Received June 8, 2007
Accepted on July 12, 2007

ORIGINAL ARTICLES

Transplant Glomerulopathy May Occur in the Absence of Donor-Specific Antibody and C4d Staining

Enver Akalin ^*1, Rajani Dinavahi ^*, Steven Dikman , Graciela de Boccardo ^*, Rex Friedlander , Bernd Schroppel ^*, Vinita Sehgal ^*, Jonathan S. Bromberg , Peter Heeger ^*, and Barbara Murphy ^*

*Renal Division, Recanati/Miller Transplantation Institute, and Department of Pathology, Mount Sinai School of Medicine, and Immunogenetics Laboratory, Rogosin Institute, New York, New York

¹ To whom correspondence should be addressed. E-mail: enver.akalin{at}msnyuhealth.org.

	Abstract

Background and objectives: Transplant glomerulopathy (TGP) has been proposed to be a component of chronic antibody-mediated rejection (AMR). We have studied 36 patients with TGP and 51 patients with chronic allograft nephropathy (CAN) but without TGP for C4d staining and donor-specific anti-HLA antibodies (DSA) to investigate the alloantibody-mediated mechanisms.

Design, setting, participants, & measurements: Allograft biopsies were stained with C4d staining and DSAs were studied by Luminex Flow Beads. Allograft biopsies were done at a mean of 5.3 ± 5.0 and 5.6 ± 4.6 yr after transplantation in patients with CAN and TGP, respectively.

Results: The mean creatinine level at the time of the biopsy was 2.7 ± 1.2 mg/dl in each group. Proteinuria of >1.0 g/d was more common in patients with TGP (61 versus 25%; P = 0.002). Whereas three patients with TGP had a history of acute AMR, none of the patients with CAN had. Mean chronicity score of the biopsies were 1.7 ± 0.7 in patients with CAN and 1.9 ± 0.8 in patients with TGP. Biopsies from only two (4%) patients with CAN and four (11%) patients with TGP had diffuse C4d positivity. DSA were found in 36% of TGP and 33% of CAN patients.

Conclusions: These results suggest that a substantial number of patients with TGP did not have positive C4d staining or DSA, indicating that a non-alloantibody-mediated process may be involved in the development of TGP in some patients.