UpToDate
Official reprint from UpToDate®
www.uptodate.com ©2017 UpToDate®

原发性醛固酮增多症的临床特点

Authors
William F Young, Jr, MD, MSc
Norman M Kaplan, MD
Burton D Rose, MD
Section Editor
André Lacroix, MD
Deputy Editor
Kathryn A Martin, MD

引言

不可抑制的(原发性)醛固酮分泌过多是高血压的一个容易漏诊的病因，其典型表现为高血压和低钾血症。

自1954年Conn首次报道了醛固酮分泌瘤后，人们已经报道了原发性醛固酮增多症(primary aldosteronism, PA)的多种亚型[1-4]。PA最常见的亚型包括：

  • 醛固酮分泌瘤
  • 双侧特发性原醛症

较少见的亚型包括：

  • 单侧肾上腺皮质增生或原发性肾上腺增生症(主要由单侧肾上腺球状带小结节或大结节增生引起)
  • 双侧肾上腺小结节或大结节增生伴PA
  • 家族性原醛症Ⅰ型[糖皮质激素可治疗性醛固酮增多症(glucocorticoid-remediable aldosteronism, GRA)]和家族性原醛症Ⅱ型(醛固酮分泌瘤或双侧特发性原醛症呈家族聚集性发病或二者同时呈家族聚集性发病)
  • 单纯性醛固酮分泌性肾上腺皮质癌和异位醛固酮分泌瘤(例如，位于卵巢或肾脏的肿瘤)

            

