When to initiate RRT in patients with AKI - Does timing matter?
 

When to initiate RRT in patients with AKI - Does timing matter?

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    When to initiate RRT in patients with AKI - Does timing matter? When to initiate RRT in patients with AKI - Does timing matter? Document Transcript

    • When to initiate RRT in patients with AKI - Does timing matter?
    • Review Article When to initiate RRT in patients with AKI e Does timing matter? Saumya Gupta* Consultant Nephrologist, Apollo Gleneagles Hospital Limited, 58 Canal Circular Road, Kolkata, India a r t i c l e i n f o Article history: Received 5 December 2012 Accepted 31 January 2013 Available online 9 February 2013 Keywords: Acute kidney injury Renal replacement therapy Timing a b s t r a c t Acute kidney injury is a serious illness which occurs commonly in the renal units and also in the ICU setting. It is an independent risk factor of increased mortality and morbidity, particularly when RRT is needed. The wide variation in utilization of RRT contributes to a lack of consensus among clinicians regarding the parameters which should guide the decision to initiate RRT. This problem is confounded by a paucity of high quality evidence in the current literature. This review examines the role of usual biochemical parameters as well as conventional clinical indications for commencing RRT. It also discusses the po- tential role of biomarkers as predictors for the need of RRT in AKI. Initiating dialysis in AKI should be based on dynamic clinical criteria and not only on specific biochemical values. Copyright ª 2013, Indraprastha Medical Corporation Ltd. All rights reserved. 1. Introduction Acute kidney injury (AKI) is a serious complication of critical illness that is associated with substantial morbidity and mortality. Renal replacement therapy (RRT) has long been used as supportive treatment of AKI, and has traditionally focused on averting the life threatening derangements asso- ciated with kidney failure (i.e. metabolic acidosis, hyper- kalemia, uraemia, and/or fluid overload) while allowing time for organ recovery. In patients with AKI, RRT is regarded as a type of organ support aimed at achieving metabolic ho- meostasis and preventing fluid overload and new organ fail- ure. The benefits of RRT must be balanced by potential harm, including risks related to vascular access, infections and anticoagulation.1 Whether or not to provide RRT, and when to start, are two of the fundamental questions facing nephrologists and intensive-care practitioners in most cases of severe AKI. In recent publications, the timing of initiation of RRT was listed as one of the top priorities in research on AKI.2 However, this dimension has not been included as a factor in any of the large RCTs in this area. In current practice, the decision to start RRT is based most often on clinical features of volume overload and biochemical features of solute imbalance. In a recently published survey of nephrologists and intensivists in Canada, serum potassium level and severity of pulmonary oedema were the most commonly utilized factors for decid- ing when RRT should be started.3 However, in the absence of these factors there is generally a tendency to avoid dialysis as long as possible, a thought process that reflects the decisions made for patients with CKD Stage 5.4 Clinicians tend to delay RRT when they suspect that patients may recover on their own, and because of concern for the well-known risks asso- ciated with the RRT procedure. There is also some concern that RRT may compromise recovery of renal function, and increase the progression of CKD.5 Whether these risks out- weigh the potential benefits of earlier initiation of RRT is still unclear. * Flat No. 3G, Orbit Heights, 33 Gariahat Road South, Kolkata 700031, West Bengal, India. Tel.: þ91 9163262325. E-mail address: sgupta36@hotmail.com. Available online at www.sciencedirect.com journal homepage: www.elsevier.com/locate/apme a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 4 1 e4 6 0976-0016/$ e see front matter Copyright ª 2013, Indraprastha Medical Corporation Ltd. All rights reserved. http://dx.doi.org/10.1016/j.apme.2013.01.016
