W.R. Litchfield, C. Coolidge, P. Silva, F. Fallo, G.H. Williams, and R.G. Dluhy
JCEM, 1997;82(5);1507-1510
Unlike other forms of primary aldosteronism, recent prospective studies have paradoxically revealed that Glucocorticoid-remediable Aldosteronism (GRA) is usually characterized by normal potassium (K+ levels). To evaluate this paradox we studied 10 GRA subjects and 14 healthy controls in two protocols: 1) the renal K+ excretory response to acute oral administration 0f 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 microEq/min), and after fludrocortisone (100 +/- 35.0 microEq/min) was not significantly different than that seen in the control (n=8) subjects(54.9 +/- 19.0, 154 +/- 35.5, 112 +/- 45.8 microEq/min). Thus the renal kaliuretic response to K+ ingestion and exogenous mineralocorticoid 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+ ingestion in control subjects (n=7), but failed to increase in GRA subjects (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 aldosterone in this ACTH-regulated syndrome probably results in a milder degree of hyperaldosteronism compared with other forms of primary aldosteronism, thereby producing volume expansion with minimal renal K+ wasting.
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