- Email: [email protected]
Predictors of early mortality in acute cardiac patients requiring renal replacement therapy
Letters to the Editor [33] Finsterer J, Schoser B, Stöllberger C. Myoadenylate-deaminase gene mutation associated with left ventricular hypertrabeculation/non-compaction. Acta Cardiol 2004;59:453–6. [34] Pignatelli RH, McMahon CJ, Dreyer WJ, et al. Clinical characterization of left ventricular noncompaction in children: a relatively common form of cardiomyopathy. Circulation 2003;108:2672–8. [35] Scaglia F, Towbin JA, Craigen WJ, et al. Clinical spectrum, morbidity, and mortality in 113 pediatric patients with mitochondrial disease. Pediatrics 2004;114:925–31. [36] Davili Z, Johar S, Hughes C, Kveselis D, Hoo J. Succinate dehydrogenase deficiency associated with dilated cardiomyopathy and ventricular noncompaction. Eur J Pediatr 2007;166:867–70. [37] Ergul Y, Nisli K, Demirel A, et al. Left ventricular non-compaction in children and adolescents: clinical features, treatment and follow-up. Cardiol J 2011;18:176–84. [38] Prada CE, Jefferies JL, Grenier MA, et al. Malonyl coenzyme A decarboxylase deficiency: early dietary restriction and time course of cardiomyopathy. Pediatrics 2012;130: e456–60. [39] Ances BM, Sullivan J, Weigele JB, et al. Stroke associated with Barth syndrome. J Child Neurol 2006;21:805–7. [40] Takeda A, Sudo A, Yamada M, et al. Barth syndrome diagnosed in the subclinical stage of heart failure based on the presence of lipid storage myopathy and isolated noncompaction of the ventricular myocardium. Eur J Pediatr 2011;170:1481–4. [41] Cosson L, Toutain A, Simard G, et al. Barth syndrome in a female patient. Mol Genet Metab 2012;106:115–20. [42] Ryan TD, Ware SM, Lucky AW, Towbin JA, Jefferies JL, Hinton RB. Left ventricular noncompaction cardiomyopathy and aortopathy in a patient with recessive dystrophic epidermolysis bullosa. Circ Heart Fail 2012;5:e81–2. [43] Tanpaiboon P, Sloan JL, Callahan PF, et al. Noncompaction of the ventricular myocardium and hydrops fetalis in cobalamin C disease. JIMD Rep 2013;10:33–8. [44] Profitlich LE, Kirmse B, Wasserstein MP, Diaz GA, Srivastava S. High prevalence of structural heart disease in children with cblC-type methylmalonic aciduria and homocystinuria. Mol Genet Metab 2009;98:344–8. [45] Finsterer J, Stöllberger C, Höftberger R. Left ventricular hypertrabeculation/ noncompaction in hereditary inclusion body myopathy. Int J Cardiol 2011;150:e67–9. [46] Alter P, Rupp H. Myocardial fibrosis in left ventricular non-compaction: is late gadolinium enhancement indeed indicative of fibrosis? Eur J Heart Fail 2011;13:577–8.
