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

尿酸性肾病

Authors
Gary C Curhan, MD, ScD
Michael A Becker, MD
Section Editor
Stanley Goldfarb, MD
Deputy Editor
John P Forman, MD, MSc
Translators
李德天, 主任医师,教授

引言

尿酸或尿酸结晶沉积可引起三种不同的肾病:急性尿酸性肾病、慢性尿酸盐肾病、尿酸性肾结石[1]。前两种疾病将总结在此,而尿酸性肾结石将单独讨论。 (参见“尿酸性肾结石”)

尿酸是一种弱有机酸,在生物系统中有两种存在形式,根据当前的pH值以其中某一种形式存在(参见“尿酸性肾结石”):几乎不溶解的非解离性尿酸结晶,这是pH小于5.5时最具有代表性的形式;溶解度大得多的尿酸盐阴离子,这是生理性PH为7.4时最具有代表性的形式(占98%)。为了便于讨论,在本文中我们使用“尿酸”来表示几乎不溶解的非解离性尿酸结晶形态,使用“尿酸盐”来表示可溶解的解离性尿酸盐阴离子。

急性尿酸性肾病

急性尿酸性肾病(uric acid nephropathy, UAN)的特征是尿酸沉积在肾小管内引起的急性少尿或无尿性肾衰竭[1,2]。其最常见的原因是淋巴瘤、白血病或骨髓增殖性疾病(例如真性红细胞增多症)患者中尿酸生成和排泄过多,特别是在放疗或化疗引起快速细胞溶解后。 (参见“肿瘤溶解综合征:定义、发病机制、临床表现、病因及危险因素”“急性髓系白血病并发症的概述”)

更少见的UAN原因包括:癫痫发作或治疗实体肿瘤导致的组织分解代谢增加、由罕见的严重次黄嘌呤-鸟嘌呤磷酸核糖转移酶缺乏综合征(Lesch-Nyhan综合征)导致的原发性尿酸产生过多、或近曲小管对尿酸盐重吸收减少而导致的高尿酸尿症[比如在Fanconi综合征[1-4]中,或是由于遗传性尿酸盐-阴离子转运体(urate-anion transporter, URAT)1活性缺乏导致的家族性肾性低尿酸血症患者在进行运动时就可能出现这种情况]。 (参见“儿童多动性运动障碍”,关于‘Lesch-Nyhan综合征’一节“低尿酸血症:病因与临床意义”,关于‘家族性肾性低尿酸血症’一节“低尿酸血症:病因与临床意义”,关于‘急性肾损伤’一节)

临床表现 — UAN通常没有尿路相关症状,但如果发生肾盂或输尿管梗阻则可出现腰痛。如在上述任何情况下出现了急性肾损伤,同时伴有明显的高尿酸血症(血浆尿酸盐浓度一般在15mg/dL893μmol/L以上),应怀疑为急性UAN。相比之下,除了肾前性疾病中近曲小管的钠和尿酸盐重吸收增加外,其他类型的急性肾损伤血浆尿酸盐浓度通常低于12mg/dL(714μmol/L)。

    

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: 2017-05-08.
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. Rose, BD. Pathophysiology of Renal Disease, 2d ed, McGraw-Hill, New York, 1987, pp. 418-425.
  2. Kjellstrand CM, Cambell DC 2nd, von Hartitzsch B, Buselmeier TJ. Hyperuricemic acute renal failure. Arch Intern Med 1974; 133:349.
  3. Crittenden DR, Ackerman GL. Hyperuricemic acute renal failure in disseminated carcinoma. Arch Intern Med 1977; 137:97.
  4. Hricik DE, Goldsmith GH. Uric acid nephrolithiasis and acute renal failure secondary to streptozotocin nephrotoxicity. Am J Med 1988; 84:153.
  5. Kelton J, Kelley WN, Holmes EW. A rapid method for the diagnosis of acute uric acid nephropathy. Arch Intern Med 1978; 138:612.
  6. Monballyu J, Zachee P, Verberckmoes R, Boogaerts MA. Transient acute renal failure due to tumor-lysis-induced severe phosphate load in a patient with Burkitt's lymphoma. Clin Nephrol 1984; 22:47.
  7. Razis E, Arlin ZA, Ahmed T, et al. Incidence and treatment of tumor lysis syndrome in patients with acute leukemia. Acta Haematol 1994; 91:171.
  8. Coiffier B, Altman A, Pui CH, et al. Guidelines for the management of pediatric and adult tumor lysis syndrome: an evidence-based review. J Clin Oncol 2008; 26:2767.
  9. Johnson RJ, Kivlighn SD, Kim YG, et al. Reappraisal of the pathogenesis and consequences of hyperuricemia in hypertension, cardiovascular disease, and renal disease. Am J Kidney Dis 1999; 33:225.
  10. Batuman V, Maesaka JK, Haddad B, et al. The role of lead in gout nephropathy. N Engl J Med 1981; 304:520.
  11. Craswell PW, Price J, Boyle PD, et al. Chronic renal failure with gout: a marker of chronic lead poisoning. Kidney Int 1984; 26:319.
  12. TALBOTT JH, TERPLAN KL. The kidney in gout. Medicine (Baltimore) 1960; 39:405.
  13. Beck LH. Requiem for gouty nephropathy. Kidney Int 1986; 30:280.
  14. Moe OW. Posing the question again: does chronic uric acid nephropathy exist? J Am Soc Nephrol 2010; 21:395.
  15. Murray T, Goldberg M. Chronic interstitial nephritis: etiologic factors. Ann Intern Med 1975; 82:453.
  16. Sorensen LB. Role of the intestinal tract in the elimination of uric acid. Arthritis Rheum 1965; 8:694.
  17. Sorensen LF. Gout secondary to chronic renal disease: studies on urate metabolism. Ann Rheum Dis 1980; 39:424.
  18. So A, Thorens B. Uric acid transport and disease. J Clin Invest 2010; 120:1791.