Rifabutin-Induced SIADH and Leucopenia in a Renal Transplant Recipient with Genitourinary Tract Tuberculosis: A Case Report and Review of the Literature.

Abstract

Tuberculosis (TB) infection of the genitourinary tract (GU TB) is rare in renal transplant recipients, with only a few published case series. GU TB is difficult to diagnose with or without immunosuppression but must always be suspected in any patient with unexplained sterile pyuria. As GU TB is associated with graft rejection, prompt diagnosis and treatment are vital. Treatment is challenging, as rifampicin, the most effective drug used to treat tuberculosis, is a significant inducer of cytochrome P-450 3A metabolism, with the potential to cause significant reductions in the serum levels of calcineurin inhibitors. For this reason, rifabutin, a weaker cytochrome P-450 3A inducer, with similar efficacy against TB, is sometimes used as an alternative to rifampicin in transplant recipients. We present a renal transplant patient diagnosed with GU TB, treated with a regime containing rifabutin, who subsequently developed profound hyponatremia and leucopenia. Serum and urine biochemistry was consistent with a diagnosis of the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Both SIADH and leucopenia resolved with rifabutin cessation. This is the first report of biochemically proven, idiosyncratic SIADH and leucopenia associated with the use of rifabutin in the treatment of GU TB in a renal transplant recipient.