Korean J Transplant.  2019 Dec;33(4):146-152. 10.4285/jkstn.2019.33.4.146.

Progression of diabetic nephropathy after successful pancreas transplantation alone: a case report

Affiliations
  • 1Department of Surgery, Pusan National University Yangsan Hospital, Pusan National University School of Medicine, Yangsan, Korea. gmoolpop@gmail.com
  • 2Department of Pathology, Pusan National University Yangsan Hospital, Pusan National University School of Medicine, Yangsan, Korea.

Abstract

Pancreas transplantation is the only method that can nearly cure insulin-dependent diabetes mellitus. However, the effect of pancreas transplantation on patients with diabetic nephropathy has recently been considered controversial. In this report, we present a case of abrupt aggravation of proteinuria after successful pancreas transplantation alone without evidence of calcineurin inhibitor (CNI) toxicity. A 22-year-old female patient with type I diabetes mellitus underwent pancreas transplantation alone. The patient already had retinopathy and mild proteinuria, which in this case, may mean diabetic nephropathy. Her glucose levels were managed within the normal range after successful pancreas transplantation. However, the amount of proteinuria fluctuated. Kidney needle biopsy was performed owing to severe elevation of proteinuria, 2 years after the transplantation. Electron microscopy revealed diabetic glomerulosclerosis without evidence of CNI toxicity. This case indicates that diabetic nephropathy can be aggravated after pancreas transplantation, despite well-managed glucose levels and absence of CNI toxicity.

Keyword

Pancreas transplantation; Diabetic nephropathies; Calcineurin inhibitors

MeSH Terms

Biopsy, Needle
Calcineurin
Calcineurin Inhibitors
Diabetes Mellitus
Diabetes Mellitus, Type 1
Diabetic Nephropathies*
Female
Glucose
Humans
Kidney
Methods
Microscopy, Electron
Pancreas Transplantation*
Pancreas*
Proteinuria
Reference Values
Young Adult
Calcineurin
Calcineurin Inhibitors
Glucose

Figure

  • Fig. 1 Diamond-shaped patch is applied to the graft portal vein. Graft pancreas is soft with no fatty change.

  • Fig. 2 Endoscopic finding of graft duodenum at postoperative 1 year. Heathy mucosa is observed. There is no evidence of rejection on duodenal mucosal biopsy.

  • Fig. 3 (A) Glycosylated hemoglobin (HbA1c) level rapidly decreased to the normal range (<6%) immediately after pancreas transplant alone. Fasting glucose level was also well controlled after transplant. (B) Blood urea nitrogen (BUN) and creatinine (Cr) levels fluctuating after transplant. Progression of diabetic nephropathy and use of immunosuppressant might deteriorate renal function. (C) Changes in posttransplant proteinuria. Proteinuria abruptly increases with three peaks, corresponding to Pneumocystis jiroveci pneumonia (PJP) infection, at postoperative 600 days and 800 days.

  • Fig. 4 (A, B) Pathologic findings of renal biopsy. Prominent glomerular basement membrane thickening is identified. Deposits of hyaline material are present under the parietal epithelium of Bowman capsule, forming Kimmelstiel-Wilson nodule in one glomerulus. Global sclerosis is identified (H&E; A: ×200, B: ×400).

  • Fig. 5 (A, B) Pathologic findings of renal biopsy. On electron microscopy, foot process effacement is diffuse. Glomerular basement membrane is thick, measuring more than 500 nm in thickness. Mesangial sclerosis is identified. Electron dense deposit is not identified.

  • Fig. 6 Linear immunofluorescence stain of immunoglobulin G shows along the glomerular basement membrane.


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