Fisiopatología de la insuficiencia renal aguda durante la sepsis

Publicado en Med Intensiva. 2011;35:424-32. - vol.35 núm 07

Resumen

Resumen

La insuficiencia renal aguda (IRA) es un factor de riesgo independiente asociado a mayor mortalidad durante la sepsis. Definiciones de consenso recientes han permitido estandarizar los trabajos de investigación en el tema. La comprensión de la fisiopatología de la IRA durante la sepsis está limitada por la escasez de estudios histológicos y por la imposibilidad de medir los flujos microcirculatorios renales. Históricamente se ha considerado a la IRA séptica como una patología dependiente de la caída del flujo sanguíneo renal (FSR). Efectivamente, en las etapas precoces de la sepsis o en la sepsis acompañada de shock cardiogénico existe compromiso del FSR; sin embargo, estudios recientes han demostrado que en la sepsis reanimada, aquella en que característicamente se observa un gasto cardiaco normal o alto y vasodilatación sistémica, el FSR es normal o incluso aumentado y no existe evidencia histológica significativa de necrosis tubular. Otros factores, distintos al puramente hemodinámico, participan en la génesis de la IRA en la sepsis. Entre éstos están la apoptosis celular, los trastornos microcirculatorios glomerulares y medulares, los cambios celulares en respuestas a la cascada proinflamatoria propia de la sepsis, el estrés oxidativo, la disfunción mitocondrial y el daño a distancia inducido por ventilación mecánica, entre otros. En la actualidad, el tratamiento de la IRA en la sepsis es de soporte. En general, las terapias de reemplazo renal pueden ser clasificadas como intermitentes o continuas, y en las que buscan primariamente el reemplazo de la función renal deteriorada, frente a aquellas cuyo objetivo principal es lograr la estabilidad hemodinámica de los pacientes mediante la remoción de mediadores proinflamatorios.

Palabras clave Sepsis. Insuficiencia renal aguda. Flujo sanguíneo renal.

Introducción

Epidemiología La incidencia de insuficiencia renal aguda (IRA) en los pacientes críticos es variable según la definición utilizada y la población estudiada, pero oscila entre el 35 y el 50%1. La sepsis y su forma más severa, el shock séptico, son las principales causas de IRA en las unidades de cuidados intensivos (UCI), correspondiéndoles hasta el 50% de los casos2. La mortalidad de la sepsis sigue siendo alta, particularmente cuando se asocia a disfunción de órganos, como la IRA, donde alcanza valores del 20 al 35%, o en presencia de compromiso hemodinámico, con una mortalidad promedio del 60%. El desarrollo de IRA durante la sepsis es un factor de riesgo independiente asociado a mayor mortalidad2; de hecho, el estudio FRAMI, realizado en 43 UCI españolas, mostró que la aparición de IRA en paciente críticos se asocia en forma independiente a mayor mortalidad, con un OR de 2,513. Definición Hasta hace poco no existía claridad en una definición de consenso para la IRA en la sepsis. Recientemente el grupo ADQI (Acute Dialysis Quality Initiative) propuso una clasificación diagnóstica de consenso que ha sido favorablemente recibida por los clínicos y ha permitido estandarizar los trabajos de investigación en el tema4, y dicha clasificación recibe el acrónimo de RIFLE (del inglés Risk, Injury, Failure, Loss, and End-stage Kidney failure) (Tabla 1). Los pacientes se clasifican de acuerdo a la pérdida de filtración glomerular (FG) (respecto al basal de cada paciente) y/o de flujo urinario (FU) normal en cinco categorías (eligiendo el criterio que arroje la peor...

Bibliografía

1. Ostermann M, Chang RW. Acute kidney injury in the intensive care unit according to RIFLE. Crit Care Med. 2007; 35:1837-43. quiz 1852
Pubmed
2. Uchino S, Kellum JA, Bellomo R, Doig GS, Morimatsu H, Morgera S, et-al. Acute renal failure in critically ill patients: a multinational, multicenter study. JAMA. 2005; 294:813-8.
