Original Article
Intensity of Continuous Renal-Replacement Therapy in Critically Ill Patients
N Engl J Med 2009; 361:1627-1638October 22, 2009
- Abstract
Background
The optimal intensity of continuous renal-replacement therapy remains unclear. We conducted a multicenter, randomized trial to compare the effect of this therapy, delivered at two different levels of intensity, on 90-day mortality among critically ill patients with acute kidney injury.
Methods
We randomly assigned critically ill adults with acute kidney injury to continuous renal-replacement therapy in the form of postdilution continuous venovenous hemodiafiltration with an effluent flow of either 40 ml per kilogram of body weight per hour (higher intensity) or 25 ml per kilogram per hour (lower intensity). The primary outcome measure was death within 90 days after randomization.
Results
Of the 1508 enrolled patients, 747 were randomly assigned to higher-intensity therapy, and 761 to lower-intensity therapy with continuous venovenous hemodiafiltration. Data on primary outcomes were available for 1464 patients (97.1%): 721 in the higher-intensity group and 743 in the lower-intensity group. The two study groups had similar baseline characteristics and received the study treatment for an average of 6.3 and 5.9 days, respectively (P=0.35). At 90 days after randomization, 322 deaths had occurred in the higher-intensity group and 332 deaths in the lower-intensity group, for a mortality of 44.7% in each group (odds ratio, 1.00; 95% confidence interval [CI], 0.81 to 1.23; P=0.99). At 90 days, 6.8% of survivors in the higher-intensity group (27 of 399), as compared with 4.4% of survivors in the lower-intensity group (18 of 411), were still receiving renal-replacement therapy (odds ratio, 1.59; 95% CI, 0.86 to 2.92; P=0.14). Hypophosphatemia was more common in the higher-intensity group than in the lower-intensity group (65% vs. 54%, P<0.001).
Conclusions
In critically ill patients with acute kidney injury, treatment with higher-intensity continuous renal-replacement therapy did not reduce mortality at 90 days. (ClinicalTrials.gov number, NCT00221013.)
Media in This Article
Figure 1
Numbers of Patients Enrolled in the Study, Randomly Assigned to a Treatment Group, and Included in the Analysis.Figure 2
Kaplan–Meier Estimates of the Probability of Death.Article Activity
- Article
Acute kidney injury is associated with substantial morbidity and mortality.1 It is a common finding among patients in the intensive care unit (ICU)2 and is an independent predictor of mortality.3 Acute kidney injury severe enough to result in the use of renal-replacement therapy affects approximately 5% of patients admitted to the ICU and is associated with a mortality rate of 60%. 4 The optimal approach to renal-replacement therapy, as well as the optimal intensity and timing of such therapy, in critically ill patients remains unclear. In one single-center, randomized, controlled study in which continuous renal-replacement therapy was the sole treatment approach, survival improved when the intensity of therapy was increased from an assigned effluent rate of 20 ml per kilogram of body weight per hour to either 35 or 45 ml per kilogram per hour.5 However, subsequent single-center studies have had conflicting results.6-8
The recently reported Veterans Affairs/National Institutes of Health Acute Renal Failure Trial Network Study (ClinicalTrials.gov number, NCT00076219)9 showed that increasing the intensity of renal-replacement therapy did not decrease mortality among patients with acute kidney injury. In contrast to other studies, which used continuous renal-replacement therapy exclusively, this study assigned patients to a protocol of either intermittent or continuous renal-replacement therapy according to whether they were hemodynamically stable or unstable, respectively. This design reflects clinical practice in the United States and elsewhere but makes it difficult to carry out a formal comparison of treatment intensities that would be independent of the particular treatment approach. We conducted a randomized, controlled study to test the hypothesis that increasing the intensity of continuous renal-replacement therapy would reduce mortality at 90 days.
Methods
Study Design
The Randomized Evaluation of Normal versus Augmented Level (RENAL) Replacement Therapy Study was a prospective, randomized, parallel-group trial designed to assess two levels of intensity of continuous renal-replacement therapy in critically ill patients with acute kidney injury. The study was conducted between December 30, 2005, and November 28, 2008, in 35 ICUs in Australia and New Zealand. The study protocol is outlined in the Supplementary Appendix, available with the full text of this article at NEJM.org. It was approved by the human research ethics committees of the University of Sydney and all participating institutions. The integrity of data collection was verified by the George Institute for International Health monitoring team. An independent data and safety monitoring committee reviewed safety data and interim results with the aim of providing advice to the trial management committee should such analyses prove beyond a reasonable doubt that augmented continuous renal-replacement therapy led to a net benefit or harm in terms of mortality.