    • In ICU patients, AKI is often observed at an early stage before traditional measures of renal function are deranged. Many specialists regard AKI as a systemic disease, rather than a single organ failure in isolation characterised by a systemic inflammatory response with distant organ injury.6 The cause of the acute kidney injury (AKI) requiring RRT is also relevant. Without an underlying cause, clinicians do not have much information other than an observed disturbance in conven- tionally measured biochemical parameters of kidney function combined with oliguria or anuria. The outcome from AKI in a young patient secondary to a crush syndrome is very dif- ferent from that of an elderly diabetic developing AKI fol- lowing systemic infection from an ischaemic limb. It may be that the aetiology of the underlying condition is also of great importance with regard to timing of treatment. This high- lights the differences between ‘single organ AKI’ and ‘multi- organ AKI’ in that timing of RRT on a renal unit may differ significantly from ICU patients in terms of both dose delivered and duration of treatment.7 The timing of initiation of RRT remains a topic of discus- sion for some years in both groups of patients suffering from chronic kidney disease8 and AKI9 respectively. A recently published systematic review and meta-analysis concluded that earlier initiation of RRT in critically ill AKI patients may have a beneficial effect on survival but that, in the absence of new evidence from suitably designed randomized trials, a definitive treatment recommendation cannot be made.9 2. Where do we stand now regarding current evidence? Studies looking at the timing of initiation of RRT need to address the criteria used for commencing therapy; but this is hampered by the lack of any universally accepted criteria for initiation. They have evaluated various arbitrary cut-offs for serum creatinine, serum urea or urine output, fluid balance, time from admission or duration of AKI and often differ- entiated between ‘early’ and ‘late’ RRT (Table 1).10e26 In the current literature, there are 2 RCTs,17,19 2 prospective cohort studies,10,14 13 retrospective cohort studies11e13,15,16,18,20e26 and 3 meta-analyses/systematic re- views.9,27,28 Significant heterogeneity still remains regarding the potential parameters which are monitored by clinicians to decide that the time has come to commence RRT. Most clinical trials used serum creatinine, serum urea and/or urine output to define timing of RRT but the exact cut-offs were variable between studies. 2.1. Serum creatinine Five studies contained data on the role of serum creatinine as a trigger for RRT (Table 1).10,11,22e24 The results are conflicting. Shiao et al11 retrospectively analysed the data of 98 patients with AKI post-abdominal surgery and showed that patients who were started on CVVH at RIFLE stage Risk (i.e. after rise in serum creatinine by 150e200%) had a significantly lower hospital mortality than patients who started RRT with either RIFLE-Injury or RIFLE-Failure (i.e. after serum creatinine rise by >200%). In contrast, Chou et al12 showed no difference in hospital mortality in 370 AKI patients between the group who started RRT with RIFLE-Risk or even before they fulfilled the RIFLE criteria and patients in whom AKI had progressed to RIFLE-Injury or RIFLE-Failure when RRT was started. Two larger studies concluded that mortality was significantly higher in patients who had a serum creatinine < 309 mmol/L when RRT was started compared to those with higher crea- tinine values.10,23 2.2. Serum urea Different levels of serum urea were used as triggers for RRT in eight studies.10,13e17,23,26 Liu et al14 reported a significantly lower mortality in 122 patients who had a serum ure- a < 27.1 mmol/L at the time of initiation of RRT compared to 121 patients with a higher value. When adjusted for age, he- patic failure, sepsis, thrombocytopaenia and serum crea- tinine, the relative risk of death with a higher urea level at the time of RRT was 1.85 [95% confidence interval (CI) 1.2e3.2]. Improved mortality was also reported in retrospective studies when RRT was instituted at a serum urea < 21 mmol/L,26 <29 mmol/L13 or <35.7 mmol/L,15 suggesting that RRT at lower serum urea levels is better than late RRT. In contrast, two larger studies