Deposition of complement product C4d in anti-glomerular basement membrane glomerulonephritis.

摘要

C4d is a complement degradation product that correlates significantly with circulating donor-specific antibodies. Detected in peritu-bular capillaries (PTCs), it can independently predict unfavorable graft outcome and usually permits the diagnosis of antibody-mediated rejection.1"4 We present a case in which the presence of diffuse C4d deposition was associated with recurrent anti-glomerular basement membrane (anti-GBM) glomerulonephritis (AGBMN) in a transplanted kidney. CASE REPORT Clinical record review of this patient was approved by the University of Pittsburgh (Pittsburgh, PA) Institutional Review Board (protocol no. 07110135). The patient was a 29-year-old woman who presented with end-stage renal disease, but no pulmonary manifestations. She was positive for anti-GBM antibodies (1:912) and myeloperoxidase pe-rinuclear antineutrophil cytoplasmic antibodies (ANCAs). Furthermore, serological testing showed hypocomple-mentemia (C3, 44 mg/dL [0.44 g/L; normal, 0.80 to 1.60 g/dL]; C4, <10 mg/dL [<0.10 g/L; normal, 0.16 to 0.38 g/L]). Kidney biopsy confirmed the diagnosis of AGBMN. The patient was maintained on peritoneal dialysis therapy, and 2 years later, she received a zero-antigen-mismatch deceased donor kidney allograft. Initial immunosuppression consisted of pretransplantation alemtuzumab (Mabcampath; Bayer, Milan, Italy) (30 mg intravenously) and 2 intravenous doses of mefhylprednisolone sodium succinate (Solu-Medrol; Pfizer, Milan, Italy) (1,000 mg intravenously), followed by tacrolimus monotherapy. The posttransplantation course was uneventful.