Following unilateral adrenalectomy, some patients experience persistent hyperkalemia. This has been attributed to hypoaldosteronism due to severe suppression of aldosterone synthesis in the contralateral adrenal gland. Additionally, excess aldosterone leads to glomerular hyperfiltration masking kidney dysfunction, which can then manifest after cure with CKD-related hyperkalemia.
We report a case of 51-year-old male who was diagnosed with hypertension in his late 30s. He required a beta-blocker and calcium channel blocker (CCB) for 10 years, and eventually developed hypertensive nephropathy. With worsening lower extremity edema, he was switched from a CCB to an angiotensin receptor blocker. Soon afterwards, he presented with hypertensive emergency and was discovered to have significant hypokalemia (K 2.1 mmol/L), prompting work up for primary aldosteronism.
Biochemical evaluation revealed an elevated aldosterone to renin ratio of 38 [(ng/dL)/(ng/mL/hr)] and adrenal protocol CT scan revealed a 1.9 cm left adrenal nodule with benign characteristics. Adrenal vein sampling showed marked lateralization of excess aldosterone to the left adrenal gland, with proper catheter placement demonstrated in each adrenal veins (5-fold cortisol gradient bilaterally). He was started on spironolactone and 6 weeks later, underwent an uncomplicated laparoscopic left adrenalectomy. Spironolactone was discontinued
Serum K level was normal at 4.8 mmol/L immediately postoperatively. Ten hours later, his K went up to 6.6 mmol/L which was confirmed by repeat blood work, accompanied by worsened renal function (Cr 2.5 mg/dL up from a of baseline 2.0). His hyperkalemia persisted in the 5.0 – 6.0 range despite IV Calcium Gluconate, Insulin and D50. Oral potassium binders were avoided due to concerns about ileus. Upon recognition of the possibility of hypoaldosteronism, we recommended a NaHCO3 gtt, with subsequent normalization of serum K. We avoided initiating fludrocortisone in the short term, due to uncertainty about duration of hypoaldosteronism, & because he was still requiring two antihypertensive agents. Plasma aldosterone 2 wks after surgery was fully suppressed, confirming suspicion of hypoaldosteronism. He has been managed successfully with oral sodium bicarbonate tablets, remaining normokalemic at 3 weeks post-surgery.
Here we present a case of persistent hyperkalemia following resection of a signficantly biochemically active and long-standing aldosteronoma, which was successfully managed with sodium bicarbonate. We attribute the post-operative hyperkalemia in this patient to a combination of hypoaldosteronism due to deep suppression of the mineralocorticoid production of the contralateral adrenal, as well as unmasking of more severe kidney dysfunction than was he previously thought to have once aldosterone excess was withdrawn.