Association of Renal Failure with Lewis Incompatibility after Allogeneic Bone Marrow Transplantation M. A. BLAJCHMAN, M.D., F.R.C.P.(C.) D. J. KING, M.R.C.P.(U.K.) NANCY M. HEDDLE, A.R.T. D. P. SINGAL, Ph.D. I. R. WALKER, M.D., F.R.C.P.(C.) M. C. BRAIN, M.D., F.R.C.P., F.R.C.P.(C.) Hamilton, Ontario, Canada From the Departments of Pathology and Medicine, McMaster University, the Canadian Red Cross Blood Transfusion Service, and the McMaster Division of the Chedoke-McMaster Hospitals, Hamilton, Ontario, Canada. Requests for reprints should be addressed to Dr. M. A. Blajchman, Room 2N31, Department of Pathology, McMaster Uni- versity Medical Centre, 1200 Main Street West, Hamilton, Ontario L8N 325, Canada. Manuscript accepted July 6, 1984. The cause of the renal failure that occurs in approximately 20 per- cent of patients following allogeneic bone marrow transplantation is poorly understood. A patient is described in whom acute renal failure occurred one week after allogeneic bone marrow trans- plantation. The onset of the renal failure was associated with the demonstration of anti-Lewis antibodies in the patient’s serum, which could only have been derived from donor lymphocytes. Recovery of renal function coincided with the disappearance of the Lewis antibody. It is postulated that Lewis incompatibility between graft and host tissue may have contributed to the renal failure in this patient and that incompatibility associated with determinants present on renal cells may account for other instances of acute renal failure following allogeneic bone marrow transplantation. Severe acute renal failure is one of the complications that may follow allogeneic bone marrow transplantation [l-5]. There are many po- tential causes of the impaired renal function: the nephrotoxicity of chemotherapy; the total-body irradiation given &r preparation for transplantation; the effects of opportunistic bacterial, fungal, or viral infections; the nephrotoxicity of antibiotics (especially the amino- glycosides and amphotericin B); and the cyclosporin A used to prevent or ameliorate acute graft-versus-host disease [ 1,3-5,6-81. Immu- nologic mechanisms as a cause of altered renal function seem unlikely because of the prolonged impairment of humoral immunity that nor- mally follows bone marrow transplantation and the lack of an asso- ciation of renal failure with acute graft-versus-host disease when uncomplicated by infection. The incidence of acute renal failure fol- lowing bone marrow transplantation is uncertain. In 1981, Shulman et al [l] stated that “the 19 percent incidence (3 of 16 patients) of severe renal failure developing with prophylactic cyclosporin A is worrisome, but no more frequent than that observed in similar patients not receiving cyclosporin A”-a comment that implies that severe renal failure is a relatively common complication. We report the onset of acute renal failure one week after allogeneic bone marrow transplantation in a patient who received neither methotrexate nor cyclosporin A for graft-versus-host disease pro- phylaxis. The onset of renal failure was associated with the finding of anti-Lea antibodies in the patient’s serum due to Lewis incompati- bility between the recipient who was Le(a-b+) and the donor who was Le(a-b-). Although it is possible that other factors may have con- tributed to the acute renal failure, recovery of renal function accom- panied disappearance of the antibody. The finding of anti-Lea anti- bodies from Day -I- 10 to + 19 is evidence of immune competence of July 1965 The American Journal of Medicine Volume 79 143