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[47] Finsterer J, Stöllberger C, Kovacs GG, Sehnal E. Left ventricular hypertrabeculation/ noncompaction coincidentally found in sporadic inclusion body myositis. Int J Cardiol 2013;168:610–2. [48] Corrado G, Checcarelli N, Santarone M, Stollberger C, Finsterer J. Left ventricular hypertrabeculation/noncompaction with PMP22 duplication-based Charcot–Marie– Tooth disease type 1A. Cardiology 2006;105:142–5. [49] Piga A, Longo F, Musallam KM, et al. Left ventricular noncompaction in patients with β-thalassemia: uncovering a previously unrecognized abnormality. Am J Hematol 2012;87:1079–83. [50] Finsterer J, Stöllberger C. Poliomyelitis and left ventricular hypertrabeculation (noncompaction). Int J Cardiol 2012;158:e15–6. [51] Azevedo O, Gaspar P, Sá Miranda C, Cunha D, Medeiros R, Lourenço A. Left ventricular noncompaction in a patient with Fabry disease: overdiagnosis, morphological manifestation of Fabry disease or two unrelated rare conditions in the same patient? Cardiology 2011;119:155–9. [52] Chen H, Zhang W, Sun X, et al. Fkbp1a controls ventricular myocardium trabeculation and compaction by regulating endocardial Notch1 activity. Development 2013;140:1946–57. [53] Shou W, Aghdasi B, Armstrong DL, et al. Cardiac defects and altered ryanodine receptor function in mice lacking FKBP12. Nature 1998;391:489–92. [54] Camuglia AC, Younger JF, McGaughran J, Lo A, Atherton JJ. Cardiac myosin-binding protein C gene mutation expressed as hypertrophic cardiomyopathy and left ventricular noncompaction within two families: insights from cardiac magnetic resonance in clinical screening: Camuglia MYBPC3 gene mutation and MRI. Int J Cardiol 2013;168:2950–2. [55] Dellefave LM, Pytel P, Mewborn S, et al. Sarcomere mutations in cardiomyopathy with left ventricular hypertrabeculation. Circ Cardiovasc Genet 2009;2:442–9. [56] Finsterer J. Cardiogenetics, neurogenetics, and pathogenetics of left ventricular hypertrabeculation/noncompaction. Pediatr Cardiol 2009;30:659–81. [57] Ojala T, Polinati P, Manninen T, et al. New mutation of mitochondrial DNAJC19 causing dilated and noncompaction cardiomyopathy, anemia, ataxia, and male genital anomalies. Pediatr Res 2012;72:432–7. [58] Finsterer J, Stöllberger C, Steger C, Cozzarini W. Complete heart block associated with noncompaction, nail–patella syndrome, and mitochondrial myopathy. J Electrocardiol 2007;40:352–4.
http://dx.doi.org/10.1016/j.ijcard.2014.03.025 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.
Predictors of early mortality in acute cardiac patients requiring renal replacement therapy☆ A single center experience Chiara Lazzeri ⁎, Marco Chiostri, Maria Grazia D'Alfonso, Silvia Passantino, Carlotta Sorini Dini, Gian Franco Gensini, Serafina Valente Intensive Cardiac Coronary Unit, Heart and Vessel Department, Azienda Ospedaliero-Universitaria Careggi, Florence, Italy
a r t i c l e
i n f o
Article history: Received 5 January 2014 Accepted 9 March 2014 Available online 15 March 2014 Keywords: Acute cardiac patients Renal replacement therapy Acute kidney injury Early mortality
Acute kidney injury (AKI) frequently complicates the clinical course of critically ill patients admitted to an intensive care unit (ICU) and constitutes an independent predictor for patient survival [1–3]. Severe acute kidney injury (AKI) requiring renal replacement therapy (RRT) occurs in about 5% of the critically ill population and is, ☆ No grant, no fund. ⁎ Corresponding author at: Intensive Cardiac Care Unit, Heart and Vessel Department, Viale Morgagni 85, 50134 Florence, Italy. Tel./fax: +39 55 7947518. E-mail address: [email protected] (C. Lazzeri).
depending on the definition used, associated with a very high inhospital mortality rate [4], ranging from 38% to 80% [5,6]. The present investigation is aimed at assessing the predictors of in-Intensive Cardiac Care Unit (ICCU) mortality in 297 acute cardiac patients requiring RRT and consecutively admitted to our ICCU from January 2004 to December 2012. Data were prospectically stored and retrospectively analyzed. Patients with end-stage renal disease dependent on hemodialysis, patients with a kidney transplant and patients with another solid organ transplantation were excluded. Continuous data are reported as mean ± SD or median (interquartile range, IQR) as needed; comparisons between subgroups were performed by means of Student's t-test (parametric data) or Kruskal–Wallis H and Mann–Whitney U-test (non parametric data). Categorical data are reported as frequencies (percentages); between-group comparisons were made with chi-square test (or Fisher's exact test when appropriate). Survival analysis was aimed to identify factors linked to in-ICCU death and to investigate acute death, logistic regression analysis was performed. According to the increasing studentized residuals in survivor/not survivor comparison, diagnosis is coded as follows: 1) Monitoring; 2) non-ST elevation myocardial infarction; 3) acute heart failure; 4) valvular heart
536
Letters to the Editor Table 1 Logistic regression analysis.
