Part of “CHAPTER 80 – HYPERALDOSTERONISM“

Mineralocorticoid excess, whether primary or secondary, and disorders that mimic it are commonly manifested clinically as hypokalemia, which usually but not always is accompanied by alkalosis. Thus, a useful strategy for diagnosing hypokalemia is to approach the evaluation as a differential diagnosis of disorders of mineralocorticoid excess. Clinical features that accompany hypokalemia and may be used to determine the specific disorders that need to be considered are illustrated in Table 80-1 and in the flow chart in Figure 80-1. This basic framework is expanded in the course of this review to include the disorders appropriate to each of the four listed patterns of abnormalities of renin and aldosterone. Ideally, evaluation of the renin and aldosterone systems should be done in the absence of medication during a standardized sodium intake (e.g., 100 mEq per day of sodium as sodium chloride). If this is not possible, then at least the use of medications that affect the production of renin and aldosterone (i.e., diuretics and angiotensin converting enzyme inhibitors) should be discontinued and the blood pressure should be controlled with a calcium channel blocking agent. The level of sodium intake immediately preceding the sampling of blood for plasma renin activity and plasma aldosteroneshould be estimated by collecting a 24-hour aliquot of urine for the determination of sodium excretion. The blood for the plasma renin activity and plasma aldosterone evaluations should be drawn after overnight bedrest (in the hospital) or after 30 minutes of bedrest (in the clinic), and then drawn again after 2 hours of standing and walking.