IMPAIRED POTASSIUM-STIMULATED ALDOSTERONE PRODUCTION - A POSSIBLE EXPLANATION FOR NORMOKALEMIC GLUCOCORTICOID-REMEDIABLE ALDOSTERONISM

Unlike other forms of primary aldosteronism, recent prospective studie s have paradoxically revealed that glucocorticoid-remediable aldostero nism (GRA) is usually characterized by normal potassium (K+) levels. T o evaluate this paradox we studied 10 GRA subjects-and 14 healthy cont rols in two protocols: 1) the renal K+ excretory response to acute ora l administration of 50 mmol K+ chloride and to fludrocortisone, 0.2 mg po q12 h x 4 doses; and 2) the aldosterone response to administration of 50 mmol K+ chloride. The K+ excretion rate (KER) in GRA subjects ( n = 6) at baseline (45.6 +/- 8.3 mu Eq/min), after K+ (134 +/- 34.2 mu Eq/min), and after fludrocortisone (100 +/- 35.0 mu Eq/min) was not s ignificantly different than that seen in the control (n = 8) subjects (54.9 +/- 19.0, 154 +/- 35.5, 112 +/- 45.8 mu Eq/min, respectively). T hus the renal kaliuretic response to Ki ingestion and exogenous minera locorticoid is normal in GRA. Serum aldosterone increased from 5.0 +/- 3.8 at baseline to a maximum of 13.1 +/- 6.6 ng/dL 60 min after K+ in gestion in control subjects (n = 7), but failed to increase in GRA sub jects (n = 14), going from 8.7 +/- 3.8 (baseline) to 8.8 +/- 5.4 ng/dL at 60 min(P = 0.004 vs. control). The blunted aldosterone response to K+ in GRA in association with the sharp diurnal decline in aldosteron e in this ACTH-regulated syndrome probably results in a milder degree of hyperaldosteronism compared with other forms of primary aldosteroni sm, thereby producing volume expansion with minimal renal K+ wasting.