syndrome, rapidly progressive glomerulonephritis (RPGN), or chronic glomerulonephritis (GN). Strict monitoring of kidney function, urine and blood abnormalities, and blood pressure must be performed in patients undergoing therapy with potentially toxic drugs. It is critical to recognize these conditions early, because in many patients, there is improvement after removing the offending medication (8). In certain scenarios, removal of the offending agent plus an immunosuppressive strategy has been employed. However, the effectiveness of immunosuppressive therapy in this context has not been determined. From a diagnostic and therapeutic standpoint, it is sometimes difficult to ascribe a drug as being directly causative versus unmasking a preexisiting syndrome.
Drug-induced glomerular diseases can also be classified into two categories: direct cellular toxicity and immune-mediated injury (Table 1).
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