Diagnosis (1 unit step) Chronic renal failure Inotropes administration More than 2 devices use Age (1 year step) LVEF at admission (1% step) TnI (10 ng/ml step)
Adjusted OR
95% CI
P value
1.22 1.29 5.32 3.60 1.03 0.97 1.01
1.07–1.39 0.72–2.30 2.17–13.05 1.86–6.95 1.00–1.05 0.95–1.00 0.99–1.02
0.003 0.385 b 0.001 b 0.001 0.029 0.018 0.194
ICCU: Intensive Cardiac Care Unit; LVEF: left ventricular ejection fraction; Tn I: troponin I.
Fig. 1.
failure; 5) sepsis; 6) ST-elevation myocardial infarction; 7) multiorgan failure. Statistical significance has been fixed at a two-tailed p value less than 5% (PASW 17.0 for Microsoft® Windows® (SPSS-IBM, USA)). Fig. 1 depicts the flow-chart of the study population which comprises 92 patients with ST elevation myocardial infarction (30.9%), 38 patients with non-ST elevation myocardial infarction (12.9%), 19 patients with multiorgan failure (6.4%), 83 patients with acute heart failure (27.8%), 22 patients with valvular heart disease (7.4%), 16 patients with post-surgical acute renal injury (5.5%) and 27 patients with sepsis (9.1%). In the overall population, coronary angiography was performed in 130 patients (43.8%). In our series 124 died (41.7%). Dead patients were older (p = 0.046) and showed lower values of admission systolic blood pressure (p b 0.001) and of left ventricular ejection fraction (p b 0.001). Intra-aortic balloon pump (p b 0.001) and mechanical ventilation (p b 0.001) were more frequently used in dead patients. Among survived patients, 161 patients (54.2%) were successfully weaned from RRT, 9 patients were submitted to urgent cardiac surgery and 3 patients showed a significant loss in renal function resulting in dialysis dependance. At logistic regression analysis (Table 1), the following variables were associated with in-ICCU mortality: inotrope administration (OR: 5.32, 95%CI 2.17–13.05, p b 0.001); more than 2 device use (OR: 3.60, 95%CI 1.86–6.95, p b 0.001); age (1 year step) (OR: 1.03, 95%CI 1.00–1.05, p = 0.029); LVEF on admission (1% step) (OR: 0.97, 95%CI 0.95–1.00, p = 0.018); diagnosis (1 unit step) (OR: 1.22, 95%CI 1.07– 1.39, p = 0.003). In our investigation, performed in 297 consecutive acute cardiac patients requiring RRT, the following factors are associated with in-ICCU mortality: age, cardiac dysfunction (as indicated by LVEF), multiorgan failure (as inferred by device use and inotropes administration) and admission diagnosis. In our series, in-ICCU mortality rate is comparable to that of previous investigations performed in critically ill patients [5–7]. Few studies [8–11] focus on prognostic factors for early mortality in AKI critically ill patients requiring RRT. The presence of multi-organ dysfunction (as indicated by the contemporary use of two or more device) is confirmed in our series as an ominous prognostic factor in AKI patients requiring RRT. Similarly Soubrier et al. [8], in an observational study including 197 patients, http://dx.doi.org/10.1016/j.ijcard.2014.03.024 0167-5273/© 2014 Published by Elsevier Ireland Ltd.
