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Abstract: TH-PO0485

Role of Glucose-Loaded Dialysate in Diabetic Ketoacidosis

Session Information

Category: Dialysis

  • 801 Dialysis: Hemodialysis and Frequent Dialysis

Authors

  • George, Lydia, Southeast Health, Dothan, Alabama, United States
  • Thomas, Greeshma A., Southeast Health, Dothan, Alabama, United States
  • Easow, Benjamin M., Southeast Health, Dothan, Alabama, United States
  • Mathew, Tijin A, Southeast Health, Dothan, Alabama, United States
  • Kodavanti, Chandra Kumar Mallick, Southeast Health, Dothan, Alabama, United States
Introduction

DKA is uncommon in patients with end-stage renal disease (ESRD) on hemodialysis due to reduced renal insulin clearance. We report a case of DKA precipitated with hemodilaysis (HD).

Case Description

A 53-year-old female with ESRD on HD, insulin-dependent type 2 diabetes mellitus and hypertension presented with shortness of breath for 2 days. She missed her last two HD sessions due to adverse weather. On arrival, she was afebrile, tachycardic, hypertensive, and hypoxemic. Chest X-ray showed bilateral pleural effusions. Labs showed BUN 49 mg/dL, creatinine 7.94 mg/dL, glucose 164 mg/dL. Diagnosed with pulmonary edema secondary to volume overload, she underwent urgent HD with removal of fluid. Subsequently, patient developed lethargy, abdominal pain and hypotension. Immediately after, labs revealed woresening anion gap metabolic acidosis with elevated ketone levels. Any Infectious etiology was ruled out. She was diagnosed with DKA and was admitted to ICU, managed with cautious IV fluids, insulin infusion, and norepinephrine. Blood glucose and anion gap normalized by day two, and she was transitioned to subcutaneous insulin.

Discussion

DKA is uncommon in ESRD patients due to decreased renal insulin clearance, which prolongs insulin activity. Standard dialysate often contains 100-200 mg/dL glucose, and in the absence of sufficient insulin, this can worsen hyperglycemia and promote ketosis. The absorbed glucose, coupled with impaired insulin mediated glucose utilization by insulin dependant tissues stimulates lipolysis and hepatic ketogenesis ultimately trigering DKA. ESRD patients lack osmotic diuresis, leading to extracellular volume overload rather than depletion, masking typical DKA signs and complicating diagnosis. Insulin therapy should be cautiously used due to decreased clearance, and volume resuscitation must be balanced with fluid status. This case underscores the need to recognize dialysate glucose as a potential precipitant of DKA and consider HD associated DKA as a differential when patients present with nausea, abdominal pain and lethargy post HD. Proactive insulin management and close metabolic monitoring during dialysis sessions are essential to prevent this potentially life-threatening complication.

Digital Object Identifier (DOI)