A 55-year-old man comes to the clinic for follow-up of hypertension. The patient was diagnosed with hypertension 3 months ago after an episode of transient vision loss in his right eye. He has occasional headaches and general fatigue but otherwise feels well. His current medications include aspirin, lisinopril, and low-dose hydrochlorothiazide. His blood pressure is 157/95 mm Hg and pulse is 69/min. BMI is 26 kg/m². Cardiac examination shows a fourth heart sound on auscultation. There are no bruits in the carotids or abdomen. Pulses are 2+ in all extremities. Laboratory results are as follows: Which of the following best explains this patient's laboratory findings?

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11ec25c8_d0bd_d007_bc81_a168903a18d8_MD0003_00 This patient with hypertension and undetectable plasma renin activity most likely has primary hyperaldosteronism (PH). PH is the most common cause of secondary hypertension and is usually due to an adrenal adenoma or bilateral adrenal hyperplasia. Patients typically develop hypertension, mild hypernatremia, hypokalemia, and metabolic alkalosis. Plasma renin activity (PRA) is low in PH due to feedback inhibition. Hypokalemia and hypertension with suppressed PRA may also be seen in congenital adrenal hyperplasia, Cushing's syndrome, or exogenous mineralocorticoid intake. secondary hypertension Serum potassium may be normal initially in patients with PH, but treatment with diuretics may trigger severe, symptomatic hypokalemia. Although aldosterone causes increased renal reabsorption of sodium, most patients with PH do not have edema or clinically significant hypernatremia due to aldosterone escape. aldosterone escape (Choice A) ACE inhibitors decrease conversion of angiotensin I to angiotensin II. Aldosterone levels are decreased and PRA is reflexively increased. ACE inhibitors are associated with hyperkalemia and a rise in creatinine due to reduced glomerular filtration rate. (Choice B) Malignant hypertension is characterized by markedly elevated blood pressure with end-organ damage to the eye (eg, retinal hemorrhages, papilledema), kidney (eg, nephrosclerosis), and central nervous system (eg, hemorrhage, encephalopathy). It also causes secondary hyperaldosteronism with elevated PRA. This patient's normal creatinine and undetectable PRA make malignant hypertension less likely. (Choice D) Diuretic use in the absence of PH may also cause hypokalemia, but it is associated with a compensatory rise in PRA. (Choice E) Unilateral renal artery stenosis is characterized by hypertension, abdominal bruits, and episodes of flash pulmonary edema. Renovascular hypertension also causes a rise in PRA, leading to secondary hyperaldosteronism. Educational objective: Primary hyperaldosteronism is characterized by hypertension, mild hypernatremia, metabolic alkalosis, and suppressed plasma renin activity. Hypokalemia is not always present at baseline but can be severe with diuretic use. Clinically significant hypernatremia and edema are not seen due to aldosterone escape. References: Primary aldosteronism. (http://www.ncbi.nlm.nih.gov/pubmed/22806599)

A 55-Year-Old Man Comes to the Clinic for Follow-Up of Hypertension