found that patients who required mechanical ventilation and inotropic support carried a poor prognosis. Schwilk et al. [10] observed that mortality rates progressively raised with increasing the number of dysfunctioning organ systems (from 12% with one organ failing system to 100% with five organ failing systems). More recently, Aldawood et al. reported that mechanical ventilation was associated with worse outcome. The novelty of our investigation, performed in a large series, is that cardiac dysfunction (as indicated by LVEF) is an independent predictor of in-ICCU mortality in AKI patients requiring RRT. AKI is known to be a causative factor for accelerated cardiovascular injury through the activation of neurohormonal, immunological, and inflammatory pathways [12]. On the other hand, when the cardiac output is reduced by 25%, the renal blood is decreased by up to 50% [13], and pressor systems like the sympathetic nervous system and the renin–angiotensin– aldosterone-system are activated leading to increased vascular resistance and subsequently reduced renal perfusion [14]. References [1] Ostermann M, Chang R. Correlation between the AKI classification and outcome. Crit Care 2008;12:R144. [2] Park WY, Hwang EA, Jang MH, et al. The risk factors and outcome of acute kidney injury in the intensive care units. Korean J Intern Med 2010;25:181–7. [3] Samimagham HR, Kheirkhah S, Haghighi A, Najmi Z. Acute kidney injury in intensive care unit: incidence, risk factors and mortality rate. Saudi J Kidney Dis Transplant 2011;22:464–70. [4] Uchino S, Kellum JA, Bellomo R, et al. Beginning and Ending Supportive Therapy for the Kidney (BEST Kidney) Investigators. Acute renal failure in critically ill patients: a multinational, multicenter study. JAMA 2005;294:813–8. [5] Brar H, Olivier J, Lebrun C, Gabbard W, Fulop T, Schmidt D. Predictors of mortality in a cohort of intensive care unit patients with acute renal failure receiving continuous renal replacement therapy. Am J Med Sci 2008;335:342–7. [6] Aldawood A. Outcome and prognostic factors of critically ill patients with acute renal failure requiring continuous renal replacement therapy. Saudi J Kidney Dis Transplant 2010;21:1106–10. [7] Fortrie G, Stads S, de Geus HR, Groeneveld AB, Zietse R, Betjes MG. Determinants of renal function at hospital discharge of patients treated with renal replacement therapy in the intensive care unit. J Crit Care Apr 2013;28(2):126–32. [8] Soubrier S, Leroy O, Devos P, et al. Epidemiology and prognostic factors of critically ill patients treated with hemodiafiltration. J Crit Care Mar 2006;21(1):66–72. [9] Sasaki S, Gando S, Kobayashi S, et al. Predictors of mortality in patients treated with continuous hemodiafiltration for acute renal failure in an intensive care setting. ASAIO J Jan-Feb 2001;47(1):86–91. [10] Schwilk B, Wiedeck H, Stein B, Reinelt H, Treiber H, Bothner U. Epidemiology of acute renal failure and outcome of haemodiafiltration in intensive care. Intensive Care Med Dec 1997;23(12):1204–11. [11] Chertow GM, Christiansen CL, Cleary PD, Munro C, Lazarus JM. Prognostic stratification in critically ill patients with acute renal failure requiring dialysis. Arch Intern Med Jul 24 1995;155(14):1505–11. [12] Ronco C, Haapio M, House AA, Anavekar N, Bellomo R. Cardiorenal syndrome. J Am Coll Cardiol 2008;52:1527–39. [13] Ljungman S, Laragh JH, Cody RJ. Role of the kidney in congestive heart failure. Relationship of cardiac index to kidney function. Drugs 1990;39(Suppl 4):10–21. [14] Waldum B, Os I. The cardiorenal syndrome: what the cardiologist needs to know. Cardiology 2013;126:175–86.