Pubmed
3. Herrera-Gutierrez ME, Seller-Perez G, Maynar-Moliner J, Sanchez-Izquierdo-Riera JA. Epidemiology of acute kidney failure in Spanish ICU. Multicenter prospective study FRAMI. Med Intensiva. 2006; 30:260-7.
Pubmed
4. Bellomo R, Ronco C, Kellum JA, Mehta Rl , Palevsky P. Acute renal failure — definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Crit Care. 2004; 8:R204-212.
Pubmed
5. Bone RC, Balk RA, Cerra FB, Dellinger RP, Fein AM, Knaus WA, et-al. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine. Chest. 1992; 101:1644-55.
Pubmed
6. Uchino S, Bellomo R, Goldsmith D, Bates S, Ronco C. An assessment of the RIFLE criteria for acute renal failure in hospitalized patients. Crit Care Med. 2006; 34:1913-7.
Pubmed
7. Mehta RL, Kellum JA, Shah SV, Molitoris BA, Ronco C, Warnock DG, et-al. Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury. Crit Care. 2007; 11:R31.
Pubmed
8. Robert AM, Kramer RS, Dacey LJ, Charlesworth DC, Leavitt BJ, Helm RE, et-al. Cardiac surgery-associated acute kidney injury: a comparison of two consensus criteria. Ann Thorac Surg. 2010; 90:1939-43.
Pubmed
9. Joannidis M, Metnitz B, Bauer P, Schusterschitz N, Moreno R, Druml W, et-al. Acute kidney injury in critically ill patients classified by AKIN versus RIFLE using the SAPS 3 database. Intensive Care Med. 2009; 35:1692-702.
Pubmed
10. Regueira T, Andresen M. Management of oxygen delivery and consumption during sepsis. Rev Med Chil. 2010; 138:233-42.
Pubmed
11. Bellomo R, Chapman M, Finfer S, Hickling K, Myburgh J. Low-dose dopamine in patients with early renal dysfunction: a placebo-controlled randomised trial. Australian and New Zealand Intensive Care Society (ANZICS) Clinical Trials Group. Lancet. 2000; 356:2139-43.
Pubmed
12. Heyman SN, Lieberthal W, Rogiers P, Bonventre JV. Animal models of acute tubular necrosis. Curr Opin Crit Care. 2002; 8:526-34.
Pubmed
13. Wan L, Bellomo R, Di Giantomasso D, Ronco C. The pathogenesis of septic acute renal failure. Curr Opin Crit Care. 2003; 9:496-502.
Pubmed
14. Kikeri D, Pennell JP, Hwang KH, Jacob AI, Richman AV, Bourgoignie JJ. Endotoxemic acute renal failure in awake rats. Am J Physiol. 1986; 250:F1098-1106.
Pubmed
15. Badr KF, Kelley VE, Rennke HG, Brenner BM. Roles for thromboxane A2 and leukotrienes in endotoxin-induced acute renal failure. Kidney Int. 1986; 30:474-80.
Pubmed
16. Zanotti-Cavazzoni Sl , Goldfarb RD. Animal models of sepsis. Crit Care Clin. 2009; 25:703-19. vii–viii
Pubmed
17. Langenberg C, Bellomo R, May C, Wan L, Egi M, Morgera S. Renal blood flow in sepsis. Crit Care. 2005; 9:R363-374.
Pubmed
18. Langenberg C, Wan L, Egi M, May CN, Bellomo R. Renal blood flow in experimental septic acute renal failure. Kidney Int. 2006; 69:1996-2002.
Pubmed
19. Ravikant T, Lucas CE. Renal blood flow distribution in septic hyperdynamic pigs. J Surg Res. 1977; 22:294-8.
Pubmed
20. Brenner M, Schaer GL, Mallory DL, Suffredini AF, Parrillo JE. Detection of renal blood flow abnormalities in septic and critically ill patients using a newly designed indwelling thermodilution renal vein catheter. Chest. 1990; 98:170-9.
