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

急性肾损伤(急性肾衰竭)的肾脏替代疗法(透析)：新陈代谢及血流动力学注意事项

Author
Thomas A Golper, MD
Section Editor
Steve J Schwab, MD
Deputy Editor
Alice M Sheridan, MD
Translators
潘阳彬, 副主任医师，副教授

引言

急性肾衰竭可干扰水、电解质及有机溶质(如尿素、肌酐和尿酸)的排泄。一些简单的计算有助于我们理解这些排泄过程的受限情况及透析对这些过程的影响。正常的肾小球滤过率为170-180L/d，该值大致等于主要通过肾小球滤过而排出的溶质(如肌酐)的清除率。

大多数急性肾衰竭患者能耐受肾小球滤过率为正常值10%(17L/d或12mL/min)时的溶质潴留[1-3]。因此，这在没有分解代谢过度的患者中是一个合理的初始目标。相比之下，分解代谢过度患者则需要更积极的溶质清除技术来维持可接受或最佳的稳态或时间平均(time-averaged)溶质浓度。

本文将总结通过透析进行溶质清除的机制及发生的血流动力学变化。急性肾衰竭患者进行透析治疗的指征、应用透析的目标、有关透析是否会延缓肾功能恢复的担忧，以及不同血液透析膜的效果将单独讨论。 (参见“成人急性肾损伤的肾脏替代疗法(透析)：适应证、时机及透析剂量”和“急性肾损伤(急性肾衰竭)的肾脏替代疗法(透析)：肾功能的恢复和血液透析膜的影响”)

溶质清除的机制

透析期间溶质清除的过程可通过两种不同的机制发生：一是溶质沿浓度梯度由高到低从血浆进入透析液的被动扩散；二是血浆超滤(或对流)过程中水分穿过血液滤过器的膜。溶质和溶液之间的摩擦力(称为溶剂拖拽)可导致中、小分子量的溶质(＜5000D)沿同一方向进行对流运输。

溶质的透析清除率部分取决于其大小，较大分子(包括结合了蛋白质的分子)的清除效率较低。筛选系数(sieving coefficient, SC)是一种对超滤期间溶质滤过性的测量指标，等于滤液中溶质浓度与动脉血浆中该溶质浓度的比值[4]。筛选系数的范围是0-1，0代表溶质完全不能被滤过，1代表溶质能自由滤过(如尿素与肌酐)。超滤期间一种溶质的总清除率等于其筛选系数与液体清除率(超滤率)的乘积。对于筛选系数为1的溶质，其在滤液中的浓度大致等于其在血浆中的浓度，且该溶质的滤过清除率等于其净超滤率。关于这些概念更详细的讨论可参见其他专题。 (参见“连续性肾脏替代治疗期间的药物清除”)

     

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: 2015-06-26.
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. Ronco C, Bellomo R, Homel P, et al. Effects of different doses in continuous veno-venous haemofiltration on outcomes of acute renal failure: a prospective randomised trial. Lancet 2000; 356:26.
  2. VA/NIH Acute Renal Failure Trial Network, Palevsky PM, Zhang JH, et al. Intensity of renal support in critically ill patients with acute kidney injury. N Engl J Med 2008; 359:7.
  3. RENAL Replacement Therapy Study Investigators, Bellomo R, Cass A, et al. Intensity of continuous renal-replacement therapy in critically ill patients. N Engl J Med 2009; 361:1627.
  4. Colton CK, Henderson LW, Ford CA, Lysaght MJ. Kinetics of hemodiafiltration. I. In vitro transport characteristics of a hollow-fiber blood ultrafilter. J Lab Clin Med 1975; 85:355.
  5. Manns M, Sigler MH, Teehan BP. Continuous renal replacement therapies: an update. Am J Kidney Dis 1998; 32:185.
  6. Clark WR, Mueller BA, Alaka KJ, Macias WL. A comparison of metabolic control by continuous and intermittent therapies in acute renal failure. J Am Soc Nephrol 1994; 4:1413.
  7. Bergstrom J, Asaba H, Furst P, Oules R. Dialysis, ultrafiltration, and blood pressure. Proc Eur Dial Transplant Assoc 1976; 13:293.
  8. Rucker D, Thadhani R, Tonelli M. Trace element status in hemodialysis patients. Semin Dial 2010; 23:389.
  9. Henrich WL, Woodard TD, Blachley JD, et al. Role of osmolality in blood pressure stability after dialysis and ultrafiltration. Kidney Int 1980; 18:480.
  10. Swartz RD, Somermeyer MG, Hsu CH. Preservation of plasma volume during hemodialysis depends on dialysate osmolality. Am J Nephrol 1982; 2:189.
  11. Kimura G, Irie A, Kuroda K, et al. Absence of transcellular fluid shift during haemofiltration. Proc Eur Dial Transplant Assoc 1980; 17:192.
  12. Schuenemann B, Borghardt J, Falda Z, et al. Reactions of blood pressure and body spaces to hemofiltration treatment. Trans Am Soc Artif Intern Organs 1978; 24:687.
  13. Wehle B, Asaba H, Castenfors J, et al. Hemodynamic changes during sequential ultrafiltration and dialysis. Kidney Int 1979; 15:411.
  14. Quellhorst E, Schuenemann B, Hildebrand U, Falda Z. Response of the vascular system to different modifications of haemofiltration and haemodialysis. Proc Eur Dial Transplant Assoc 1980; 17:197.
  15. Baldamus CA, Ernst W, Frei U, Koch KM. Sympathetic and hemodynamic response to volume removal during different forms of renal replacement therapy. Nephron 1982; 31:324.
  16. Paganini EP, Fouad F, Tarazi RC, et al. Hemodynamics of isolated ultrafiltration in chronic hemodialysis patients. Trans Am Soc Artif Intern Organs 1979; 25:422.
  17. Zucchelli P, Santoro A, Sturani A, et al. Effects of hemodialysis and hemofiltration on the autonomic control of circulation. Trans Am Soc Artif Intern Organs 1984; 30:163.
  18. Chen WT, Chaignon M, Omvik P, et al. Hemodynamic studies in chronic hemodialysis patients with hemofiltration/ultrafiltration. Trans Am Soc Artif Intern Organs 1978; 24:682.
  19. Kooman JP. The role of the venous system in the regulation of hemodynamics during hemodialysis (Thesis). Universitaire Pers, Maastricht, 1992.
  20. van Kuijk WH, Hillion D, Savoiu C, Leunissen KM. Critical role of the extracorporeal blood temperature in the hemodynamic response during hemofiltration. J Am Soc Nephrol 1997; 8:949.
  21. Hoffmann JN, Hartl WH, Deppisch R, et al. Hemofiltration in human sepsis: evidence for elimination of immunomodulatory substances. Kidney Int 1995; 48:1563.
  22. Grootendorst AF, van Bommel EF, van der Hoven B, et al. High volume hemofiltration improves right ventricular function in endotoxin-induced shock in the pig. Intensive Care Med 1992; 18:235.
  23. Stein B, Pfenninger E, Grünert A, et al. Influence of continuous haemofiltration on haemodynamics and central blood volume in experimental endotoxic shock. Intensive Care Med 1990; 16:494.
  24. Stein B, Pfenninger E, Grünert A, et al. The consequences of continuous haemofiltration on lung mechanics and extravascular lung water in a porcine endotoxic shock model. Intensive Care Med 1991; 17:293.
  25. Sander A, Armbruster W, Sander B, et al. Hemofiltration increases IL-6 clearance in early systemic inflammatory response syndrome but does not alter IL-6 and TNF alpha plasma concentrations. Intensive Care Med 1997; 23:878.