diphenyihydantoin or phenobarbital, or when lymphocytes from control subjects were incubated with carbamazepine. From these results, we conclude that carbamazepine was the agent responsible for the acute tubulointerstitial fiephritis. At the time our patient presented, a review of the literature revealed widely divergent views regarding the use of corticosteroids or immunosuppressive agents in the treatment of acute tubulointerstitial nephritis. We elected to treat him as if he were undergoing acute cellular renal transpl~int rejection by giving iv bolus methylprednisolone therapy followed by prednisone orally. Although he improved rapidly and eventuallv recovered normal renal functiOn, it xs not possible to conclude that the steroid therapy and the subsequent recovery represent a causeand-effect relationship. However. the temporal relationship of the two and the more recent demonstration of the effectiveness of prednisone in methicillin-induced acute interstitial nephritis 9 lead us to propose that the treatment and the response were causally related. Whether such therapy will be efficacious m patients with other types of drug-induced acute tubulointerstitial nephritis will only be ascertained by additional controlled studies. In the meantime, it would appear that consideration should be given to the use of intravenous methylprednisolone infusions in patients who have severe renal failure associated with acute tubulointerstitial nephritis. In addition, we believe th~at when this disease presents in a patient receiving multiple drugs, it is appropriate to conduct lymphocyte ti-ansformation studies in which responses of the patient's lymphocytes to each drug may be examined in vitro.