Study Population
Patients were eligible for enrollment if they were critically ill, were 18 years of age or older, had acute kidney injury, were deemed by the treating clinician to require renal-replacement therapy, and met at least one of the following criteria: oliguria (urine output <100 ml in a 6-hour period) that was unresponsive to fluid resuscitation measures, a serum potassium concentration exceeding 6.5 mmol per liter, severe acidemia (pH <7.2), a plasma urea nitrogen level above 70 mg per deciliter (25 mmol per liter), a serum creatinine concentration above 3.4 mg per deciliter (300 μmol per liter), or the presence of clinically significant organ edema (e.g., pulmonary edema). Written informed consent was obtained from the patient or responsible surrogate by means of either a priori or delayed consent. (For a detailed description of delayed consent, see the Supplementary Appendix.)
Patients who had received any previous renal-replacement therapy during the same hospital admission or who were on maintenance dialysis for end-stage kidney disease were ineligible for the study. (For a detailed list of inclusion and exclusion criteria and the criteria for discontinuing the study treatment, see the Supplementary Appendix.)
Intervention
The patients in both groups were treated with continuous venovenous hemodiafiltration. Replacement fluid was delivered into the extracorporeal circuit after the filter (i.e., postdilution), with a ratio of dialysate to replacement fluid of 1:1. The effluent flow prescribed was based on the patient's body weight at the time of randomization and was either 40 ml per kilogram per hour (for the higher-intensity group) or 25 ml per kilogram per hour (for the lower-intensity group). Blood flow was kept above 150 ml per minute. Fluid was removed by decreasing the flow of the replacement fluid and of the dialysate in equal proportion, so that effluent exceeded them both by any amount prescribed by the clinician. Filters with the AN69 membrane (Gambro) were used. Hemosol BO fluid (Gambro) was used as the dialysate and replacement fluid. Gambro had no role in the initiation, design, analysis, or reporting of the study.
Study Outcomes
The primary study outcome was death from any cause within 90 days after randomization. Secondary and tertiary outcomes included death within 28 days after randomization, death in the ICU, in-hospital death, cessation of renal-replacement therapy, duration of ICU and hospital stays, duration of mechanical ventilation and renal-replacement therapy, dialysis status at day 90, and any new organ failures.
Statistical Analysis
All statistical analyses were conducted according to a predefined plan.10,11 The target enrollment was 1500 patients, which provided 90% power to detect an 8.5% absolute reduction in 90-day mortality from a baseline of 60% (alpha level, <0.05). Two interim analyses were performed and reviewed by an independent data and safety monitoring committee. Since the Haybittle–Peto rule with a maximum of three analyses was used to limit the overall probability of a type I error to 0.05, the final analysis was conducted at an alpha level of 0.048.
All analyses were performed according to the intention-to-treat principle, with no imputation for missing values. Data from patients who were lost to follow-up were not analyzed. Proportions were compared with the use of the chi-square test, and continuous variables were analyzed with the use of Student's t-test. Mantel–Haenszel adjusted odds ratios and their corresponding 95% confidence intervals were calculated. Analysis of the primary outcome for the two groups was also performed by means of the log-rank test, with the results presented as a Kaplan–Meier cumulative-incidence plot.
Prespecified subgroup analyses were performed according to the presence or absence of sepsis; failure of one or more nonrenal organs; a Sequential Organ Failure Assessment (SOFA) cardiovascular score of 3 or 4 at baseline (on a scale ranging from 0 to 4, with a higher score indicating more severe organ dysfunction); and an estimated glomerular filtration rate of less than 60 ml per minute within 6 months prior to randomization. We assessed subgroups for heterogeneity of treatment effect according to accepted clinical guidelines.12
Statistical analyses were performed, independently checked, and replicated with the use of SAS software, version 9.1.