535
[47] Finsterer J, Stöllberger C, Kovacs GG, Sehnal E. Left ventricular hypertrabeculation/ noncompaction coincidentally found in sporadic inclusion body myositis. Int J Cardiol 2013;168:610–2. [48] Corrado G, Checcarelli N, Santarone M, Stollberger C, Finsterer J. Left ventricular hypertrabeculation/noncompaction with PMP22 duplication-based Charcot–Marie– Tooth disease type 1A. Cardiology 2006;105:142–5. [49] Piga A, Longo F, Musallam KM, et al. Left ventricular noncompaction in patients with β-thalassemia: uncovering a previously unrecognized abnormality. Am J Hematol 2012;87:1079–83. [50] Finsterer J, Stöllberger C. Poliomyelitis and left ventricular hypertrabeculation (noncompaction). Int J Cardiol 2012;158:e15–6. [51] Azevedo O, Gaspar P, Sá Miranda C, Cunha D, Medeiros R, Lourenço A. Left ventricular noncompaction in a patient with Fabry disease: overdiagnosis, morphological manifestation of Fabry disease or two unrelated rare conditions in the same patient? Cardiology 2011;119:155–9. [52] Chen H, Zhang W, Sun X, et al. Fkbp1a controls ventricular myocardium trabeculation and compaction by regulating endocardial Notch1 activity. Development 2013;140:1946–57. [53] Shou W, Aghdasi B, Armstrong DL, et al. Cardiac defects and altered ryanodine receptor function in mice lacking FKBP12. Nature 1998;391:489–92. [54] Camuglia AC, Younger JF, McGaughran J, Lo A, Atherton JJ. Cardiac myosin-binding protein C gene mutation expressed as hypertrophic cardiomyopathy and left ventricular noncompaction within two families: insights from cardiac magnetic resonance in clinical screening: Camuglia MYBPC3 gene mutation and MRI. Int J Cardiol 2013;168:2950–2. [55] Dellefave LM, Pytel P, Mewborn S, et al. Sarcomere mutations in cardiomyopathy with left ventricular hypertrabeculation. Circ Cardiovasc Genet 2009;2:442–9. [56] Finsterer J. Cardiogenetics, neurogenetics, and pathogenetics of left ventricular hypertrabeculation/noncompaction. Pediatr Cardiol 2009;30:659–81. [57] Ojala T, Polinati P, Manninen T, et al. New mutation of mitochondrial DNAJC19 causing dilated and noncompaction cardiomyopathy, anemia, ataxia, and male genital anomalies. Pediatr Res 2012;72:432–7. [58] Finsterer J, Stöllberger C, Steger C, Cozzarini W. Complete heart block associated with noncompaction, nail–patella syndrome, and mitochondrial myopathy. J Electrocardiol 2007;40:352–4.
http://dx.doi.org/10.1016/j.ijcard.2014.03.025 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.
Predictors of early mortality in acute cardiac patients requiring renal replacement therapy☆ A single center experience Chiara Lazzeri ⁎, Marco Chiostri, Maria Grazia D'Alfonso, Silvia Passantino, Carlotta Sorini Dini, Gian Franco Gensini, Serafina Valente Intensive Cardiac Coronary Unit, Heart and Vessel Department, Azienda Ospedaliero-Universitaria Careggi, Florence, Italy
a r t i c l e
i n f o
Article history: Received 5 January 2014 Accepted 9 March 2014 Available online 15 March 2014 Keywords: Acute cardiac patients Renal replacement therapy Acute kidney injury Early mortality
Acute kidney injury (AKI) frequently complicates the clinical course of critically ill patients admitted to an intensive care unit (ICU) and constitutes an independent predictor for patient survival [1–3]. Severe acute kidney injury (AKI) requiring renal replacement therapy (RRT) occurs in about 5% of the critically ill population and is, ☆ No grant, no fund. ⁎ Corresponding author at: Intensive Cardiac Care Unit, Heart and Vessel Department, Viale Morgagni 85, 50134 Florence, Italy. Tel./fax: +39 55 7947518. E-mail address: [email protected] (C. Lazzeri).