did not find a correlation between serum urea at the time of RRT and outcome.10,23 2.3. Urine output Data on the role of specific urine volumes as triggers for RRT were included in eight studies12,16e19,23e25 often com- bined with serum urea or creatinine criteria. The majority of studies showed better outcomes; when oliguria was used as the trigger for RRT instead of serum creatinine or urea values.12,16,18,24,25 However, the definitions for oliguria varied from urine output < 100 ml/h in 8 h16,24 to <400 ml/24 h23 and <30 ml/h for 6 h.17 2.4. Fluid overload There is increasing evidence that fluid overload in patients with AKI is associated with poor outcome.21,29 Bouchard et al29 showed that ICU mortality was significantly higher in patients whose body weight on the first day of RRT was 1e20% above that on ICU admission compared to patients without weight gain during this period. There was a direct correlation be- tween the degree of fluid gain and ICU mortality. Similar re- sults were reported by Payen et al21 who performed a subgroup analysis of the multicentre ‘Sepsis Occurrence in Acutely Ill Patients (SOAP) study’. Two hundred and thirteen patients were treated with RRT within 2 days of ICU admission compared to 65 patients who had RRT after 2 days in ICU. Although patients in the early RRT group had higher severity of illness scores, their ICU and 60-day mortality was lower. A potential explanation for this difference was the higher cu- mulative fluid balance and greater need for mechanical ven- tilation in the late RRT group. Consequently, it may be appropriate to consider starting RRT in patients with AKI prior to fluid accumulation of 10% of body weight.30 a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 4 1 e4 642
    • Table 1 e Parameters at the time of RRT and subsequent outcome. Study RRT mode Patient population Parameters at the time of RRT Outcome (early vs late RRT) Early Late Bagshaw et al10 prospective study CRRT; IHD 1238 mixed ICU patients Serum Cr  3.5 mg/dl serum urea  136 mg/dl Serum Cr > 3.5 mg/dl serum urea > 136 mg/dl Hospital mortality 71 vs 53.4% P < 0.0001 P ¼ 0.48 Shiao et al11 retrospective study CVVH; IH 98 patients post-abdominal surgery AKI as per RIFLE classification; no AKI or RIFLE-Risk AKI as per RIFLE classification RIFLE Injury or Failure Hospital mortality 43 vs 75% P ¼ 0.002 Chou et al12 retrospective CVVH; SLED; SLED-f; IHD 370 patients with AKI and sepsis RIFLE-0 or RIFLE-Risk RIFLE-Injury or RIFLE-Failure Hospital mortality 70.8 vs 69.7% P > 0.05 Wu et al13 retrospective study CRRT; IHD 80 patients with AKI and acute liver failure Serum urea < 160 mg/dl Serum urea > 160 mg/dl ICU mortality 57 vs 85% P ¼ 0.02 Liu et al14 prospective study CRRT; IHD 243 mixed ICU patients Serum urea < 152 mg/dl Serum urea  152 mg/dl Hospital mortality RR 1.85 with higher urea (95% CI 1.2 e3.2) Carl et al15 retrospective study CRRT 147 patients with AKI and sepsis Serum urea < 200 mg/dl Serum urea > 200 mg/dl 28 day mortality 52.3 vs 68% P < 0.05 Elahi et al16 retrospective study CRRT 64 patients post-cardiac surgery Urine output < 100 ml in 8 h Serum urea > 168 mg/dl serum Cr  2.82 mg/dl or K > 6 mmol/ L Hospital mortality 22 vs 43% P < 0.05 Bouman et al17 RCT CRRT 106 patients with AKI circulatory and respiratory failure Urine output 30 ml/h for 6 h and Cr Cl 20 ml/min Serum urea > 224 mg/dl or K > 6.5 mmol/L or severe pulmonary oedema 28 day mortality 29 vs 25% P ¼ 0.08 Manche et al18 retrospective study IHD 71 patients with AKI post- cardiac surgery Urine output < 0.5 ml/kg despite fluid challenge and single dose of diuretic AKI which failed to respond to all supportive medical measures ICU mortality 25 vs 87% P ¼ 0.00001 Sugahara et al19 RCT CRRT 28 patients post-cardiac surgery Urine output < 30 ml/h for 3 h Urine output < 20 ml/h for 2 h 14 day mortality 14 vs 86% P < 0.01 Piccinni et al20 retrospective study CRRT 80 patients with AKI, ALI and septic shock Within 12 h of admission to ICU ‘Classic’ indications for RRT ICU mortality 30 vs 60% P ¼ 0.003 28 day mortality 72.5 vs 45%, P ¼ 0.005 Payen et al21 retrospective study RRT 278 patients with sepsis and AKI Period from admission to ICU to RRT < 2 days Period from admission to ICU to RRT  2 days 60 day mortality 44.8 