Results
Enrollment
Between December 1, 2005, and August 31, 2008, we enrolled 1508 patients, of whom 747 were assigned to the higher-intensity treatment group and 761 to the lower-intensity treatment group (Figure 1Figure 1
Numbers of Patients Enrolled in the Study, Randomly Assigned to a Treatment Group, and Included in the Analysis.). Consent was subsequently withheld or withdrawn for 43 patients (2.9%), 25 of whom had been assigned to higher-intensity therapy and 18 to lower-intensity therapy; only 1 patient was lost to follow-up, thus the primary outcome was available for 1464 patients (97.1%).Baseline Characteristics
All baseline characteristics were similar between the two groups (Table 1Table 1
Baseline Characteristics of the Study Patients.). The serum creatinine concentrations before randomization in the higher-intensity and lower-intensity treatment groups were 3.8 mg per deciliter (338 μmol per liter) and 3.7 mg per deciliter (330 μmol per liter), respectively. In all, 73.9% of patients were receiving mechanical ventilation, 49.4% had severe sepsis, and 82.5% were receiving vasoactive drugs.Study and Supportive Treatments
Table 2Table 2
Characteristics of Study Treatments and Subsequent Use of Renal-Replacement Therapy. lists the characteristics of the study therapy. The mean duration of treatment in the two groups was similar, but during therapy, they had significantly different mean daily serum creatinine concentrations (1.9 mg per deciliter [170 μmol per liter] in the higher-intensity group vs. 2.3 mg per deciliter [204 μmol per liter] in the lower-intensity group, P<0.001) and blood urea nitrogen levels (35.6 mg per deciliter [12.7 mmol per liter] vs. 44.5 mg per deciliter [15.9 mmol per liter], P<0.001). These differences were consistent with the difference in the intensity of the delivered treatment (mean effluent rate, 33.4 ml per kilogram of body weight per hour in the higher-intensity group vs. 22.0 in the lower-intensity group; P<0.001). Patients receiving higher-intensity continuous renal-replacement therapy were more likely to receive regional extracorporeal-circuit anticoagulation with heparin and protamine (P=0.007) and required more filters per day (0.93 vs. 0.84, P<0.001). Only 7.6% and 7.0% of the patients in the higher-intensity and the lower-intensity groups, respectively, underwent intermittent hemodialysis at any time during their ICU stay, for a total of 314 dialysis sessions by day 28 after randomization.Treatment Limitations
Among patients who died, limitations of ICU treatment were instituted for 289 of 322 patients in the higher-intensity group and 301 of 332 patients in the lower-intensity group (89.8% and 90.7%, respectively; P=0.52). Among these patients, treatment was withdrawn or limited because death was considered to be imminent in 219 of 322 patients in the higher-intensity group and in 232 of 332 patients in the lower-intensity group (68.0% and 69.9%, respectively; P=0.49). Intensive treatment was withheld, since further maximal therapy was not indicated in 70 patients (21.7%) in the higher-intensity group and in 69 patients (20.8%) in the lower-intensity group.
Primary Outcome
Within 90 days after randomization, death occurred in 322 (44.7%) of 721 patients in the higher-intensity group and in 332 (44.7%) of 743 patients in the lower-intensity group (odds ratio in the higher-intensity group, 1.00; 95% confidence interval [CI], 0.81 to 1.23; P=0.99) (Table 3Table 3
Primary and Secondary Outcomes. and Figure 2Figure 2Kaplan–Meier Estimates of the Probability of Death.). Mortality was also similar between the two treatment groups in all prespecified subgroups (Figure 3Figure 3
Mortality in the Prespecified Subgroups and among All Patients.).Secondary and Tertiary Outcomes
There were no significant differences between the groups in any of the secondary or tertiary outcomes (Table 3). At 28 days after randomization, 64 patients (14.5% of survivors) in the higher-intensity group and 57 patients (12.2% of survivors) in the lower-intensity group were still receiving renal-replacement therapy. At 90 days, these numbers had dropped to 27 patients (6.8% of survivors) and 18 patients (4.4% of survivors), respectively (odds ratio in the higher-intensity group, 1.59; 95% CI, 0.86 to 2.92; P=0.14). Oliguria (urinary excretion, <400 ml per day) was present in 59.7% of patients at randomization.
