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Clinical Transplantation |



* The Brown Foundation Institute of Molecular Medicine and the Department of Pediatrics, Division of Pediatric Nephrology and Hypertension, University of Texas Health Science Center at Houston, Houston, Texas;
The EMMES Corporation, Rockville, Maryland;
Division of Pediatric Nephrology, Alberta Childrens Hospital University of Calgary, Calgary, Alberta, Canada;
Montreal Childrens Hospital, McGill University Heath Centre, Department of Pediatrics, Division of Pediatric Nephrology, Montreal, Quebec, Canada; || Department of Pediatrics, University of Wisconsin, University of Wisconsin Childrens Hospital, Madison, Wisconsin; and ¶ Department of Pediatrics, Division of Nephrology and Hypertension, University of Cincinnati College of Medicine, and The Childrens Hospital Research Foundation, Cincinnati, Ohio
Address correspondence to: Dr. Michael C. Braun, The Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston, 2121 W. Holcombe Boulevard, Houston, TX 77030. Phone: 713-500-2438; Fax: 713-500-2424; E-mail: michael.c.braun{at}uth.tmc.edu
Received for publication February 16, 2005. Accepted for publication March 28, 2005.
Membranoproliferative glomerulonephritis type II (MPGN II) is an uncommon form of complement-dependent acquired renal disease. Although it has been recognized since the 1970s that MPGN II recurs almost universally in renal transplants, data regarding the long-term consequences of disease recurrence are limited. Therefore, a retrospective comparative analysis of 75 patients with MPGN II contained in the North American Pediatric Renal Transplant Cooperative Study transplantation database was performed. Five-year graft survival for patients with MPGN II was significantly worse (50.0 ± 7.5%) compared with the database as a whole (74.3 ± 0.6%; P < 0.001). Living related donor organs had a significantly better 5-yr survival (65.9 ± 10.7%) compared with cadaveric donor organs (34.1 ± 9.8%; P = 0.004). The primary cause of graft failure in 11 (14.7%) patients was recurrent disease. Supplemental surveys were obtained on 29 (38%) of 75 patients. Analysis of these data indicated that recurrent disease occurred in 12 (67%) of the 18 patients with posttransplantation biopsies. Although there was no correlation between pretransplantation presentation, pre- or posttransplantation C3 levels, and either disease recurrence or graft failure, there was a strong association between heavy proteinuria and disease recurrence. The presence of glomerular crescents in allograft biopsies had a significant negative correlation with graft survival. At last follow-up, patients with recurrent disease had significantly higher serum creatinine and qualitatively more proteinuria than patients without biopsy-proven disease. These data indicate that recurrent MPGN II has a significant negative impact on renal allograft function and survival.
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