SAT-001 - Vasopressin resistance (Diabetes Insipidus) as a complication of Diabetic Ketoacidosis: Management challenge.

Vasopressin resistance (Diabetes Insipidus) as a complication of Diabetic Ketoacidosis: Management challenge.

Background
Severe hypokalemia during DKA can cause transient arginine vasopressin (AVP) resistance by reducing aquaporin-2 expression and function, resulting in diabetes insipidus (DI). This overlap is underrecognized and potentially challenging to manage because DI therapies are contraindicated in DKA. Early diagnosis and management can prevent life-threatening complications.

Case
A 53-year-old man with diabetes and HIV on Tenofovir arrived with altered mental status and was diagnosed with severe DKA, showing glucose of 976 mg/dL (ref < 100), bicarbonate less than 5 mmol/L(ref 22-29), beta-hydroxybutyrate at 9.53 mM (ref < 0.6), and anion-gap metabolic acidosis. He also had acute kidney injury, with creatinine at 3.4 mg/dL (ref 0.7-1.2), and acute pancreatitis, with lipase at 23,552 U/L (ref 8-78). A CT scan revealed pancreatitis. Treatment included intravenous fluids, insulin infusion, and aggressive electrolyte correction in the ICU. What’s concerning is that he developed refractory hypokalemia at 2 mEq/L (ref 3.5-5.0). On day 2 of admission, his serum sodium rapidly increased to 182 mEq/L from 134 (ref 135-145), with a urine output of 8 L/day (ref 0.8-2) and a Urine osmolality of 177 mOsm/kg (ref 300-900).
This led to the diagnosis of transient nephrogenic diabetes insipidus in the setting of severe hypokalemia, septic shock due to ESBL-UTI, and tenofovir use. Treatment included free-water replacement, isotonic saline, and short-term desmopressin 2 mcg twice daily for 7 days, with close monitoring to avoid rapid osmotic shifts. Thiazides, amiloride, and NSAIDs were avoided given contraindications in DKA. With meticulous electrolyte correction, fluid resuscitation, hypokalemia resolved; AVP resistance eventually resolved; renal function improved; and desmopressin was discontinued.
Conclusion
This case highlights reversible AVP resistance as a critical complication of severe DKA, driven by profound hypokalemia and reduced expression of aquaporin2 water channels. Early recognition, careful fluid and electrolyte management, and short-term use of desmopressin are essential to prevent life-threatening osmotic complications, particularly in immunocompromised patients with multisystem involvement.

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