Complications of Therapy
In the higher-intensity group, there were seven serious adverse events (three cases of the disequilibrium syndrome, one case of cerebral edema, one of rectal bleeding, one of cardiac arrest, and one of too rapid correction of hyponatremia) that were considered by the site investigators to be potentially related to treatment (Table 4Table 4
Summary of Complications Associated with Study Treatment.). In the lower-intensity group, there were five serious adverse events (three cases of heparin-induced thrombocytopenia, one case of hypoxemia, and one of cardiogenic shock). Hypophosphatemia was detected in 461 patients (65.1%) in the higher-intensity group and in 396 patients (54.0%) in the lower-intensity group (P<0.001). Discussion
In this multicenter, randomized, controlled trial of the intensity of continuous renal-replacement therapy, we found that the higher-intensity treatment did not decrease mortality as compared with the lower-intensity treatment. There were also no significant differences in the rate of recovery (i.e., cessation of dialysis because it was no longer needed) or in the occurrence of organ failure, the need for mechanical ventilation, time spent in the ICU, or time spent in the hospital.
Our findings do not agree with those of two previous randomized, controlled studies of continuous renal-replacement therapy intensity,5,6 which showed decreased mortality with increased intensity of treatment. In a study of 425 patients, Ronco et al.5 reported a decrease in mortality from 59 to 43% when the prescribed effluent flow was increased from 20 ml per kilogram per hour to 35 or 45 ml per kilogram per hour. In a similar study involving 206 patients, Saudan et al.6 observed a 20% reduction in all-cause mortality at 90 days (from 61 to 41%) with an increase in the prescribed effluent flow from 25 ml per kilogram per hour to approximately 43 ml per kilogram per hour. However, the results in our study are consistent with those of two other randomized, controlled studies. Bouman et al.7 reported no increase in survival among 106 patients in a comparison of prescribed effluent flows of 48 and 20 ml per kilogram per hour. Similarly, Tolwani et al.8 found no difference in outcome among 200 patients randomly assigned to an effluent flow of either 20 or 35 ml per kilogram per hour.
The lower-intensity treatment in our trial was similar to that usually prescribed in ICUs in Australia and New Zealand13 and was also identical to that prescribed for the control group in one of the trials of continuous renal-replacement therapy intensity in which the results were positive.6 For the higher-intensity dose, we chose a value of 40 ml per kilogram per hour, which was intermediate between the two higher doses in the study by Ronco et al.5 and similar to the higher-intensity treatment group in the study by Saudan et al.6 In addition, the prescribed difference between treatment intensities (15 ml per kilogram per hour) in our study was identical to that prescribed in these studies.5,6,14 Although the target doses were always achieved when continuous renal-replacement therapy was delivered, treatments were frequently interrupted owing to clotting of the filter, surgery, diagnostic investigations, or other procedures. In the Acute Renal Failure Trial Network Study,9 the dose delivered was 89% of that prescribed for higher-intensity treatment, whereas Tolwani et al.8 reported a value of 83% and the value in our study was 84%. For the lower-intensity treatment, the doses delivered were 95% in the Acute Renal Failure Trial Network Study as compared with 85% in the study by Tolwani et al. and 88% in our study. In all previous studies, delivered doses were less than 85% of the prescribed doses.15-17
Our findings are consistent with those of the Acute Renal Failure Trial Network Study,9 which used a combination of continuous and intermittent renal-replacement therapy. In contrast to that study, however, we used continuous renal-replacement therapy exclusively — the preferred approach to renal-replacement therapy in ICUs in Australia, New Zealand, the United Kingdom, and many centers worldwide1,18 — and ours included patients with stage 4 chronic kidney disease.19
Despite the similarities in primary outcome in our study and the Acute Renal Failure Trial Network Study, there were some differences in the characteristics of the patients. Our patients were older and had a lower body weight, a lower incidence of sepsis, and higher mean scores on the cardiovascular and respiratory system SOFA. There were also differences in the processes of care. Our patients had not undergone renal-replacement therapy before randomization, whereas 64% of patients in the Acute Renal Failure Trial Network Study had undergone renal-replacement therapy in the 24 hours before randomization. In our study, the mean time from ICU admission to randomization was 50 hours, as compared with 150 hours in the other trial. Finally, our patients received only 314 intermittent hemodialysis treatments during the study therapy phase, as compared with 5077 hemodialysis treatments in the other trial. The rate of dependence on dialysis among study survivors at 28 days was 15.8% in our study as compared with 45.2% in the Acute Renal Failure Trial Network Study and 5.6% at 90 days in our study, as compared with 24.6% at 60 days in the other study.
