Drug-induced acute interstitial nephritis in renal allografts: Histopathologic features and clinical course in six patients

Drug-induced acute interstitial nephritis is a common cause of dysfunction in native kidneys, but is rarely reported in renal allografts. This report describes six renal transplant recipients with acute renal allograft dysfun ction or delayed allograft function in whom a renal transplant biopsy showe d histopathologic features of drug-induced interstitial nephritis with no d iagnostic evidence of acute rejection, cyclosporine or tacrolimus nephrotox icity, or other lesion that could account for the graft dysfunction. In fiv e of the six patients, interstitial nephritis occurred within 4 weeks of tr ansplantation. All the patients were receiving trimethaprim-sulfamethoxazol e and/or other drugs associated with interstitial nephritis. After disconti nuation of these drugs and short-term corticosteroid treatment, all patient s showed improvement in renal function, although the time course of this im provement varied considerably, with three patients showing a return to base line serum creatinine level within 2 weeks and two patients showing a gradu al improvement over 8 weeks. Four of the five patients followed up for more than 1 year (range, 14 to 33 months) after the episode of interstitial nep hritis had good allograft function (serum creatinine level less than or equ al to 1.6 mg/dL) at most recent follow-up, with one patient who had graft l oss because of severe rejection 7.5 months after the development of interst itial nephritis. These findings suggest drug-induced interstitial nephritis may be an infrequent cause of graft dysfunction in kidney transplant recip ients. Drug induced interstitial nephritis is a reversible lesion that shou ld be considered in the differential diagnosis of acute renal allograft dys function. (C) 1999 by the National Kidney Foundation, Inc.