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

Renal replacement therapy (dialysis) in acute kidney injury: Metabolic and hemodynamic considerations

Thomas A Golper, MD
Section Editor
Steve J Schwab, MD
Deputy Editor
Alice M Sheridan, MD


Acute kidney injury interferes with the excretion of water, electrolytes, and organic solutes (such as urea, creatinine, and uric acid). A few simple calculations will permit us to understand the limits on these processes and how they may be affected by dialytic procedures. The normal glomerular filtration rate is approximately 170 to 180 L/day, which is roughly the clearance of those solutes like creatinine that are excreted primarily by glomerular filtration.

Most patients with acute kidney injury tolerate the solute retention that accompanies a glomerular filtration rate that is 10 percent of normal (17 L/day or 12 mL/min) [1-3]. This is therefore a reasonable initial target among patients who are not hypercatabolic. In comparison, hypercatabolic patients require more aggressive solute removal techniques to maintain acceptable or optimal steady-state or time-averaged concentrations of solutes.

The mechanisms of solute removal by dialysis and the hemodynamic changes that occur will be reviewed here. The indications for dialysis in patients with acute kidney injury, the goals for dialysis delivery, concerns related to whether dialysis delays the recovery of renal function, and the effects of different hemodialysis membranes are discussed separately. (See "Renal replacement therapy (dialysis) in acute kidney injury in adults: Indications, timing, and dialysis dose" and "Dialysis-related factors that may influence recovery of renal function in acute kidney injury (acute renal failure)".)


For dialysis to remove a solute, it must be present in the circulation. The process of solute removal during dialysis can occur by two different mechanisms: passive diffusion down a favorable concentration gradient from the plasma into the dialysis fluid and during the ultrafiltration (or convection) of plasma water across the membrane of the hemofilter. The frictional forces between water and solutes (called solvent drag) result in the convective transport of small- and middle-molecular-weight solutes (less than 5000 daltons) in the same direction.

The dialytic clearance of a solute is dependent in part upon size, with larger molecules (including those that are protein bound) being less efficiently removed. The sieving coefficient (SC) is a measure of a solute's filterability during ultrafiltration, being equal to the ratio of the solute concentration in the filtrate to that in the arterial plasma water [4]. The SC ranges from 0, for a solute that is completely rejected, to 1, for a solute that is freely filtered (such as urea and creatinine). The total clearance of a solute during ultrafiltration is equal to the product of the SC and the rate of fluid removal (the ultrafiltration rate). For a solute with an SC of 1, the concentration of the solute in the filtrate is roughly the same as that in the plasma water, and the solute clearance by filtration is equal to the net ultrafiltration rate. A more detailed discussion of these concepts can be found elsewhere. (See "Drug removal during continuous renal replacement therapy".)


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: Aug 2017. | This topic last updated: Aug 10, 2017.
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.
  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. Burton JO, Jefferies HJ, Selby NM, McIntyre CW. Hemodialysis-induced cardiac injury: determinants and associated outcomes. Clin J Am Soc Nephrol 2009; 4:914.
  21. 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.
  22. Hoffmann JN, Hartl WH, Deppisch R, et al. Hemofiltration in human sepsis: evidence for elimination of immunomodulatory substances. Kidney Int 1995; 48:1563.
  23. 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.
  24. 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.
  25. 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.
  26. 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.