depending on the definition used, associated with a very high inhospital mortality rate [4], ranging from 38% to 80% [5,6]. The present investigation is aimed at assessing the predictors of in-Intensive Cardiac Care Unit (ICCU) mortality in 297 acute cardiac patients requiring RRT and consecutively admitted to our ICCU from January 2004 to December 2012. Data were prospectically stored and retrospectively analyzed. Patients with end-stage renal disease dependent on hemodialysis, patients with a kidney transplant and patients with another solid organ transplantation were excluded. Continuous data are reported as mean ± SD or median (interquartile range, IQR) as needed; comparisons between subgroups were performed by means of Student's t-test (parametric data) or Kruskal–Wallis H and Mann–Whitney U-test (non parametric data). Categorical data are reported as frequencies (percentages); between-group comparisons were made with chi-square test (or Fisher's exact test when appropriate). Survival analysis was aimed to identify factors linked to in-ICCU death and to investigate acute death, logistic regression analysis was performed. According to the increasing studentized residuals in survivor/not survivor comparison, diagnosis is coded as follows: 1) Monitoring; 2) non-ST elevation myocardial infarction; 3) acute heart failure; 4) valvular heart
536
Letters to the Editor Table 1 Logistic regression analysis.
Diagnosis (1 unit step) Chronic renal failure Inotropes administration More than 2 devices use Age (1 year step) LVEF at admission (1% step) TnI (10 ng/ml step)
Adjusted OR
95% CI
P value
1.22 1.29 5.32 3.60 1.03 0.97 1.01
1.07–1.39 0.72–2.30 2.17–13.05 1.86–6.95 1.00–1.05 0.95–1.00 0.99–1.02
0.003 0.385 b 0.001 b 0.001 0.029 0.018 0.194
ICCU: Intensive Cardiac Care Unit; LVEF: left ventricular ejection fraction; Tn I: troponin I.
Fig. 1.
failure; 5) sepsis; 6) ST-elevation myocardial infarction; 7) multiorgan failure. Statistical significance has been fixed at a two-tailed p value less than 5% (PASW 17.0 for Microsoft® Windows® (SPSS-IBM, USA)). Fig. 1 depicts the flow-chart of the study population which comprises 92 patients with ST elevation myocardial infarction (30.9%), 38 patients with non-ST elevation myocardial infarction (12.9%), 19 patients with multiorgan failure (6.4%), 83 patients with acute heart failure (27.8%), 22 patients with valvular heart disease (7.4%), 16 patients with post-surgical acute renal injury (5.5%) and 27 patients with sepsis (9.1%). In the overall population, coronary angiography was performed in 130 patients (43.8%). In our series 124 died (41.7%). Dead patients were older (p = 0.046) and showed lower values of admission systolic blood pressure (p b 0.001) and of left ventricular ejection fraction (p b 0.001). Intra-aortic balloon pump (p b 0.001) and mechanical ventilation (p b 0.001) were more frequently used in dead patients. Among survived patients, 161 patients (54.2%) were successfully weaned from RRT, 9 patients were submitted to urgent cardiac surgery and 3 patients showed a significant loss in renal function resulting in dialysis dependance. At logistic regression analysis (Table 1), the following variables were associated with in-ICCU mortality: inotrope administration (OR: 5.32, 95%CI 2.17–13.05, p b 0.001); more than 2 device use (OR: 3.60, 95%CI 1.86–6.95, p b 0.001); age (1 year step) (OR: 1.03, 95%CI 1.00–1.05, p = 0.029); LVEF on admission (1% step) (OR: 0.97, 95%CI 0.95–1.00, p = 0.018); diagnosis (1 unit step) (OR: 1.22, 95%CI 1.07– 1.39, p = 0.003). In our investigation, performed in 297 consecutive acute cardiac patients requiring RRT, the following factors are associated with in-ICCU mortality: age, cardiac dysfunction (as indicated by LVEF), multiorgan failure (as inferred by device use and inotropes administration) and admission diagnosis. In our series, in-ICCU mortality rate is comparable to that of previous investigations performed in critically ill patients [5–7]. Few studies [8–11] focus on prognostic factors for early mortality in AKI critically ill patients requiring RRT. The presence of multi-organ dysfunction (as indicated by the contemporary use of two or more device) is confirmed in our series as an ominous prognostic factor in AKI patients requiring RRT. Similarly Soubrier et al. [8], in an observational study including 197 patients, http://dx.doi.org/10.1016/j.ijcard.2014.03.024 0167-5273/© 2014 Published by Elsevier Ireland Ltd.
