Kidney Week

Abstract: FR-PO1169

Diabetes Without Diabetes: Unexplained Diabetic-Pattern Glomerulopathy in a Kidney Transplant Recipient

Session Information

• Transplantation: Clinical - Transplant Access, Recipient Evaluation, Living Donors, Pregnancy, and More
  October 23, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Transplantation

• 2002 Transplantation: Clinical

Authors

• Siddiqi, Mahwash, Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States

Mahwash Siddiqi, MD

• Raza, Muhammad, Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States

Muhammad Raza, MD

• Tahir, Maria, Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States

Maria Tahir, MD

• Abendroth, Catherine, Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States

Catherine Abendroth, MD

• Kaur, Gurwant, Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States

Gurwant Kaur, MD, FASN

• Portela-Colon, Rafael, Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States

Rafael Portela-Colon, MD, FASN

• Farooq, Umar, Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States

Umar Farooq, MD, MS, MBA, FASN

• Verma, Navin, Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States

Navin Verma, MD

• Ghahramani, Nasrollah, Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States

Nasrollah Ghahramani, MD, FASN

• Shah, Vaqar H., Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States

Vaqar H. Shah, MD, FASN

Introduction

Diabetic glomerulopathy is defined by mesangial expansion, glomerular basement membrane (GBM) thickening, and capsular drop lesions it poses a significant diagnostic challenge when found in a non-diabetic patient, particularly post-transplant, where tacrolimus toxicity and hypertensive nephropathy must also be considered.

Case Description

A 64-year-old non-diabetic male with ESRD from chronic glomerulonephritis received a living-related transplant 24 years ago. Despite consistently normal HbA1c (5.4–6.1%), Fructosamine, and random glucose levels, he developed progressive allograft dysfunction (creatinine 5.32 mg/dL, UPCR 12.2 g/g, eGFR declining from 40 to 15 mL/min in the last few years). Myeloma workup and urinary protein electrophoresis (UPEP) were negative. Allograft biopsy performed three times showed diffuse mesangial expansion, GBM thickening, capsular drop lesion, and marked arteriolar hyalinosis, all consistent with diabetic glomerulopathy. Congo red was negative. Immunofluorescence showed linear polytypic GBM staining consistent with protein trapping. Electron microscopy confirmed GBM thickening two to three times normal without electron-dense deposits. Absence of GBM duplication excluded chronic allograft nephropathy. Etiology remained uncertain.

Discussion

This case highlights a well-recognized but uncommon diagnostic challenge: diabetic-pattern glomerulopathy in the absence of diabetes. In the post-transplant setting, this morphology raises a broad differential including tacrolimus-induced nephrotoxicity (which can cause arteriolar hyalinosis and GBM changes), hypertensive nephropathy, monoclonal immunoglobulin deposition disease (excluded by negative myeloma workup and polytypic IF staining), idiopathic nodular glomerulosclerosis, and donor-transmitted glomerular disease. The capsular drop lesion, often cited as pathognomonic of diabetes, adds further diagnostic complexity when encountered in a non-diabetic host. The linear polytypic IF pattern reflects non-specific GBM protein entrapment rather than true immune complex deposition, supporting a metabolic or hemodynamic rather than immune-mediated etiology.