Pubmed
21. Langenberg C, Bagshaw SM, May CN, Bellomo R. The histopathology of septic acute kidney injury: a systematic review. Crit Care. 2008; 12:R38.
Pubmed
22. Lerolle N, Nochy D, Guerot E, Bruneval P, Fagon JY, Diehl JL, et-al. Histopathology of septic shock induced acute kidney injury: apoptosis and leukocytic infiltration. Intensive Care Med. 2010; 36:471-8.
Pubmed
23. Doi K, Leelahavanichkul A, Yuen PS, Star RA. Animal models of sepsis and sepsis-induced kidney injury. J Clin Invest. 2009; 119:2868-78.
Pubmed
24. Fink MP, Delude RL. Epithelial barrier dysfunction: a unifying theme to explain the pathogenesis of multiple organ dysfunction at the cellular level. Crit Care Clin. 2005; 21:177-96.
Pubmed
25. Krown KA, Page MT, Nguyen C, Zechner D, Gutierrez V, Comstock KL, et-al. Tumor necrosis factor alpha-induced apoptosis in cardiac myocytes. Involvement of the sphingolipid signaling cascade in cardiac cell death. J Clin Invest. 1996; 98:2854-65.
Pubmed
26. Kaushal GP, Basnakian AG, Shah SV. Apoptotic pathways in ischemic acute renal failure. Kidney Int. 2004; 66:500-6.
Pubmed
27. Langenberg C, Wan L, Egi M, May CN, Bellomo R. Renal blood flow and function during recovery from experimental septic acute kidney injury. Intensive Care Med. 2007; 33:1614-8.
Pubmed
28. Spain DA, Wilson MA, Garrison RN. Nitric oxide synthase inhibition exacerbates sepsis-induced renal hypoperfusion. Surgery. 1994; 116:322-30. discussion 330-321
Pubmed
29. Brezis M, Rosen S. Hypoxia of the renal medulla — its implications for disease. N Engl J Med. 1995; 332:647-55.
Pubmed
30. Di Giantomasso D, Morimatsu H, May CN, Bellomo R. Intrarenal blood flow distribution in hyperdynamic septic shock: Effect of norepinephrine. Crit Care Med. 2003; 31:2509-13.
Pubmed
31. Abraham E. Neutrophils and acute lung injury. Crit Care Med. 2003; 31:S195-199.
Pubmed
32. Marshall JC, Vincent JL, Fink MP, Cook DJ, Rubenfeld G, Foster D, et-al. Measures, markers, and mediators: toward a staging system for clinical sepsis. A report of the Fifth Toronto Sepsis Roundtable, Toronto, Ontario, Canada, October 25-26, 2000. Crit Care Med. 2003; 31:1560-7.
Pubmed
33. Camussi G, Ronco C, Montrucchio G, Piccoli G. Role of soluble mediators in sepsis and renal failure. Kidney Int Suppl. 1998; 66:S38-42.
Pubmed
34. Knotek M, Rogachev B, Wang W, Ecder T, Melnikov V, Gengaro PE, et-al. Endotoxemic renal failure in mice: Role of tumor necrosis factor independent of inducible nitric oxide synthase. Kidney Int. 2001; 59:2243-9.
Pubmed
35. Cunningham PN, Dyanov HM, Park P, Wang J, Newell KA, Quigg RJ. Acute renal failure in endotoxemia is caused by TNF acting directly on TNF receptor-1 in kidney. J Immunol. 2002; 168:5817-23.
Pubmed
36. Rodriguez-Wilhelmi P, Montes R, Matsukawa A, Nariuchi H, Hurtado V, Montes M, et-al. Tumor necrosis factor-alpha inhibition reduces CXCL-8 levels but fails to prevent fibrin generation and does not improve outcome in a rabbit model of endotoxic shock. J Lab Clin Med. 2003; 141:257-64.