vs 64.6% P < 0.01 Ji et al22 retrospective study CVVHD 58 patients with AKI post- cardiac surgery Urine output < 0.5 ml/kg/h for <12 h Urine output < 0.5 ml/kg/h for >12 h Hospital mortality 8.8 vs 37.5% P ¼ 0.02 Ostermann et al23 retrospective study CRRT; IHD 1847 mixed ICU patients Serum Cr  3.5 mg/dl serum pH  7.2 Serum Cr >3.5 mg/dl serum pH < 7.2 ICU mortality 59 vs 48% P < 0.0001 74 vs 48% P < 0.0001 Demirkilic et al24 retrospective study CRRT 61 patients with AKI post- cardiac surgery Urine output < 100 ml within 8 h post surgery Serum Cr > 5.0 mg/dl or K > 5.5 ICU mortality 18 vs 48% P ¼ 0.014 hospital mortality 23.5 vs 56% P ¼ 0.016 Iyem et al25 retrospective study CVVH 185 patients with AKI post- cardiac surgery Urine output  0.5 ml/kg/h and a 50% increase in pre op urea and creatinine 48 h after urine output  0.5 ml/kg/hr and a 50% increase in pre op urea and creatinine Hospital mortality 5.2 vs 6.6% P > 0.05 Gettings et al26 retrospective study CRRT 100 trauma patients Serum urea < 120 mg/dl Serum urea  120 mg/dl Hospital mortality 61 vs 80% P ¼ 0.041 CRRT, continuous renal replacement therapy; IHD, intermittent haemodialysis; RR, relative risk; ALI, acute lung injury; RIFLE, Risk Injury Failure Loss of renal function End stage renal disease; SLED, slow extended dialysis; SLEDf, slow extended dialysis with haemofiltration; CVVHD, continuous veno-venous haemodialysis. apollomedicine10(2013)41e4643
    • 2.5. Hyperkalemia Untreated hyperkalemia is universally fatal. 1 RCT17 and 2 ret- rospective studies16,24 have used serum potassium as a marker regarding the timing to initiate RRT. It is interesting to note that the cut-off in each of these studies were different, namely >6.5 mmol/L,17 >6 mmol/L16 and >5.5 mmol/L24 respectively. 2.6. Metabolic acidosis A retrospective study conducted by Ostermann et al23 found that ICU mortality was significantly high (48% vs 74%, P < 0.0001) in the late group as defined by serum pH < 7.2. 2.7. Non-renal factors A large retrospective analysis of 1847 ICU patients treated with RRT for AKI highlighted that the most important independent risk factors for ICU mortality were need for mechanical ven- tilation, associated organ failure, pre-existing chronic health problems, acidosis, oliguria and age.23 Patients who were oli- guric (urine output <400 ml/24 h) and acidotic with serum pH < 7.2 at the time of RRT had an ICU mortality of 79.1%. Serum urea and creatinine were not found to be independ- ently associated with outcome. The results of this study sug- gest that the decision to start RRT should depend less on specific serum creatinine or urea values but more on degree of acidosis, urine output and associated organ failure. 3. Discussion The idea that earlier initiation of treatment should be bene- ficial stems from our belief that sometimes complex in- terventions may change the course of a serious disease process. Recently published KDIGO guidelines regarding this question mention to initiate RRT emergently when life threatening changes in fluid, electrolyte and acid-base bal- ance exist. It also mentions that consideration needs to be given to the broader clinical context, modifiable conditions with relation to RRT and trends of biochemical parameters rather than their thresholds alone.4 In the common clinical scenario of AKI and sepsis, many clinicians believe that initiating RRT early in sepsis can remove circulating levels of inflammatory cytotoxins and may there- fore have a beneficial effect on the pathophysiologic mecha- nisms. Unfortunately, the validity of this hypothesis has never been proven, and existing evidence rather points to the con- trary.31 In patients with septic AKI, RRT should not be seen as a curative therapy, but rather as a supportive intervention, preventing the patient from dying due to hyperkalemia or fluid overload during the time period when AKI was present. Whatever criteria are used to define ‘early’ vs ‘late’ RRT, it is clear that what may be ‘early’ for one patient could be ‘late’ for another patient depending on the patient’s comorbidity and clinical course.30 Since the course of patients with AKI can be very variable, it is essential that clinicians assess these patients regularly to ensure that RRT is started at the ‘right’ time. As