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Diabetic retinopathy after combined kidney–pancreas transplantation
Author(s) -
Chow Vincent Cc,
Pai Rami P,
Chapman Jeremy R,
O'connell Philip J,
Allen Richard Dm,
Mitchell Paul,
Nankivell Brian J
Publication year - 1999
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 - 10.1034/j.1399-0012.1999.130413.x
Subject(s) - medicine , pancreas transplantation , diabetic retinopathy , transplantation , retinopathy , kidney transplantation , kidney , pancreas , diabetes mellitus , endocrinology
Diabetic retinopathy (DR) is amenable to good diabetic control; however, only successful pancreas transplantation can achieve sustained normoglycaemia. The aim of this long‐term study was to examine the course of DR in insulin‐dependent diabetic recipients of a simultaneous kidney and pancreas transplant (SPK). Successful SPK recipients (n=46) and failed pancreas transplant with a functioning kidney transplant (n=8) were assessed by baseline and regular post‐transplant ophthalmic examinations (n=432) for up to 10 yr after SPK. At the time of SPK (n=108 eyes), the mean duration of diabetes was 25±7 yr, ten eyes were blind, and 79% of eyes had advanced DR that had panretinal laser (panretinal photocoagulation, PRP). Successful SPK recipients had normal glucose control with a mean HBA 1 C of 5.2±0.6%. DR remained stable in 75% of both the study and control groups, with no difference between groups. The DR mostly evolved towards inactive proliferative DR. After SPK, 14% of non‐blind eyes showed improvement of DR, 76% remained stable and 10% progressed. Early vitreous haemorrhage occurred in 6.1% of eyes, and was related to established DR. Cataract of all types increased after transplantation (p<0.01), which reduced visual acuity (VA) in affected eyes. The mean overall VA remained unchanged for the study duration. In summary, uremic patients from diabetic nephropathy had a high prevalence of severe proliferative DR and blindness at the time of presentation for SPK. This was subsequently stabilised to inactive proliferative DR by appropriate laser therapy followed by metabolic control achieved by SPK.