Pubmed
37. Thijs A, Thijs LG. Pathogenesis of renal failure in sepsis. Kidney Int Suppl. 1998; 66:S34-7.
Pubmed
38. Messmer UK, Briner VA, Pfeilschifter J. Tumor necrosis factor-alpha and lipopolysaccharide induce apoptotic cell death in bovine glomerular endothelial cells. Kidney Int. 1999; 55:2322-37.
Pubmed
39. Andresen HM, Regueira HT, Leighton F. Oxidative stress in critically ill patients. Rev Med Chil. 2006; 134:649-56.
Pubmed
40. Wang W, Jittikanont S, Falk SA, Li P, Feng L, Gengaro PE, et-al. Interaction among nitric oxide, reactive oxygen species, and antioxidants during endotoxemia-related acute renal failure. Am J Physiol Renal Physiol. 2003; 284:F532-537.
Pubmed
41. Himmelfarb J, Mcmonagle E, Freedman S, Klenzak J, Mcmenamin E, Le P, et-al. Oxidative stress is increased in critically ill patients with acute renal failure. J Am Soc Nephrol. 2004; 15:2449-56.
Pubmed
42. Nisoli E, Clementi E, Paolucci C, Cozzi V, Tonello C, Sciorati C, et-al. Mitochondrial biogenesis in mammals: the role of endogenous nitric oxide. Science. 2003; 299:896-9.
Pubmed
43. Petros A, Lamb G, Leone A, Moncada S, Bennett D, Vallance P. Effects of a nitric oxide synthase inhibitor in humans with septic shock. Cardiovasc Res. 1994; 28:34-9.
Pubmed
44. Radi R, Cassina A, Hodara R. Nitric oxide and peroxynitrite interactions with mitochondria. Biol Chem. 2002; 383:401-9.
Pubmed
45. Kantrow SP, Taylor DE, Carraway MS, Piantadosi CA. Oxidative metabolism in rat hepatocytes and mitochondria during sepsis. Arch Biochem Biophys. 1997; 345:278-88.
Pubmed
46. Unno N, Wang H, Menconi MJ, Tytgat SH, Larkin V, Smith M, et-al. Inhibition of inducible nitric oxide synthase ameliorates endotoxin-induced gut mucosal barrier dysfunction in rats. Gastroenterology. 1997; 113:1246-57.
Pubmed
47. Zingarelli B, Day BJ, Crapo JD, Salzman AL, Szabo C. The potential role of peroxynitrite in the vascular contractile and cellular energetic failure in endotoxic shock. Br J Pharmacol. 1997; 120:259-67.
Pubmed
48. Brealey D, Karyampudi S, Jacques TS, Novelli M, Stidwill R, Taylor V, et-al. Mitochondrial dysfunction in a long-term rodent model of sepsis and organ failure. Am J Physiol Regul Integr Comp Physiol. 2004; 286:R491-497.
Pubmed
49. Radi R, Rodriguez M, Castro L, Telleri R. Inhibition of mitochondrial electron transport by peroxynitrite. Arch Biochem Biophys. 1994; 308:89-95.
Pubmed
50. Murray AJ, Anderson RE, Watson GC, Radda GK, Clarke K. Uncoupling proteins in human heart. Lancet. 2004; 364:1786-8.
Pubmed
51. Brealey D, Brand M, Hargreaves I, Heales S, Land J, Smolenski R, et-al. Association between mitochondrial dysfunction and severity and outcome of septic shock. Lancet. 2002; 360:219-23.
Pubmed
52. Goode HF, Cowley HC, Walker BE, Howdle PC, Webster NR. Decreased antioxidant status and increased lipid peroxidation in patients with septic shock and secondary organ dysfunction. Crit Care Med. 1995; 23:646-51.
Pubmed
53. Takeda K, Shimada Y, Amano M, Sakai T, Okada T, Yoshiya I. Plasma lipid peroxides and alpha-tocopherol in critically ill patients. Crit Care Med. 1984; 12:957-9.
