Aldosterone, a steroid hormone secreted by the adrenal cortex, is important in the overall control of sodium and potassium balance. Abnormalities in aldosterone concentrations are seen in a variety of clinical conditions. Overproduction (hyperaldosteronism) may result both from a primary cause such as adrenal adenoma (1) or a secondary cause, e.g., stimulation by increased renin release (2). Underproduction of the hormone is seen in such diseases as Addison disease (3). Many methods for measurement of plasma aldosterone have been based on the extraction method of James and Wilson (4). However, technical progress has enabled the production of direct kit methods for measuring plasma aldosterone. Previous studies (5)(6) have demonstrated that direct methods gave anomalous results in certain circumstances, possibly because of the presence of polar metabolites. The purpose of the current study was to compare a direct method with an existing extraction method for measuring aldosterone—first, in a large number of samples from clinical sources, and second, after physiological alterations of sodium intake. Plasma was obtained in the morning from 89 individuals after they had sat for 5–10 min: 40 patients with essential hypertension, average age 52 years (range 25–80 years; 21 men, 19 women); 28 presumed healthy volunteers, average age 45 years (range 24–77 years; 19 men, 9 women); 17 patients with chronic renal failure (serum creatinine 349 ± 32.2; range 189–535 μmol/L), average age 59 years (range 29–83 years; 9 men, 8 women); a 42-year-old woman with a pheochromocytoma; 2 patients with Conn syndrome (a 37-year-old woman and a 35-year-old man); and a 75-year-old woman with persistent hypertension and hypokalemia. Except for the chronic renal failure patients, none of the subjects had any sign of renal failure as determined by serum creatinine values (all <110 μmol/L). In addition, two or three quality-control pools were analyzed …
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Miller et al. (1997) studied this question.
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