In our efforts to achieve a high degree of internal and external validity, we ensured allocation concealment before randomization and used a primary outcome that was not subject to ascertainment bias. We enrolled 88.8% of fully eligible patients,20 followed a predetermined statistical-analysis plan,10 and were able to follow up on all but one patient. The management of renal-replacement therapy was designed to be in accord with standard practice in Australia and New Zealand.12 Nearly all the patients received their assigned treatments, and there was a substantial difference in the intensity of the delivered doses of renal-replacement therapy. By including patients with preexisting stage 4 chronic kidney disease and by using continuous renal-replacement therapy (the preferred form of renal-replacement therapy in many countries and centers), we sought to increase the external validity of our results. We acknowledge, however, that a substantial number of the serum creatinine measurements within 6 months prior to randomization were unavailable (Table 1), thus limiting the conclusions that could be drawn regarding the effect of chronic kidney disease on the study outcomes.
The trial had several limitations: the study personnel and staff were aware of patients' treatment status, the timing of dialysis initiation was not standardized, and data to assess the costs of the interventions were not gathered. In addition, operational characteristics such as frequent filter clotting could have influenced solute clearance. The difference between the prescribed dose and the delivered dose highlights the risk of overestimating the effective delivery of therapy and the need to improve operational measures in continuous renal-replacement therapy. Specifically, basing the delivered dose on effluent volume most likely overestimates true solute clearance. Future trials should measure solute clearance rather than simply relying on effluent volume. Furthermore, we cannot exclude the possibility that individual patients may benefit from personalized prescriptions. We did not use a prespecified creatinine clearance to trigger the cessation of therapy, since this was not standard practice in the study centers. Accordingly, we used cessation of renal-replacement therapy as a clinically relevant measure of the recovery of kidney function. The greater frequency of morning hypophosphatemia in the higher-intensity treatment group is consistent with the increased phosphate losses that would be expected with more intense treatment and was similarly noted in the Acute Renal Failure Trial Network Study.9
In countries where continuous renal-replacement therapy is now the preferred form of renal-replacement therapy in the ICU, our study has implications for clinical practice. We found that a prescribed treatment intensity that exceeds 25 ml of effluent flow per kilogram per hour adds no significant benefit and exposes patients to the risk of hypophosphatemia. There has been a widespread increase in the use of higher-intensity continuous renal-replacement therapy,4,19 and our findings indicate that such practice is not justified. However, it must be emphasized that the dose delivered in our lower-intensity group was higher than the doses that are used in many centers.4,15-17 Furthermore, the lower dose in our control group was associated with a lower mortality than was reported in a large international study of the treatment of acute renal failure in critically ill patients.4 Thus, our findings suggest not that the intensity of renal-replacement therapy is unimportant but rather that increases beyond an adequate level of intensity provide no additional benefit in critically ill patients. The results also suggest that some specific aspects of renal-replacement therapy in critically ill patients — that is, the effect of the timing of treatment initiation on mortality and the effect of continuous as compared with intermittent treatment on renal recovery — should be prioritized for investigation in future trials.
In conclusion, this large, randomized, controlled trial showed that increasing the intensity of continuous renal-replacement therapy from 25 to 40 ml of effluent flow per kilogram per hour does not reduce mortality or the rate of dependence on dialysis among critically ill patients.
Supported by grants from the National Health and Medical Research Council of Australia (352550) and the Health Research Council of New Zealand (06-357).
Dr. Bellomo reports receiving consulting fees from Gambro Biosite, Abbott Diagnostics, and Philips Medical Systems, and grant support from Fresenius Kabi, Bard, Pfizer, and Gambro; Dr. Cass, grant support from Fresenius Kabi, Roche, and Gambro; Dr. Finfer, travel support to present research results at scientific meetings from Eli Lilly, Cardinal Health, and CSL Bioplasma; Dr. Gallagher, lecture fees from Roche and Amgen; Dr. McArthur, grant support from Bard, Pfizer, and Gambro; and Dr. Myburgh, grant support from Fresenius Kabi. The George Institute for International Health, an independent not-for-profit institute affiliated with the University of Sydney, has received reimbursement for Dr. Finfer's time as a steering-committee member for studies sponsored by Eli Lilly and Eisai and has received research funding from Servier, Novartis, Eisai, Merck Sharp & Dohme, Pfizer Australia, Fresenius Kabi Deutschland, and Sanofi-Aventis. No other potential conflict of interest relevant to this article was reported.