Pubmed
54. Andresen M, Regueira T, Bruhn A, Perez D, Strobel P, Dougnac A, et-al. Lipoperoxidation and protein oxidative damage exhibit different kinetics during septic shock. Mediators Inflamm. 2008; 168652.
55. Deneke SM, Lynch BA, Fanburg BL. Effects of low protein diets or feed restriction on rat lung glutathione and oxygen toxicity. J Nutr. 1985; 115:726-32.
Pubmed
56. Messmer UK, Briner VA, Pfeilschifter J. Basic fibroblast growth factor selectively enhances TNF-alpha-induced apoptotic cell death in glomerular endothelial cells: effects on apoptotic signaling pathways. J Am Soc Nephrol. 2000; 11:2199-211.
Pubmed
57. Elbers PW, Ince C. Mechanisms of critical illness — classifying microcirculatory flow abnormalities in distributive shock. Crit Care. 2006; 10:221.
Pubmed
58. Regueira T, Andresen M, Djafarzadeh S. Mitochondrial dysfunction during sepsis, impact and possible regulating role of hypoxia-inducible factor-1alpha. Med Intensiva. 2009; 33:385-92.
Pubmed
59. Szabo C. Poly (ADP-ribose) polymerase activation and circulatory shock. Novartis Found Symp. 2007; 280:92-103. discussion 103-107, 160-104
Pubmed
60. Goldfarb RD, Marton A, Szabo E, Virag L, Salzman AL, Glock D, et-al. Protective effect of a novel, potent inhibitor of poly(adenosine 5’-diphosphate-ribose) synthetase in a porcine model of severe bacterial sepsis. Crit Care Med. 2002; 30:974-80.
Pubmed
61. Larche J, Lancel S, Hassoun SM, Favory R, Decoster B, Marchetti P, et-al. Inhibition of mitochondrial permeability transition prevents sepsis-induced myocardial dysfunction and mortality. J Am Coll Cardiol. 2006; 48:377-85.
Pubmed
62. Regueira T, Lepper PM, Brandt S, Ochs M, Vuda M, Takala J, et-al. Hypoxia inducible factor-1 alpha induction by tumour necrosis factor-alpha, but not by toll-like receptor agonists, modulates cellular respiration in cultured human hepatocytes. Liver Int. 2009; 29:1582-92.
Pubmed
63. Vary TC. Increased pyruvate dehydrogenase kinase activity in response to sepsis. Am J Physiol. 1991; 260:E669-74.
Pubmed
64. Vary TC, Siegel JH, Nakatani T, Sato T, Aoyama H. Effect of sepsis on activity of pyruvate dehydrogenase complex in skeletal muscle and liver. Am J Physiol. 1986; 250:E634-640.
Pubmed
65. Crouser ED, Julian MW, Huff JE, Struck J, Cook CH. Carbamoyl phosphate synthase-1: a marker of mitochondrial damage and depletion in the liver during sepsis. Crit Care Med. 2006; 34:2439-46.
Pubmed
66. Fredriksson K, Hammarqvist F, Strigard K, Hultenby K, Ljungqvist O, Wernerman J, et-al. Derangements in mitochondrial metabolism in intercostal and leg muscle of critically ill patients with sepsis-induced multiple organ failure. Am J Physiol Endocrinol Metab. 2006; 291:E1044-1050.
Pubmed
67. Porta F, Takala J, Weikert C, Bracht H, Kolarova A, Lauterburg BH, et-al. Effects of prolonged endotoxemia on liver, skeletal muscle and kidney mitochondrial function. Crit Care. 2006; 10:R118.
Pubmed
68. Kozlov AV, Van Griensven M, Haindl S, Kehrer I, Duvigneau JC, Hartl RT, et-al. Peritoneal inflammation in pigs is associated with early mitochondrial dysfunction in liver and kidney. Inflammation. 2010; 33:295-305.
Pubmed
69. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. N Engl J Med. 2000;342:1301–8.