found that patients who required mechanical ventilation and inotropic support carried a poor prognosis. Schwilk et al. [10] observed that mortality rates progressively raised with increasing the number of dysfunctioning organ systems (from 12% with one organ failing system to 100% with five organ failing systems). More recently, Aldawood et al. reported that mechanical ventilation was associated with worse outcome. The novelty of our investigation, performed in a large series, is that cardiac dysfunction (as indicated by LVEF) is an independent predictor of in-ICCU mortality in AKI patients requiring RRT. AKI is known to be a causative factor for accelerated cardiovascular injury through the activation of neurohormonal, immunological, and inflammatory pathways [12]. On the other hand, when the cardiac output is reduced by 25%, the renal blood is decreased by up to 50% [13], and pressor systems like the sympathetic nervous system and the renin–angiotensin– aldosterone-system are activated leading to increased vascular resistance and subsequently reduced renal perfusion [14]. References [1] Ostermann M, Chang R. Correlation between the AKI classification and outcome. Crit Care 2008;12:R144. [2] Park WY, Hwang EA, Jang MH, et al. The risk factors and outcome of acute kidney injury in the intensive care units. Korean J Intern Med 2010;25:181–7. [3] Samimagham HR, Kheirkhah S, Haghighi A, Najmi Z. Acute kidney injury in intensive care unit: incidence, risk factors and mortality rate. Saudi J Kidney Dis Transplant 2011;22:464–70. [4] Uchino S, Kellum JA, Bellomo R, et al. Beginning and Ending Supportive Therapy for the Kidney (BEST Kidney) Investigators. Acute renal failure in critically ill patients: a multinational, multicenter study. JAMA 2005;294:813–8. [5] Brar H, Olivier J, Lebrun C, Gabbard W, Fulop T, Schmidt D. Predictors of mortality in a cohort of intensive care unit patients with acute renal failure receiving continuous renal replacement therapy. Am J Med Sci 2008;335:342–7. [6] Aldawood A. Outcome and prognostic factors of critically ill patients with acute renal failure requiring continuous renal replacement therapy. Saudi J Kidney Dis Transplant 2010;21:1106–10. [7] Fortrie G, Stads S, de Geus HR, Groeneveld AB, Zietse R, Betjes MG. Determinants of renal function at hospital discharge of patients treated with renal replacement therapy in the intensive care unit. J Crit Care Apr 2013;28(2):126–32. [8] Soubrier S, Leroy O, Devos P, et al. Epidemiology and prognostic factors of critically ill patients treated with hemodiafiltration. J Crit Care Mar 2006;21(1):66–72. [9] Sasaki S, Gando S, Kobayashi S, et al. Predictors of mortality in patients treated with continuous hemodiafiltration for acute renal failure in an intensive care setting. ASAIO J Jan-Feb 2001;47(1):86–91. [10] Schwilk B, Wiedeck H, Stein B, Reinelt H, Treiber H, Bothner U. Epidemiology of acute renal failure and outcome of haemodiafiltration in intensive care. Intensive Care Med Dec 1997;23(12):1204–11. [11] Chertow GM, Christiansen CL, Cleary PD, Munro C, Lazarus JM. Prognostic stratification in critically ill patients with acute renal failure requiring dialysis. Arch Intern Med Jul 24 1995;155(14):1505–11. [12] Ronco C, Haapio M, House AA, Anavekar N, Bellomo R. Cardiorenal syndrome. J Am Coll Cardiol 2008;52:1527–39. [13] Ljungman S, Laragh JH, Cody RJ. Role of the kidney in congestive heart failure. Relationship of cardiac index to kidney function. Drugs 1990;39(Suppl 4):10–21. [14] Waldum B, Os I. The cardiorenal syndrome: what the cardiologist needs to know. Cardiology 2013;126:175–86.