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Abstract
In such patients, however, renin and aldosterone secretion may be suppressed appropriately for the level of sodium retention4; this is particularly true for patients with hypertension. Since the hyperkalemia may be unrelated to aldosterone deficiency, considering hyporeninemic hypoaldosteronism a disease in this instance may be incorrect. Type I pseudohypoaldosteronism may result from an inherited abnormality in the mineralocorticoid receptor, leading to the loss of mineralocorticoid responsiveness, salt wasting, hyperkalemia, low blood pressure, and markedly elevated plasma renin activity and plasma aldosterone levels.5 In addition, the Type I syndrome may also occur as a result of an acquired defect in aldosterone action caused by a variety of renal diseases and associated with salt wasting. The role of aldosterone in the hyperkalemia and hyperchloremic acidosis seen in Type II pseudohypoaldosteronism remains unclear. Since the complete syndrome can be transmitted in an autosomal dominant fashion, a single abnormality causing sodium chloride hyperabsorption, hyperkalemia, and hyperchloremic acidosis is likely.