Additional case of acute cellular kidney rejection associated with the presence of antibodies to the red blood cell Kidd antigen

Earlier we reported a case of plasma cell-rich acute cellular rejection of a transplanted kidney, which was associated with a serum antibody to the red blood cell (RBC) Kidd antigen, Jk-b, without a history of recent transfusion. We presented data to suggest that the plasma cells in the kidney made antibodies to the Jk-b antigen, which is also present in the kidney and may, in turn, have contributed to the rejection process (1). Since that time, we have identified a second patient with a milder but similar clinical course and antibodies to Jk-a, the polymorphic allele Kidd antigen. The patient was a 19-yr-old female who had received a kidney transplant from her father (three of six HLA match) seven yr earlier after developing end-stage renal disease secondary to focal segmental glomerulosclerosis. Her transplant status had been stable with a serum creatinine of 1.2–1.5 mg/dL with her immunosuppression consisting of alternate day prednisone, mycophenolate mofetile, and cyclosporine. She had a history of nephrolithiasis in the transplanted kidney and had recently experienced several urinary tract infections. A rise in her serum creatinine to 2.5 mg/dL and a recent history of medication non-adherence, as reflected by undetectable cyclosporine levels, prompted the performance of a kidney biopsy. The needle biopsy of the renal allograft revealed chronic allograft nephropathy with acute cellular rejection. The interstitium was infiltrated by lymphocytes and plasma cells that occupied 60% of its area. The plasma cells comprised less than 5% of the infiltrating mononuclear inflammatory cells. The tubules were infiltrated by lymphocytes that ranged from four to 10 lymphocytes per tubular cross-section. The blood vessels were free of inflammation. There were no viral inclusions or cytopathic viral changes. Immunohistochemical studies for CMV, EBV, and BK virus were negative. An immunofluorescence study for C4d using indirect immunofluorescence technique on frozen tissue with a monoclonal antibody (AbD Serotec, dilution 1:100) revealed no labeling of interstitial capillaries. The acute cellular rejection was graded as IA by the Banff criteria. Polymerase chain reaction (PCR) on blood was negative for BK and CMV virus, and there were only 500 copies/mL of EBV virus. PCR on urine revealed only 10 900 copies/mL of BK virus. The patient was treated with high dose steroids for three days and a repeat biopsy in one wk showed decreased lymphocytic infiltrates in the interstitium with only rare plasma cells. There was resolution of the acute cellular rejection with disappearance of lymphocytes from the tubular epithelium. The patient was discharged in stable condition and has remained so with a serum creatinine of 1.6–2.0 mg/dL. Although the patient had received two units of RBCs in association with her transplant seven yr earlier, her antibody screen for antibodies to red cells had been negative six months following the transplant and she had received no additional transfusions or treatment with intravenous immunoglobulin. Nevertheless, at the time of the first biopsy, the patient was noted to have low titer IgG serum antibodies to the RBC Kidd antigen, Jka. The patient s phenotype is Jk-a negative, Jk-b positive. The kidney donor was her father and his RBC phenotype is Jk-a positive, Jk-b positive. An eluate of the kidney biopsy contained anti-Jk-a antibodies. We previously discussed the possible functional relationship between kidney rejection and antibodies to the RBC Kidd antigen (1). The Pediatr Transplantation 2008: 12: 918–919 2008 Wiley Periodicals, Inc.