ISONIAZID HEPATOTOXICITY IN RENAL-TRANSPLANT RECIPIENTS

Tuberculosis occurs at higher rates in renal transplant recipients tha n in the general population. It would be desirable to use isoniazid pr ophylaxis in renal transplant recipients at risk for reactivation of t uberculosis; yet many transplant centers do not routinely employ INH p rophylaxis because they perceive transplant recipients to be at an enh anced risk of hepatotoxicity from isoniazid. Data on the risk of isoni azid in renal transplant patients receiving cyclosporine-based immunos uppression are limited. We retrospectively studied 83 renal transplant recipients (mean age 39.1 +/- 11.7 yr) who had received INH prophylax is between 1985 and 1994. Eight patients had laboratory evidence of ch ronic 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 fo llow 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 necess itated discontinuation of INH. No patient had jaundice or other eviden ce of clinical hepatotoxicity. The 95% confidence interval for the obs erved frequency of clinical hepatitis was 0% to 4.3%. At the end of IN H therapy the mean SGOT was 22.7 +/- 6.2 I.U. (p>0.2, compared with st art SGOT) and only one patient had an abnormal SGOT. In conclusion, it appears that the risk of renal transplant recipients developing serio us hepatotoxicity with the administration of INH is low and not differ ent from normal individuals.