ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Please note that you are viewing an archived section from 2020 and some content may be unavailable. To unlock all content for 2020, please visit the archives.

Abstract: PO0999

ESKD due to an Atypical Cause of Diabetes Mellitus

Session Information

Category: Trainee Case Report

  • 602 Diabetic Kidney Disease: Clinical

Authors

  • Giordano McAuliffe, Christin M., Vanderbilt University Medical Center, Nashville, Tennessee, United States
  • Luther, James M., Vanderbilt University Medical Center, Nashville, Tennessee, United States
Introduction

Diabetes mellitus (DM) is the most common cause of chronic kidney disease (CKD) in the United States. This case describes CKD caused by an atypical, potentially reversible cause of type 2 DM.

Case Description

A 70 year-old male presented to our Hypertension Clinic with new onset lower extremity edema, CKD, and hypertension. He had had type 2 DM for 20 years complicated by retinopathy and gastroparesis. Although body mass index was 29.8, he required more than 100 units of long-acting insulin daily. His blood pressure measured 200/115 and had been refractory to multiple medications. Initial laboratory evaluation demonstrated creatinine 2.7 mg/dL, glucose 245 mg/dL, urine protein-to-creatinine (uPCR) of 8.5, hemoglobin A1c of 7.5%, and negative serum and urine protein electrophoresis. Echocardiogram revealed severe left ventricular hypertrophy. CT of his abdomen demonstrated a 4 x 4 cm pancreatic cystic mass which had been biopsied 15 years previously and showed no malignant cells. Due to persistent gastrointestinal complaints, imaging was repeated 2 years later and demonstrated an increase in the pancreatic mass size to 5.8 x 5.1 cm without any evidence of metastasis. Further laboratory evaluation demonstrated C-peptide 2.4 ng/ml (normal) and glucagon 1760 ng/L (normal <208 ng/L). Elevated pancreatic polypeptide and chromogranin A levels confirmed the diagnosis: glucagonoma. He declined surgery and was intolerant of octreotide. Although uPCR decreased to a nadir of 1.5 with improved blood pressure control, his kidney function progressively declined and he required hemodialysis (HD). HD only minimally improved his nausea and vomiting. His physical condition declined over the course of a year, until he entered hospice and expired. At time of death, his pancreatic lesion measured 6 cm.

Discussion

Glucagonomas are rare tumors with an incidence of approximately 0.1 cases per 100,000, most commonly presenting in the 5th decade of life. Secondary causes of DM should be considered in patients without obesity, normal C-peptide levels despite advanced disease, and/or a pancreatic mass. Additionally, glucagon excess or mechanical obstruction by a pancreatic mass may cause gastrointestinal complaints attributed to uremia or diabetic gastropathy. Timely diagnosis and resection could prevent this disease cascade of diabetes, nephropathy, and end-stage kidney disease.