EARLY GRAFT LOSS DUE TO RECURRENCE OF DIABETIC NEPHROPATHY FOLLOWING LIVE DONOR KIDNEY TRANSPLANTATION

JE HERON1, BL NEUEN1, SJ CHADBAN1,2

1Department of Renal Medicine, Royal Prince Alfred Hospital, Sydney, NSW; 2Charles Perkins Centre, University of Sydney, Sydney, NSW

Background: The epidemiology and natural history of recurrent diabetic nephropathy following kidney transplantation are not well described. Although histological changes of diabetic nephropathy have been detected two years after transplantation, renal impairment typically progresses slowly and graft loss is uncommon. Optimal glycaemic control is thought to protect against recurrence of diabetic nephropathy. The role of other risk factors remains unclear. We herein report a case of graft loss with advanced changes of diabetic nephropathy 26 months following transplantation in a patient with good glycaemic control.

Case Report: A 60-year-old male underwent ABO incompatible live donor transplantation for end-stage kidney disease secondary to diabetic nephropathy. The patient had a 15-year history of type 2 diabetes that was well controlled with lifestyle modification and oral hypoglycaemic agents. At the time of transplantation the patient’s HbA1c was 5.8% and donor kidney biopsy was normal. The peri-operative period was complicated by hyperglycaemia and insulin was commenced. Over the following 15 months the patient developed progressive proteinuria, hypertension and deteriorating renal function. During this time his HbA1c was consistently less than 6.7% and home blood glucose recordings were essentially in the target range. A biopsy performed at 19 months for progressive proteinuria was consistent with recurrent diabetic nephropathy. At 24 months the patient presented with symptomatic end-stage kidney disease. A biopsy of the transplant kidney revealed acute rejection with background changes of severe diabetic nephropathy affecting all glomeruli. The patient was soon after recommenced on haemodialysis.

Conclusion: Recurrent diabetic nephropathy should be considered as a cause of graft dysfunction even in a previously normal transplant kidney within two years of transplantation.

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