Isoniazid hepatotoxicity in renal transplant recipients.

Tuberculosis occurs at higher rates in renal transplant recipients than in the general population. It would be desirable to use isoniazid prophylaxis in renal transplant recipients at risk for reactivation of tuberculosis; yet many transplant centers do not routinely employ INH prophylaxis because they perceive transplant recipients to be an enhanced risk of hepatotoxicity from isoniazid. Data on the risk of isoniazid in renal transplant patients receiving cyclosporine-based immunosuppression are limited. We retrospectively studied 83 renal transplant recipients (mean age 39.1 +/- 11.7 yr) who had received INH prophylaxis between 1985 and 1994. Eight patients had laboratory evidence of chronic hepatitis B or chronic hepatitis C infection. The mean duration of INH therapy was 344 +/- 163 d. The mean serum glutamate oxalacetic transferase (SGOT) at the start of INH therapy was 24.1 +/- 10.9 I.U., and 10% of patients had mildly elevated SGOTs. Mean peak SGOT during therapy was 36.4 +/- 15.3 I.U. (p < 0.001 compared to start (SGOT). In follow up, 31% of patients had an abnormal SGOT (> 40 I.U.); however, the elevations were small (the highest SGOT was 88.I.U.) and never necessitated discontinuation of INH. No patient had jaundice or other evidence of clinical hepatotoxicity. The 95% confidence interval for the observed frequency of clinical hepatitis was 0% to 4.3%. At the end of INH therapy the mean SGOT was 22.7 +/- 6.2 I.U. (p > 0.2, compared with start SGOT) and only one patient had an abnormal SGOT. In conclusion, it appears that the risk of renal transplant recipients developing serious hepatotoxicity with the administration of INH is low and not different from normal individuals.