mentioned before, there are only 2 RCT’s17,19 in the literature, which have tried to address this issue. Bouman et al17 randomized 106 severely ill patients into three groups; 35 patients were treated with early high volume hemofiltra- tion, 35 patients with early low volume hemofiltration and 36 patients with late low volume hemofiltration. Median ultra- filtrate rate was 48.2 ml/kg/h, 20.1 ml/kg/h and 19 ml/kg/h respectively in the 3 groups. There was no statistically sig- nificant difference in survival rates among the 3 groups (P ¼ 0.8). Median duration of renal failure in hospital survivors also did not reach statistical significance (P ¼ 0.25) in the 3 groups. Another RCT by Sugahara et al19 conducted in 28 post- cardiac surgery patients showed significant improvement in 14 day mortality (P < 0.01) in the early group. Three meta-analyses9,27,28 concluded that earlier initiation of RRT in critically ill AKI patients might be associated with a survival benefit though the studies were heterogenous, of variable quality with a paucity of RCTs. Of studies reporting secondary outcomes in the meta-analysis by Karvellas et al,9 majority reported greater renal recovery, decreased duration of RRT and decreased ICU length of stay in the early RRT group. Currentlythere islittledata to accurately distinguish inadvance between the injured kidney that will need dialytic support and theonethatwill recoverspontaneously.Studies inthe literature most commonly used serum creatinine, serum urea and urine output as the parameters to trigger RRT with varying cut-off values. However, their value is limited due to the fact that they are not always renal specific. In the early stages of AKI, GFR can decrease significantly without any major shift in serum creatinine measurements.32 Serum urea concentrations may also vary as a result of changes in urea production and tubular reabsorption without changes in GFR.33 The usefulness of urine criteria for the definition of AKI has also been discussed widely.34 Proponents argue that a fall in urine output often precedes renal dysfunction in patients before changes in serum creatinine. In contrast, critics argue that urine output is affected by volume status, intrinsic levels of anti-diuretic hormone, presence of obstruction and use of diuretics. Despite this, there is increasing evidence that urine output of <500e600 ml/24 h should be viewed as an ominous sign and trigger an evaluation of the indications for RRT. Furthermore, oliguria is closely cor- related with fluid accumulation. Recent data suggest that fluid overload of >10% of body weight is an independent risk factor for mortality in AKI.29 Consequently, it may be appropriate to consider starting RRT prior to fluid accumulation reaching a threshold of 10% of body weight. The current literature shows that individual stages of AKI are not adequate in identifying the optimal time for RRT either. The RIFLE and AKIN classifications are scoring systems which were developed to grade prognosis of AKI.35,36 Although they correlate with mortality, they were never intended to predict the need for RRT. Two retrospective studies11,12 con- ducted amongst patients after abdominal surgery and pa- tients with AKI and sepsis in a surgical ICU utilized the RIFLE criteria while separating the groups who underwent ‘early’ or ‘late’ RRT. Unfortunately they showed conflicting results. Shiao et al11 showed that the hospital mortality was sig- nificantly lower (43% vs 75%, P ¼ 0.002) in the group who commenced RRT ‘early’ when in the RIFLE-Risk stage. The other study by Chou et al12 showed that there was no signifi- cant difference in the hospital mortality (70.8% vs 69.7%, P > 0.05) between the ‘early’ and ‘late’ groups. a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 4 1 e4 644
