Abstract: PO2522
Diabetic Nephropathy: Is It All About Hyperglycemia?
Session Information
- Transplant Complications: Cardiovascular, Metabolic, and Societal
October 22, 2020 | Location: On-Demand
Abstract Time: 10:00 AM - 12:00 PM
Category: Trainee Case Report
- 1902 Transplantation: Clinical
Authors
- Alabdul Razzak, Iyiad, Alfaisal University, Riyadh, Riyadh Province, Saudi Arabia
- Arend, Lois J., Johns Hopkins University, Baltimore, Maryland, United States
- Alasfar, Sami, Johns Hopkins University, Baltimore, Maryland, United States
Introduction
Diabetic nephropathy (DN) is the most common cause of end stage renal disease (ESRD). Hyperglyemia has been suggested to be necessary for the development and maintenance of DN. Simultaneous pancreas and kidney transplantation (SPK) has revolutionized the treatment of type 1 diabetic patients with end-stage renal disease (ESRD), and prevention of recurrent DN is one of the main proposed benefits. We present a case of recurrence of DN after SPK despite normal endocrine pancreas allograft function
Case Description
A 47-year-old man with past medical history of ESRD due to diabetes type I who underwent a SPK transplant from a deceased donor in December 2003. His nadir serum Creatinine was 1.5 mg/dl and baseline urine protein creatinine ratio (UPC) is 110-250 mg/g. Maintenance immunosuppression consisted of tacrolimus, mycophenolate, and prednisone. His home medications also included benazepril for hypertension. Sixteen years after transplant, he was noted to have increase in UPC to 2100 mg/g and serum Creatinine to 1.9 mg/dL. Trough tacrolimus levels in the preceding 6 months ranged between 4.8 and 10.9 ng/mL. Donor specific antibodies were negative. He underwent renal allograft biopsy which showed early nodular mesangial matrix expansion and thickened glomerular basement membranes on electron microscopy consistent with diabetic nephropathy (Figure 1), early chronic transplant glomerulopathy, and severe arteriolar hyalinosis. Additional laboratory findings showed serum lipase 34 (Normal 7-60 U/L), amylase 103 (Normal 21-101 U/L), fasting glucose 79 (Normal 65-99 mg/dL), hemoglobin A1c 5.3, and C peptide was 2.03 (Normal 0.80 - 3.85 ng/mL). Despite increasing Benazepril dose to 40 mg daily, UPC and Cr continued to increase but stabilized in a range of 3800-4500 mg/g and 2.5 mg/dL respectively.
Discussion
Our case suggests that development of DN can be linked to mechanisms independent of hyperglycemia and the usual metabolic disturbances seen in patients with diabetes. A comprehensive restudying of the pathophysiology of DN could further enhance our existing knowledge of the factors implicated in DN, and possibly our ability to develop a more targeted therapy.