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Endocrine Abstracts (2015) 37 EP520 | DOI: 10.1530/endoabs.37.EP520

1Endocrinology, Diabetes and Metabolism Department, Coimbra Hospital and University Centre, Coimbra, Portugal; 2Nephrology Department, Coimbra Hospital and University Centre, Coimbra, Portugal; 3Pathological Anatomy Department, Coimbra Hospital and University Centre, Coimbra, Portugal; 4Endocrinology, Diabetes and Nutrition Department, Baixo Vouga Hospital Centre, Aveiro, Portugal; 5Urology and Renal Transplantation Department, Coimbra Hospital and University Centre, Coimbra, Portugal.


Introduction: Diabetes mellitus is a common metabolic complication after kidney transplantation, occurring with a frequency of 15–30% in the first year. However, despite the high incidence, there are described few cases of diabetic nephropathy with nodular glomerulosclerosis of the allograft.

Case: Female patient, 49, with autosomal dominant familial renal poliquistose diagnosed at 17 and progression for chronic end-stage renal disease, underwent renal transplantation of cadaver in June 2004. Five months after transplant and having started immunosuppressive therapy with tacrolimus, sirolimus, and prednisone, was diagnosed with diabetes mellitus. Initiated conventional intensive insulin therapy, with gradual decrease of the total daily dose after suspension of prednisone and reduction of the remaining immunosuppressants.

Instead of maintaining an optimized glycaemic control (HbA1c <7%), it was found chronic renal allograft dysfunction, 9 years and 5 months after transplantation, the patient had marked reduction of glomerular filtration rate (<20 ml/min) with proteinuria in nephrotic range. Graft biopsy was performed and histopathological and immunohistochemical evaluation demonstrated ‘nodular glomerulosclerosis in diabetes mellitus context, without acute rejection, with observed mild chronic rejection phenomena with mild tubular atrophy and fibrosis’. In April 2014, the patient kept worsening glomerular filtration rate of ~15 ml/min per 1.73 m2 and an HbA1c of 6.6%, under exclusive immunosuppression with tacrolimus.

Conclusions: In the case described, there was progressive graft dysfunction despite good glycemic control, with confirmed nodular glomerulosclerosis typical lesions. Thus, in the NODAT with renal allograft dysfunction, it is not excluded the possibility of association with diabetic nephropathy. This case also shows that in NODAT there are the same risk factors for the occurrence of late diabetic complications.

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