This is a 36‐year‐old African American man who suffered from a 1‐year history of progressive decline in kidney function (lithium‐induced nephrotoxicity) leading to discontinuation of the lithium. However, during the hospital stay, he was minimally symptomatic, mainly nocturia. His medical history was remarkable for hypertension and schizophrenia. His medications were valsartan, paliperidone, and sertraline. Family history was remarkable for hypertension, with no known history of renal disease. Physical exam showed suboptimally controlled hypertension, obese with a BMI of 39. Other systemic examination was unremarkable. Laboratory analysis was significant for renal insufficiency with creatinine determinations between 4.2 and 4.4 mg/dL, hypokalemia (K 2.6), mixed metabolic alkalosis and respiratory acidosis (pH 7.40, PCO2 48, HCO3 29.7) and serum Na 145. Urinalysis findings were consistent with inappropriately diluted urine due to nephrogenic diabetes insipidus related to his chronic lithium use. Renal ultrasound showed normal sized kidneys and echogenicity. Because of suspicion of a secondary cause of hypertension, workup for hperaldosteronism was pursued, and results showed low plasma renin activity (PRA) 0.38 ng/mL, inappropriately elevated plasma aldosterone concentration (PAC) 35 ng/dL and PAC/PRA ratio elevated > 20. A preliminary diagnosis of primary hyperaldosteronism was made, and diagnosis was confirmed by aldosterone suppression test (Intravenous saline infusion test). CT scan abdomen revealed both adrenal glands mildly thickened, and findings were consistent with bilateral idiopathic hyperplasia (IHA). The patient was started on spironolactone which resulted in improvement of blood pressure levels and normalization of his hypokalemia.
Although most clinicians had thought primary aldosteronism to be a rare form of hypertension for more than 3 decades, it is now recognized to be the most common form of secondary hypertension. Using the PAC/PRA ratio as a case‐finding test, followed by aldosterone suppression confirmatory testing, has resulted in much higher prevalence estimates up to 13% of all patients with hypertension. Subtype evaluation tests using the CT scan and adrenal venous sampling (AVS) are essential to determine the lines of management. Unilateral adrenalectomy in patients with aldosterone‐producing adenoma or unilateral adrenal hyperplasia results in normalization of hypokalemia and hypertension is improved in all these patients. Otherwise, patient with bilateral adrenal disease, like our patient, should be treated medically with a mineralocorticoid receptor antagonist.
The recognition of aldosterone‐specific cardiovascular morbidity and mortality associated with aldosterone excess should stimulate clinicians to increase efforts at case finding, which has become a simple 2‐step process; PAC/PRA ratio screening followed by aldosterone suppression confirmation test.