    • The recent literature has seen an expansion in studies examining potential ‘biomarkers’ for the early detection of AKI. Candidate molecules include neutrophil gelatinase associated lipocalin (NGAL), kidney injury molecule (KIM)-1 and cystatin C, and the list continues to grow, although the quest for the renal ‘troponin’ has been hampered by a desire for one biomarker to be seen as superior over others. A meta- analysis including 1948 patients from nine studies confirmed that urinary or plasma NGAL indeed predicted the need for RRT.37 Cystatin C has been shown to predict AKI, but its su- periority over serum creatinine has not been observed uni- versally in conducted studies.38 Currently available data are insufficient to conclude that timing of RRT should be based on these new biomarkers but results of future clinical trials are awaited. 4. Conclusion There is no doubt that RRT should be initiated in the case where life threatening conditions such as refractory hyperkalemia, severe acidosis and fluid overload is evident. There is also a broad consensus among clinicians that RRT should be started, if possible, before frank uraemic symptoms develop. Ostermann et al33 recently proposed an algorithm (Fig. 1) for initiation of RRT, incorporating the AKIN criteria and also including the non-renal indications. The message is that the criteria for initiating RRT should be individualized based on the existing dynamic parameters rather than abso- lute values with the aim to support organ function and pre- vent complications. The question whether RRT in AKI should be started ‘early’ or ‘late’ remains unanswered with the current available evi- dence. May be we cannot answer this question now because it may be the wrong question; as dialysis is a supportive rather than a curative therapy. Future research in this very impor- tant field is desperately needed and should include a combi- nation of clinical and emerging biomarkers. What we need, is to look forward to doing away with comparisons of ‘early’ vs ‘late’ dialysis and focus on improving outcomes with timely interventions of renal support tailored to individual patient need. Fig. 1 e Algorithm to guide decision regarding the timing of initiating RRT. MAP [ mean arterial blood pressure. Diagnosis of AKI based on the AKIN classification.35 a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 4 1 e4 6 45
    • Conflicts of interest The author has none to declare. r e f e r e n c e s 1. Oudemans-van Straaten HM. Primum non nocere, safety of continuous renal replacement therapy. Curr Opin Crit Care. 2007;13:635e637. 2. Kellum JA, Mehta RL, Levin A, et al. Development of a clinical research agenda for acute kidney injury using an international, interdisciplinary, three-step modified Delphi process. Clin J Am Soc Nephrol. 2008;3:887e894. 3. Clark E, Wald R, Walsh M, Bagshaw SM. Timing of initiation of renal replacement therapy for acute kidney injury: a survey of nephrologists and intensivists in Canada. Nephrol Dial Transplant. 2012;27(7):2761e2767. 4. KDIGO clinical practice guideline for acute kidney injury. Kidney Int Suppl. 2012;2:89e115. 5. Palevsky PM, Baldwin I, Davenport A, et al. Renal replacement therapy and the kidney: minimizing the impact of renal replacement therapy on recovery of acute renal failure. Curr Opin Crit Care. 2005;11:548e554. 6. Druml W. Acute renal failure is not a “cute” renal failure!. Intensive Care Med. 2004;30:1886e1890. 7. Joannidis M, Forni LG. Clinical review: timing of renal replacement therapy. Crit Care. 2011;15:223. 8. Lameire N, Van BW. The initiation of renal replacement therapy e just-in-time delivery. N Engl J Med. 2010;363:678e680. 9. Karvellas CJ, Farhat MR, Saijad I, et al. A comparison of early versus late initiation of renal replacement therapy in critically ill patients with RRT for AKI: a systematic review and meta-analysis. Crit Care. 2011;15:R72. 10. Bagshaw SM, Uchino S, Bellomo R, et al. Timing of renal replacement therapy and clinical outcomes in critically ill patients with severe acute kidney injury. J Crit Care. 2009;24:129e140. 11. Shiao CC, Wu VC, Li WY, et al. Late initiation of renal replacement therapy is associated with worse outcomes in acute kidney injury after major abdominal surgery. Crit Care. 2009;13:R171. 12. Chou YH, Huang TM, Wu VC, et al. Impact of timing of renal replacement therapy initiation on outcome of septic acute kidney injury. Crit Care. 2011;15:R134. 13. Wu VC, Ko WJ, Chang HW, et al. Early renal replacement therapy in patients with postoperative acute liver failure associated with acute renal failure: effect on postoperative outcomes. J Am Coll Surg. 2007;205:266e276. 14. Liu KD, Himmelfarb J, Paganini E, et al. Timing of initiation of dialysis in critically ill patients with acute kidney injury. Clin J Am Soc Nephrol. 