SUN-573 - The Use of Diazoxide in Refractory Hypoglycemia in ESRD: A Case of Relative Hyperinsulinism

Introduction:

The kidney is a major site of peripheral insulin and c-peptide clearance, accounting for approximately 50% of peripheral insulin and 70% of C-peptide clearance. In patients with end-stage renal disease (ESRD), spontaneous hypoglycemia may occur due to decreased renal gluconeogenesis and impaired insulin clearance. During hypoglycemia, insulin, C-peptide, and proinsulin may appear inappropriately non-suppressed in ESRD, presenting a diagnostic challenge to distinguish relative hyperinsulinism from insulinoma.

Case Description:

An 89-year-old female with history of ESRD on hemodialysis (HD) and type 2 diabetes mellitus not on any medications presented with weakness and found to have blood glucose of 40 mg/dL. During a documented blood glucose of 46 mg/dL, laboratory evaluation showed beta-hydroxybutyrate of < 0.1 mmol/L (0-0.3), insulin 6 mU/L, proinsulin 6.6 pmol/L ( ≤ 7.2), C-peptide 2.5 ng/mL (0.8-3.9), consistent with endogenous hyperinsulinemic hypoglycemia by usual thresholds. Morning cortisol was 13.4 µg/dL (5.2-22.5), insulin antibodies were negative, and HbA1c was 4.1%. Imaging included computed tomography of the abdomen and endoscopic ultrasound, which showed no pancreatic lesion. Chromogranin A level was elevated at 705 ng/mL (0-187), with a negative hypoglycemic panel.

She required dextrose infusion, nutritional support, and was started on diazoxide, titrated to 100 mg twice daily with dose adjustment on dialysis days due to hypotension. Hypoglycemia improved, and she was discharged with outpatient endocrinology follow-up. Further neuroendocrine imaging was deferred as hyperinsulinemia was attributed to ESRD given absence of significant findings on conventional imaging and clinical response to diazoxide therapy.

Conclusion/

Discussion:

This case highlights ESRD-associated relative hyperinsulinism as a cause of spontaneous hypoglycemia, which can mimic insulinoma. Reduced renal clearance of insulin, pro-insulin, and C-peptide in patients with ESRD may lead to inappropriately non-suppressed values during hypoglycemia and complicate the biochemical evaluation between ERSD-associated hypoglycemia and true insulinoma. Chromogranin A levels can also be falsely elevated during renal failure due to reduced clearance.

While Insulinoma should be considered in cases of refractory hypoglycemia, it is important to recognize ESRD-associated relative hyperinsulinism prior to pursuing invasive testing. Published evidence for diazoxide use in ESRD-associated hypoglycemia is limited to case reports and small case series. More data is needed regarding long-term efficacy and tolerability, particularly in elderly hemodialysis patients.

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