70. Imai Y, Parodo J, Kajikawa O, De Perrot M, Fischer S, Edwards V, et-al. Injurious mechanical ventilation and end-organ epithelial cell apoptosis and organ dysfunction in an experimental model of acute respiratory distress syndrome. JAMA. 2003; 289:2104-12.
Pubmed
71. Mishra J, Ma Q, Prada A, Mitsnefes M, Zahedi K, Yang J, et-al. Identification of neutrophil gelatinase-associated lipocalin as a novel early urinary biomarker for ischemic renal injury. J Am Soc Nephrol. 2003; 14:2534-43.
Pubmed
72. Mishra J, Mori K, Ma Q, Kelly C, Barasch J, Devarajan P. Neutrophil gelatinase-associated lipocalin: a novel early urinary biomarker for cisplatin nephrotoxicity. Am J Nephrol. 2004; 24:307-15.
Pubmed
73. Haase M, Haase-Fielitz A, Bellomo R, Mertens PR. Neutrophil gelatinase-associated lipocalin as a marker of acute renal disease. Curr Opin Hematol. 2011. [Published ahead of print]
74. Martensson J, Bell M, Oldner A, Xu S, Venge P, Martling CR. Neutrophil gelatinase-associated lipocalin in adult septic patients with and without acute kidney injury. Intensive Care Med. 2010; 36:1333-40.
Pubmed
75. Cruz DN, De Cal M, Garzotto F, Perazella MA, Lentini P, Corradi V, et-al. Plasma neutrophil gelatinase-associated lipocalin is an early biomarker for acute kidney injury in an adult ICU population. Intensive Care Med. 2010; 36:444-51.
Pubmed
76. Siew ED, Ware LB, Gebretsadik T, Shintani A, Moons KG, Wickersham N, et-al. Urine neutrophil gelatinase-associated lipocalin moderately predicts acute kidney injury in critically ill adults. J Am Soc Nephrol. 2009; 20:1823-32.
Pubmed
77. Melnikov VY, Faubel S, Siegmund B, Lucia MS, Ljubanovic D, Edelstein CL. Neutrophil-independent mechanisms of caspase-1- and IL-18-mediated ischemic acute tubular necrosis in mice. J Clin Invest. 2002; 110:1083-91.
Pubmed
78. Parikh CR, Mishra J, Thiessen-Philbrook H, Dursun B, Ma Q, Kelly C, et-al. Urinary IL-18 is an early predictive biomarker of acute kidney injury after cardiac surgery. Kidney Int. 2006; 70:199-203.
Pubmed
79. Parikh CR, Abraham E, Ancukiewicz M, Edelstein CL. Urine IL-18 is an early diagnostic marker for acute kidney injury and predicts mortality in the intensive care unit. J Am Soc Nephrol. 2005; 16:3046-52.
Pubmed
80. Liangos O, Perianayagam MC, Vaidya VS, Han WK, Wald R, Tighiouart H, et-al. Urinary N-acetyl-beta-(D)-glucosaminidase activity and kidney injury molecule-1 level are associated with adverse outcomes in acute renal failure. J Am Soc Nephrol. 2007; 18:904-12.
Pubmed
81. Mehta Rl , Mcdonald B, Gabbai FB, Pahl M, Pascual MT, Farkas A, et-al. A randomized clinical trial of continuous versus intermittent dialysis for acute renal failure. Kidney Int. 2001; 60:1154-63.
Pubmed
82. Lins RL, Elseviers MM, Van der Niepen P, Hoste E, Malbrain ML, Damas P, et-al. Intermittent versus continuous renal replacement therapy for acute kidney injury patients admitted to the intensive care unit: results of a randomized clinical trial. Nephrol Dial Transplant. 2009; 24:512-8.
Pubmed
83. Augustine JJ, Sandy D, Seifert TH, Paganini EP. A randomized controlled trial comparing intermittent with continuous dialysis in patients with ARF. Am J Kidney Dis. 2004; 44:1000-7.
