Category: Diabetes/Prediabetes/Hypoglycemia

Type: e-Poster

Monitor: 23


Friday, Apr 26
12:00 PM – 12:30 PM

Objective : The objective of this report is to discuss a case of hypoglycemia in a non-diabetic patient with end-stage renal disease (ESRD) and how the workup of hypoglycemia may be affected by renal impairment.

Methods : We present the findings of a patient with ESRD and hypoglycemia and a literature review.

Results : A 68 year-old female with ESRD on hemodialysis presented with altered mental status from hypoglycemia. Blood glucose of 22 mg/dL on point-of-care testing improved with 75 mL of dextrose 50% intravenous injection. She had poor appetite, weight loss, and no history of diabetes. She continued to have recurrent symptomatic hypoglycemia. During 72 hour fast, plasma glucose was 56 mg/dL with proinsulin 11.7 pmol/L (<18.8 pmol/L), C-peptide 4.18 ng/mL, beta-hydroxybutyrate 0.5 mg/dL (0.2-2.8 mg/dL), cortisol 9.6 ug/dL, and ACTH 100 pg/mL at the time of this plasma glucose. At plasma glucose of 46 mg/dL, beta-hydroxybutyrate was 1.2 mg/dL, insulin 1.7 uIU/mL (2.0-19.6 uIU/mL), proinsulin 13.9 pmol/L, C-peptide 2.36 ng/mL, cortisol 7 ug/dL. Cosyntropin 0.25 mg stimulation test showed baseline cortisol 10.8 ug/dL, 30-minute post-stimulation cortisol 22.4 ug/dL, 60-minute post-stimulation cortisol 25.7 ug/dL. Hemoglobin A1c <4.0%. Insulin autoantibody <0.4 U/mL. CT Abdomen, endoscopic ultrasound, serum testing for oral hypoglycemic agents were negative. Hypoglycemia was successfully controlled with octreotide.

Discussion :

Discrepant laboratory values including low insulin with elevated proinsulin, C-peptide and low beta-hydroxybutyrate did not allow differentiation of insulin mediated versus non-insulin mediated hypoglycemia. This may be due to the prolonged half-life of insulin and proinsulin, and reduced rate of C-peptide clearance in chronic kidney disease (CKD) due to decreased degradation or excretion by the kidney1. There are no guidelines to determine appropriate levels of these values during hypoglycemia in patients with CKD. We concluded that hypoglycemia was likely from malnutrition and reduced renal gluconeogenesis in ESRD. Ruling out adrenal insufficiency is also challenging in CKD as cortisol and its metabolites are excreted by the kidney resulting in prolonged half-life of cortisol, despite typically an appropriate response with ACTH stimulation2.

Conclusion : Workup of hypoglycemia in CKD is challenging as insulin, proinsulin, C-peptide, and cortisol are affected by renal insufficiency. There is need for further research in developing adjusted guidelines for hypoglycemia evaluation in patients with renal disease.


Christine Mathai

Endocrinology Fellow
Temple University Hospital
Philadelphia, Pennsylvania

I am currently an Endocrinology Fellow at Temple University Hospital in Philadelphia, PA. I graduated from Rutgers New Jersey Medical School and completed Internal Medicine Residency at Thomas Jefferson University Hospital.

Alec Talsania

Medical Student
Lewis Katz School of Medicine

I am currently a second year medical student at Lewis Katz School of Medicine. I have my BA from Hamilton College.

Cherie L. Vaz

Assistant Professor of Medicine
Lewis Katz School of Medicine at Temple University

I am faculty at Lewis Katz School of Medicine and practicing Endocrinologist at Temple University, Philadelphia PA.