2006;1:915e919. 15. Carl DE, Grossman C, Behnke M, et al. Effect of timing of dialysis on mortality in critically ill, septic patients with acute renal failure. Hemodial Int. 2010;14:11e17. 16. Elahi MM, Lim MY, Joseph RN, et al. Early hemofiltration improves survival in post-cardiotomy patients with acute renal failure. Eur J Cardiothorac Surg. 2004;26:1027e1031. 17. Bouman CS, Oudemans-Van Straaten HM, Tijssen JG, et al. Effects of early high-volume continuous veno-venous hemofiltration on survival and recovery of renal function in intensive care patients with acute renal failure: a prospective, randomized trial. Crit Care Med. 2002;30:2205e2211. 18. Manche A, Casha A, Rychter J, et al. Early dialysis in acute kidney injury after cardiac surgery. Interact Cardiovasc Thorac Surg. 2008;7:829e832. 19. Sugahara S, Suzuki H. Early start on continuous hemodialysis therapy improves survival rate in patients with acute renal failure following coronary bypass surgery. Hemodial Int. 2004;8:320e325. 20. Piccinni P, Dan M, Barbacini S, et al. Early isovolaemic haemofiltration in oliguric patients with septic shock. Intensive Care Med. 2006;32:80e86. 21. Payen D, de Pont AC, Sakr Y, et al. A positive fluid balance is associated with a worse outcome in patients with acute renal failure. Crit Care. 2008;12:R74. 22. Ji Q, Mei Y, Wang X, et al. Timing of continuous veno-venous hemodialysis in the treatment of acute renal failure following cardiac surgery. Heart Vessels. 2011;26:183e189. 23. Ostermann M, Chang RWS. Correlation between parameters at initiation of renal replacement therapy and outcome in patients with acute kidney injury. Crit Care. 2009;13:R175. 24. Demirkilic U, Kuralay E, Yenicesu M, et al. Timing of replacement therapy for acute renal failure after cardiac surgery. J Cardiovasc Surg. 2004;19:17e20. 25. Iyem H, Tavli M, Akcicek F, et al. Importance of early dialysis for acute renal failure after an open-heart surgery. Hemodial Int. 2009;13:55e61. 26. Gettings LG, Reynolds HN, Scalea T. Outcome in posttraumatic acute renal failure when continuous renal replacement therapy is applied early versus late. Intensive Care Med. 1999;25:805e813. 27. Pannu N, Klarenbach S, Wiebe N, et al. Renal replacement therapy in patients with acute renal failure: a systematic review. J Am Med Assoc. 2008;299:793e805. 28. Seabra VF, Balk EM, Liangos O, et al. Timing of renal replacement therapy in acute renal failure: a meta-analysis. Am J Kidney Dis. 2008;52:272e284. 29. Bouchard J, Soroko SB, Chertow GM, et al. Fluid accumulation, survival and recovery of kidney function in critically ill patients with acute kidney injury. Kidney Int. 2009;76:422e427. 30. Macedo E, Mehta R. When should renal replacement therapy be initiated for acute kidney injury? Semin Dial. 2011;24:132e137. 31. De Vriese AS, Colardyn FA, Philippe JJ, et al. Cytokine removal during continuous hemofiltration in septic patients. J Am Soc Nephrol. 1999;10:846e853. 32. Lameire N, Hoste E. Reflections on the definition, classification, and diagnostic evaluation of acute renal failure. Curr Opin Crit Care. 2004;10:468e475. 33. Ostermann M, Dickie H, Barrett NA. Renal replacement therapy in critically ill patients with acute kidney injury e when to start. Nephrol Dial Transplant. 2012;27:2242e2248. 34. Yerram P, Karuparthi PR, Misra M. Fluid overload and acute kidney injury. Hemodial Int. 2010;14:348e354. 35. Mehta RL, Kellum JA, Shah SV, et al. Acute Kidney Injury Network (AKIN): report of an initiative to improve outcomes in acute kidney injury. Crit Care. 2007;11:R31. 36. Bellomo R, Ronco C, Kellum JA, et al. Acute renal failure e 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:R204eR212. 37. Haase M, Bellomo R, Devarajan P, et al. Accuracy of neutrophil gelatinase-associated lipocalin (NGAL) in diagnosis and prognosis in acute kidney injury: a systematic review and meta-analysis. Am J Kidney Dis. 2009;54:1012e1024. 38. Cruz DN, De Geus HR, Bagshaw SM. Biomarker strategies to predict need for renal replacement therapy in acute kidney injury. Semin Dial. 2011;24:124e131. a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 4 1 e4 646
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