6600 Hyperkalemia Shortly After Surgical Treatment For Primary Hyperaldosteronism

Abstract Disclosure: M. Hernandez Hernandez: None. J. Colon Castellano: None. Primary hyperaldosteronism was thought to be a rare cause of secondary hypertension in the United States. However, recent epidemiologic data estimates that approximately 5-15% of patients with a diagnosis of hypertension are due to hyperaldosteronism. This number may be higher due to patients being widely underdiagnosed. Most of these patients can be cured with a surgical approach. Patients who undergo adrenalectomy for primary hyperaldosteronism need to be closely monitored for electrolyte disturbances. Post-adrenalectomy hyperkalemia in hyperaldosteronism is thought to be secondary to resultant hypoaldosteronism caused by suppression of the juxtaglomerular apparatus on the contralateral adrenal gland secondary to the volume-expanded state before unilateral adrenalectomy. It has been reported in a subset of patients and it is a known cause of increased morbidity and mortality as patients may present with severe hyperkalemia. We present the case of a 63-year-old male patient with medical history of hypertension who was diagnosed with primary hyperaldosteronism when he presented with hypokalemia in routine laboratories performed after an elective laparoscopic cholecystectomy. The patient’s laboratories were remarkable for potassium levels at <2mEq/L, normal sodium levels, and further workup obtained which was remarkable for plasma aldosterone concentration: plasma renin activity (PAC/PRA) at 216. The medication regimen at home included Lisinopril 40mg p.o. daily, Nifedipine 60mg p.o. daily, and oral potassium replacement. The patient was consulted to the Endocrinology service which recommended further imaging studies. Abdomino-pelvic CT scan was remarkable for a right adrenal adenoma measuring 1.5 cm with 24 Hounsfield units. The patient was initially managed with aldosterone antagonists and then a right adrenalectomy was performed successfully after adrenal vein sampling. Approximately two weeks after the adrenalectomy, the patient was called back to the Emergency Room (ER) due to hyperkalemia 6.5mEq/L. Upon arrival at the ER, there were no EKG changes associated with hyperkalemia, and he was given appropriate treatment for potassium levels. The patient was started on Fludrocortisone with excellent clinical response and is currently being followed at Endocrinology clinics. The etiology of this patient’s hyperkalemia soon after adrenalectomy demonstrates the effect of relative hypoaldosteronism from chronic suppression of the left adrenal gland due to aldosterone excess produced by the right adrenal adenoma. Fludrocortisone is a synthetic mineralocorticoid and it has potent effects in reducing potassium levels mediated by sodium reabsorption and potassium excretion at the distal renal tubules. Early treatment in these patients is crucial to prevent the development of electrolyte disturbances that may ultimately lead to life-threatening arrhythmias. Presentation: 6/2/2024