Subscribers log in here

To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information or to purchase a personal subscription, click below on the option that best describes you:
Literature review current through: 2017-06 . | This topic last updated: 2016-10-19.
The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2017 UpToDate, Inc.
References
Top
  1. CONN JW. Aldosterone in clinical medicine; past, present, and future. AMA Arch Intern Med 1956; 97:135.
  2. Bravo EL, Tarazi RC, Dustan HP, et al. The changing clinical spectrum of primary aldosteronism. Am J Med 1983; 74:641.
  3. Mattsson C, Young WF Jr. Primary aldosteronism: diagnostic and treatment strategies. Nat Clin Pract Nephrol 2006; 2:198.
  4. Young WF. Primary aldosteronism: renaissance of a syndrome. Clin Endocrinol (Oxf) 2007; 66:607.
  5. AUGUST JT, NELSON DH, THORN GW. Response of normal subjects to large amounts of aldosterone. J Clin Invest 1958; 37:1549.
  6. Gonzalez-Campoy JM, Romero JC, Knox FG. Escape from the sodium-retaining effects of mineralocorticoids: role of ANF and intrarenal hormone systems. Kidney Int 1989; 35:767.
  7. Hall JE, Granger JP, Smith MJ Jr, Premen AJ. Role of renal hemodynamics and arterial pressure in aldosterone "escape". Hypertension 1984; 6:I183.
  8. Yokota N, Bruneau BG, Kuroski de Bold ML, de Bold AJ. Atrial natriuretic factor significantly contributes to the mineralocorticoid escape phenomenon. Evidence for a guanylate cyclase-mediated pathway. J Clin Invest 1994; 94:1938.
  9. Wang XY, Masilamani S, Nielsen J, et al. The renal thiazide-sensitive Na-Cl cotransporter as mediator of the aldosterone-escape phenomenon. J Clin Invest 2001; 108:215.
  10. Guyton AC. Blood pressure control--special role of the kidneys and body fluids. Science 1991; 252:1813.
  11. Kinoshita Y, Knox FG. Role of prostaglandins in proximal tubule sodium reabsorption: response to elevated renal interstitial hydrostatic pressure. Circ Res 1989; 64:1013.
  12. Clore J, Schoolwerth A, Watlington CO. When is cortisol a mineralocorticoid? Kidney Int 1992; 42:1297.
  13. Pedrinelli R, Bruschi G, Graziadei L, et al. Dietary sodium change in primary aldosteronism. Atrial natriuretic factor, hormonal, and vascular responses. Hypertension 1988; 12:192.
  14. Blumenfeld JD, Sealey JE, Schlussel Y, et al. Diagnosis and treatment of primary hyperaldosteronism. Ann Intern Med 1994; 121:877.
  15. Zarifis J, Lip GY, Leatherdale B, Beevers G. Malignant hypertension in association with primary aldosteronism. Blood Press 1996; 5:250.
  16. Douma S, Petidis K, Doumas M, et al. Prevalence of primary hyperaldosteronism in resistant hypertension: a retrospective observational study. Lancet 2008; 371:1921.
  17. Vantyghem MC, Ronci N, Provost F, et al. Aldosterone-producing adenoma without hypertension: a report of two cases. Eur J Endocrinol 1999; 141:279.
  18. Vasan RS, Evans JC, Larson MG, et al. Serum aldosterone and the incidence of hypertension in nonhypertensive persons. N Engl J Med 2004; 351:33.
  19. Young DB. Quantitative analysis of aldosterone's role in potassium regulation. Am J Physiol 1988; 255:F811.
  20. George JM, Wright L, Bell NH, Bartter FC. The syndrome of primary aldosteronism. Am J Med 1970; 48:343.
  21. Mulatero P, Stowasser M, Loh KC, et al. Increased diagnosis of primary aldosteronism, including surgically correctable forms, in centers from five continents. J Clin Endocrinol Metab 2004; 89:1045.
  22. Fraser R, Murray GD, Connell JM. Conn's syndrome: no longer a needle in a haystack? Clin Endocrinol (Oxf) 1998; 49:709.
  23. Loh KC, Koay ES, Khaw MC, et al. Prevalence of primary aldosteronism among Asian hypertensive patients in Singapore. J Clin Endocrinol Metab 2000; 85:2854.
  24. Litchfield WR, Coolidge C, Silva P, et al. Impaired potassium-stimulated aldosterone production: a possible explanation for normokalemic glucocorticoid-remediable aldosteronism. J Clin Endocrinol Metab 1997; 82:1507.
  25. Rossi GP, Bernini G, Caliumi C, et al. A prospective study of the prevalence of primary aldosteronism in 1,125 hypertensive patients. J Am Coll Cardiol 2006; 48:2293.
  26. Gregoire JR. Adjustment of the osmostat in primary aldosteronism. Mayo Clin Proc 1994; 69:1108.
  27. Quamme GA. Control of magnesium transport in the thick ascending limb. Am J Physiol 1989; 256:F197.
  28. Ribstein J, Du Cailar G, Fesler P, Mimran A. Relative glomerular hyperfiltration in primary aldosteronism. J Am Soc Nephrol 2005; 16:1320.
  29. Sechi LA, Novello M, Lapenna R, et al. Long-term renal outcomes in patients with primary aldosteronism. JAMA 2006; 295:2638.
  30. Reincke M, Rump LC, Quinkler M, et al. Risk factors associated with a low glomerular filtration rate in primary aldosteronism. J Clin Endocrinol Metab 2009; 94:869.
  31. Shigematsu Y, Hamada M, Okayama H, et al. Left ventricular hypertrophy precedes other target-organ damage in primary aldosteronism. Hypertension 1997; 29:723.
  32. Rossi GP, Sacchetto A, Visentin P, et al. Changes in left ventricular anatomy and function in hypertension and primary aldosteronism. Hypertension 1996; 27:1039.
  33. Yoshihara F, Nishikimi T, Yoshitomi Y, et al. Left ventricular structural and functional characteristics in patients with renovascular hypertension, primary aldosteronism and essential hypertension. Am J Hypertens 1996; 9:523.
  34. Pimenta E, Gordon RD, Ahmed AH, et al. Cardiac dimensions are largely determined by dietary salt in patients with primary aldosteronism: results of a case-control study. J Clin Endocrinol Metab 2011; 96:2813.
  35. Milliez P, Girerd X, Plouin PF, et al. Evidence for an increased rate of cardiovascular events in patients with primary aldosteronism. J Am Coll Cardiol 2005; 45:1243.
  36. Catena C, Colussi G, Nadalini E, et al. Cardiovascular outcomes in patients with primary aldosteronism after treatment. Arch Intern Med 2008; 168:80.
  37. Pitt B, Zannad F, Remme WJ, et al. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators. N Engl J Med 1999; 341:709.
  38. Pitt B, Remme W, Zannad F, et al. Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction. N Engl J Med 2003; 348:1309.
  39. Williams JS, Williams GH. 50th anniversary of aldosterone. J Clin Endocrinol Metab 2003; 88:2364.
  40. Young WF Jr. Minireview: primary aldosteronism--changing concepts in diagnosis and treatment. Endocrinology 2003; 144:2208.
  41. Jaffe IZ, Mendelsohn ME. Angiotensin II and aldosterone regulate gene transcription via functional mineralocortocoid receptors in human coronary artery smooth muscle cells. Circ Res 2005; 96:643.
  42. Leopold JA, Dam A, Maron BA, et al. Aldosterone impairs vascular reactivity by decreasing glucose-6-phosphate dehydrogenase activity. Nat Med 2007; 13:189.