SAT-285 Use of High Dose Spironolactone in a Hypertensive Post-Stroke Patient Suspected with Secondary Hyperaldosteronism with a Concomitant Acute Kidney Failure & Severe Hypokalemia

Abstract Disclosure: J.L. Reyes: None. J.G. Sazon: None. M.G. Famorcan: None. R.L. Navarro: None. A.F. Diaz: None. A.A. Atilano: None. L.B. Mercado-Asis: None. Background: Hypokalemia due to increased kaliuresis in hyperaldosteronism results from unregulated hypersecretion of circulating aldosterone that leads to volume expansion, increased renal perfusion and glomerular hyperfiltration. The disrupted aldosterone secretion leads secondary hyperaldosteronism (SH) which worsens the hypokalemia. SH can further exacerbate fluid retention, electrolyte imbalances, and hypertension (HTN) especially in patients with kidney injury. The hesitancy to use spironolactone in patients with kidney problems has been a concern and obviously offsets its benefit. Thus, this case report. Clinical case: This is a 58-year-old male with acute intracerebral hemorrhage due to hypertensive emergency. Despite nicardipine drip administration, BP remained elevated at 140-180/90-100 mmHg, and his creatinine clearance declined with eGFR from 46 to 5 mL/min/1.73 m², necessitating dialysis. Conspicuously was the hypokalemia with a potassium level ranging from 3.13 to 3.82 mmol/L (NV: 3.5-5.2 mmol/L) with difficult correction despite intravenous potassium and was complicated with ileus and difficulty in extubating. The suspicion of secondary hypertension led to an endocrine referral. Spironolactone at an initial dose of 25 mg OD titrated up to 150 mg BID increased the serum potassium to 5.36 mmol/L. This provided a window for hormonal work up: plasma aldosterone concentration (PAC) was 5 ng/dl (Supine NV: 3.78- 23.3) and plasma renin activity (PRA) was 3.49 ng/ml/hr (Supine: 0.30-1.90). The values were suggestive of secondary hyperaldosteronism (SH) with a low aldosterone renin ratio of 1.43 (positive for primary aldosteronism is >20). The SH could have resulted from the kidney insufficiency of the patient. Spironolactone dosage was adjusted and serum potassium stabilized at 3.58-4.46 nmol/L with the highest dose at 400 mg per day. As the kidney function improved (eGFR of 47 mL/min/1.73 m²), BP control also improved (120-130/70-90 mmHg), and potassium level normalized (4.5 mmol/L) with resolution of ileus and eventual extubation. With other anti-HTN drugs, spironolactone dose was titrated down and maintained at 50 mg BID upon discharge. Conclusion and Recommendation: Secondary hyperaldosteronism may not be uncommon in ICU patients with resistant hypertension and unresponsive to intravenous potassium treatment. With utmost caution of monitoring urine output, kidney function, and serum potassium, spironolactone administration at a dose high enough to suppress the mineralocorticoid receptors from the excess circulating aldosterone can be significantly beneficial. Our case clearly demonstrated this clinical phenomenon with evidence of resolution of hypokalemia-related acute co-morbidities (ileus and difficult extubation). Multidisciplinary approach on the case at the outset led to the successful and optimal outcome. Presentation: Saturday, July 12, 2025