Impaired potassium-stimulated aldosterone production: A possible explanation for normokalemic glucocorticoid-remediable aldosteronism

被引:30
作者
Litchfield, WR
Coolidge, C
Silva, P
Lifton, RP
Fallo, F
Williams, GH
Dluhy, RG
机构
[1] HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA
[2] YALE UNIV, SCH MED, HOWARD HUGHES MED INST, BOYER CTR MOL GENET, NEW HAVEN, CT 06510 USA
[3] UNIV PADUA, DIV ENDOCRINOL, I-35122 PADUA, ITALY
[4] NEW ENGLAND DEACONESS HOSP, DEPT MED, NEW HAVEN, CT 06510 USA
关键词
D O I
10.1210/jc.82.5.1507
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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 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 significantly different than that seen in the control (n = 8) subjects (54.9 +/- 19.0, 154 +/- 35.5, 112 +/- 45.8 mu Eq/min, respectively). Thus the renal kaliuretic response to Ki 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.
引用
收藏
页码:1507 / 1510
页数:4
相关论文
共 28 条
[1]   RAT ADRENAL-CELL SENSITIVITY TO ANGIOTENSINII, ALPHA-1-24-ACTH, AND POTASSIUM - COMPARATIVE-STUDY [J].
BRALEY, LM ;
WILLIAMS, GH .
AMERICAN JOURNAL OF PHYSIOLOGY, 1977, 233 (05) :E402-E406
[2]   THE CHANGING CLINICAL SPECTRUM OF PRIMARY ALDOSTERONISM [J].
BRAVO, EL ;
TARAZI, RC ;
DUSTAN, HP ;
FOUAD, FM ;
TEXTOR, SC ;
GIFFORD, RW ;
VIDT, DG .
AMERICAN JOURNAL OF MEDICINE, 1983, 74 (04) :641-651
[3]   THE ABSENCE OF LONG-TERM THERAPEUTIC EFFECT OF CALCIUM-CHANNEL BLOCKADE IN THE PRIMARY ALDOSTERONISM OF ADRENAL ADENOMAS [J].
BURSZTYN, M ;
GROSSMAN, E ;
ROSENTHAL, T .
AMERICAN JOURNAL OF HYPERTENSION, 1988, 1 (03) :S88-S90
[4]  
Capponi AM, 1996, CURR OPIN ENDOCRINOL, V3, P248, DOI [10.1097/00060793-199606000-00010, DOI 10.1097/00060793-199606000-00010]
[5]   GLUCOCORTICOID-REMEDIABLE ALDOSTERONISM [J].
DLUHY, RG ;
LIFTON, RP .
ENDOCRINOLOGY AND METABOLISM CLINICS OF NORTH AMERICA, 1994, 23 (02) :285-297
[6]  
FALLO F, 1991, MINER ELECTROL METAB, V17, P185
[7]   A NEW FAMILY WITH DEXAMETHASONE-SUPPRESSIBLE HYPER-ALDOSTERONISM - ALDOSTERONE UNRESPONSIVENESS TO ANGIOTENSIN-II [J].
FALLO, F ;
SONINO, N ;
ARMANINI, D ;
LUZZI, T ;
PEDINI, F ;
PASINI, C ;
MANTERO, F .
CLINICAL ENDOCRINOLOGY, 1985, 22 (06) :777-785
[8]   ADRENAL-STEROID RESPONSES TO ACTH IN GLUCOCORTICOID-SUPPRESSIBLE ALDOSTERONISM [J].
GANGULY, A ;
WEINBERGER, MH ;
GUTHRIE, GP ;
FINEBERG, NS .
HYPERTENSION, 1984, 6 (04) :563-567
[9]   ANOMALOUS POSTURAL RESPONSE OF PLASMA ALDOSTERONE CONCENTRATION IN PATIENTS WITH ALDOSTERONE-PRODUCING ADRENAL ADENOMA [J].
GANGULY, A ;
DOWDY, AJ ;
LUETSCHER, JA ;
MELADA, GA .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1973, 36 (02) :401-404
[10]   KINDRED WITH FAMILIAL GLUCOCORTICOID-SUPPRESSIBLE ALDOSTERONISM [J].
GIEBINK, GS ;
GOTLIN, RW ;
BIGLIERI, EG ;
KATZ, FH .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1973, 36 (04) :715-723