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Kidney graft dysfunction in simultaneous pancreas–kidney recipients after pancreas failure: analysis of early and late protocol biopsies
Author(s) -
Viglietti Denis,
Serrato Tomas,
Abboud Imad,
Antoine Corinne,
Pillebout Evangéline,
Busson Marc,
Desgrandchamps François,
Meria Paul,
Godin Michel,
Hurault de Ligny Bruno,
Thervet Eric,
Legendre Christophe,
Suberbielle Caroline,
Verine Jérome,
Glotz Denis,
Peraldi MarieNoëlle
Publication year - 2013
Publication title -
clinical transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 76
eISSN - 1399-0012
pISSN - 0902-0063
DOI - 10.1111/ctr.12095
Subject(s) - medicine , pancreas , pancreas transplantation , kidney , urology , proteinuria , transplantation , kidney disease , biopsy , diabetic nephropathy , gastroenterology , diabetes mellitus , kidney transplantation , surgery , endocrinology
Background Kidney graft survival in simultaneous pancreas–kidney ( SPK ) recipients is known to decrease after pancreas graft failure. Methods Sixty‐three consecutive SPK recipients were retrospectively reviewed. Kidney graft function and proteinuria were evaluated at three months after the transplantation and at last follow‐up. Histopathologic findings of protocol biopsies performed three months and one yr after transplantation were analyzed. Results Twelve patients lost the pancreas graft. Donors' characteristics were similar in patients with or without pancreas failure. After a median follow‐up of 36 months, mean eGFR with a functional pancreas was 69.5 mL/min/1.73 m² vs. 56.3 mL/min/1.73 m² (p = 0.01) after pancreas loss. Patients who lost pancreas had a median proteinuria of 0.28 g vs. 0.13 g per 24 h (p = 0.02). Analysis of three‐month protocol biopsies revealed more frequent isolated glomerulitis after pancreas failure (p = 0.0001), without peritubular capillaritis or C4d deposition. No donor‐specific anti‐HLA antibodies were detectable in these patients. Chronic tubulointerstitial changes were more frequent in patients with pancreas loss. There was no evidence of diabetic nephropathy recurrence. Conclusion SPK recipients develop an early kidney graft dysfunction after pancreas failure. Histopathologic findings revealed frequent glomerulitis without antibody‐mediated rejection and early chronic changes.