Pubmed
84. Bagshaw SM, Berthiaume LR, Delaney A, Bellomo R. Continuous versus intermittent renal replacement therapy for critically ill patients with acute kidney injury: a meta-analysis. Crit Care Med. 2008; 36:610-7.
Pubmed
85. Pannu N, Klarenbach S, Wiebe N, Manns B, Tonelli M. Renal replacement therapy in patients with acute renal failure: a systematic review. JAMA. 2008; 299:793-805.
Pubmed
86. Tetta C, Bellomo R, Ronco C. Artificial organ treatment for multiple organ failure, acute renal failure, and sepsis: recent new trends. Artif Organs. 2003; 27:202-13.
Pubmed
87. Honore PM, Matson JR. Extracorporeal removal for sepsis: Acting at the tissue level — the beginning of a new era for this treatment modality in septic shock. Crit Care Med. 2004; 32:896-7.
Pubmed
88. Di Carlo JV, Alexander SR. Hemofiltration for cytokine-driven illnesses: the mediator delivery hypothesis. Int J Artif Organs. 2005; 28:777-86.
Pubmed
89. Honore PM, Joannes-Boyau O. High volume hemofiltration (HVHF) in sepsis: a comprehensive review of rationale, clinical applicability, potential indications and recommendations for future research. Int J Artif Organs. 2004; 27:1077-82.
Pubmed
90. Cole L, Bellomo R, Journois D, Davenport P, Baldwin I, Tipping P. High-volume haemofiltration in human septic shock. Intensive Care Med. 2001; 27:978-86.
Pubmed
91. Romero CM, Downey P, Hernandez G. High volume hemofiltration in septic shock. Med Intensiva. 2010; 34:345-52.
Pubmed
92. Cornejo R, Downey P, Castro R, Romero C, Regueira T, Vega J, et-al. High-volume hemofiltration as salvage therapy in severe hyperdynamic septic shock. Intensive Care Med. 2006; 32:713-22.
Pubmed
93. Boussekey N, Chiche A, Faure K, Devos P, Guery B, D’Escrivan T, et-al. A pilot randomized study comparing high and low volume hemofiltration on vasopressor use in septic shock. Intensive Care Med. 2008; 34:1646-53.
Pubmed
94. Ruiz C, Hernandez G, Godoy C, Downey P, Andresen M, Bruhn A. Sublingual microcirculatory changes during high-volume hemofiltration in hyperdynamic septic shock patients. Crit Care. 2010;14:R170.
95. Rabindranath K, Adams J, Macleod AM, Muirhead N. Intermittent versus continuous renal replacement therapy for acute renal failure in adults. Cochrane Database Syst Rev. 2007;CD003773.
96. Vinsonneau C, Camus C, Combes A, Costa de Beauregard MA, Klouche K, Boulain T, et-al. Continuous venovenous haemodiafiltration versus intermittent haemodialysis for acute renal failure in patients with multiple-organ dysfunction syndrome: A multicentre randomised trial. Lancet. 2006; 368:379-85.
Pubmed
97. Baeza-Roman A, Latour-Perez J, Gomez-Tello V, Garcia-Garcia MA. Hemofiltration in sepsis: what is the evidence?. Med Intensiva. 2010; 34:571-2. author reply 572–3
Pubmed
98. Phu NH, Hien TT, Mai NT, Chau TT, Chuong LV, Loc PP, et-al. Hemofiltration and peritoneal dialysis in infection-associated acute renal failure in Vietnam. N Engl J Med. 2002; 347:895-902.
Pubmed

Regueira, T.a; Andresen, M.a; Mercado, M.a; Downey, P.b

aDepartamento de Medicina Intensiva, Hospital Clínico Universidad Católica de Chile, Pontificia Universidad Católica de Chile, Santiago, Chile

bDepartamento de Nefrología, Hospital Clínico Universidad Católica de Chile, Pontificia Universidad Católica de Chile, Santiago, Chile