STEROID-INDUCED DIABETIC KETOACIDOSIS WITH HYPERNATREMIC DEHYDRATION AND HYPOKALEMIA IN BIOPSY-PROVEN MINIMAL CHANGE DISEASE: A DIAGNOSTIC AND THERAPEUTIC CHALLENGE

Abstract

Background: Diabetic ketoacidosis (DKA) is typically associated with absolute or relative insulin deficiency; however, glucocorticoids can precipitate hyperglycemic crises even in individuals without previously diagnosed diabetes. Patients receiving corticosteroid therapy for nephrotic syndromes such as minimal change disease (MCD) may develop metabolic instability due to enhanced gluconeogenesis, insulin resistance, and accelerated lipid oxidation. Concomitant electrolyte disturbances such as hypernatremia and hypokalemia in the setting of steroid-associated DKA are uncommon and may complicate metabolic management. Case Presentation: A 50Kg/42-year-old woman with biopsy-proven minimal change disease receiving oral corticosteroid therapy presented with progressive fatigue, dizziness, dysphagia, and difficulty ambulating for three days. On admission she appeared drowsy and dehydrated with tachycardia. Capillary blood glucose ranged between 505–579 mg/dL. Laboratory investigations revealed serum sodium of 158.6 mEq/L, potassium 2.7 mEq/L, chloride 121.8 mEq/L, ketonuria (2+), and glucosuria (3+). Arterial blood gas analysis showed a pH of 7.24 with bicarbonate of 9 mmol/L and high anion-gap metabolic acidosis consistent with diabetic ketoacidosis. Ultrasonography demonstrated a collapsed inferior vena cava suggestive of significant intravascular volume depletion. Inflammatory markers were not elevated and renal function remained preserved. Management: The patient was treated with intravenous fluid resuscitation using isotonic saline followed by gradual free-water replacement. Hypokalemia was corrected with intravenous potassium supplementation prior to initiation of insulin therapy. Continuous insulin infusion was initiated using a weight-based dosing protocol (approximately 0.5 units/kg/day) with close monitoring of blood glucose levels. Electrolytes and arterial blood gases were monitored serially. Dyselectrolytemia and metabolic acidosis improved progressively over the following 24 hours. Corticosteroid therapy was subsequently stopped after receiving 1mg/kg/day for 3 weeks. Patient received IV Hydrocortisone 100mg twice  daily for 3 days and there was gradual improvement sensorium, Hemodynamic parameters and metabolic profile. Patient was restarted with oral steoids after 24hours urine protein showed 2.4gms/day. Corticosteroid therapy was subsequently tapered under nephrology supervision, with improvement in sensorium, hemodynamic parameters, and metabolic profile. Conclusion: This report describes an uncommon presentation of steroid-associated diabetic ketoacidosis occurring in a patient with minimal change disease and accompanied by hypernatremic dehydration and hypokalemia. The coexistence of nephrotic syndrome, corticosteroid exposure, and intravascular volume depletion can create a complex metabolic environment requiring careful correction of fluid deficits and electrolyte imbalance. Early identification of steroid-related dysglycemia and vigilant metabolic monitoring are essential to ensure safe management in patients receiving corticosteroid therapy.