The Randomized Evaluation of Normal versus Augmented Level (RENAL) Replacement Therapy Study is a collaboration of the Australian and New Zealand Intensive Care Society Clinical Trials Group and the George Institute for International Health. The members of the Writing Committee for the RENAL Replacement Therapy Study (Rinaldo Bellomo, M.D., Alan Cass, M.D., Ph.D., Louise Cole, M.D., Ph.D., Simon Finfer, M.D., Martin Gallagher, M.D., Serigne Lo, Ph.D., Colin McArthur, M.D., Shay McGuinness, M.D., John Myburgh, M.D., Ph.D., Robyn Norton, M.D., Ph.D., M.P.H., Carlos Scheinkestel, M.D., and Steve Su, Ph.D.) take responsibility for the content of this article.
We thank Gambro for providing Hemosol dialysate and replacement fluids at a favorable price; the nurses in our intensive care units, our physician colleagues, and our patients and their families; Professor Carol Pollock and Professor Peter Kerr for their assistance with protocol development; and Dr. Peter Stow for his assistance with the Acute Physiology and Chronic Health Evaluation (APACHE III) software application.
Source Information
Address reprint requests to Dr. Bellomo at ANZICS CTG, Level 3, 10 Ievers St., Carlton, VIC 3053, Australia, or at ctg@anzics.com.au.
The members of the Randomized Evaluation of Normal versus Augmented Level (RENAL) Replacement Therapy Study Group and their affiliations are listed in the Appendix.
Appendix
The RENAL Replacement Therapy Study is a collaboration of the Australian and New Zealand Intensive Care Society Clinical Trials Group (ANZICS CTG) and the George Institute for International Health. Writing Committee: R. Bellomo — Austin Hospital; A. Cass, R. Norton, M. Gallagher, S. Lo, S. Su — George Institute for International Health; L. Cole — Nepean Hospital: S. Finfer — Royal North Shore Hospital; C. McArthur, S. McGuinness — Auckland City Hospital; J. Myburgh — St. George Hospital (Sydney); C. Scheinkestel — Alfred Hospital. Management Committee: R. Bellomo (chair), J. Lee (senior project manager), D. Ali, A. Cass, L. Cole, S. Finfer, M. Gallagher, D. Goldsmith, S. McGuinness, J. Myburgh, R. Norton, C. Scheinkestel. Steering Committee: R. Bellomo (chair), A. Banerjee, D. Bhonagiri, D. Blythe, J. Botha, J. Cade, L. Cole, G. Dobb, J. Eddington, S. Finfer, A. Flabouris, C. French, P. Garrett, S. Henderson, B. Ihle, C. Joyce, M. Kalkoff, J. Lipman, C. McArthur, S. McGuinness, D. Milliss, I. Mitchell, J. Morgan, J. Myburgh, P. Nair, N. Orford, A. Raza, C. Scheinkestel, Y. Shehabi, A. Tobin, R. Totaro, A. Turner, C. Wright. Project Management Team: D. Ali, J. Lee, L. Little, A. Morrison, G. Regaglia, R. Shukla. Data Safety and Monitoring Committee: C. Baigent (chair), J. Emberson, D. Wheeler, D. Young. Statistics Committee: L. Billot, S. Bompoint, S. Heritier, S.N. Lo, A. Pillai, S. Su. Data Management and Information Technology/Programming: S. Pandey, S. Ryan, M. Schmidt, G. Starzec, B. Vijayan. Site Investigators and Research Coordinators: Australian Capital Territory — Canberra Hospital: I. Mitchell, R. Ashley, J. Gissane, K. Malchukova, J. Ranse. New South Wales — Blacktown Hospital: A. Raza, K. Nand, T. Sara; Concord Hospital: W. Cheung, E. Fugaccia, P. Lawrence, D. Millis, J. Tan, G. Thankrishnan, H. Wong; John Hunter Hospital: P. Harrigan, E. Crowfoot, M. Hardie; Liverpool Hospital: D. Bhonagiri, S. Micallef; Newcastle — Mater Calvary Hospital: J. Brieva, M. Lintott; Nepean Hospital: L. Cole, I. Seppelt, R. Gresham, M. Nikas, L. Weisbrodt; Prince of Wales Hospital: Y. Shehabi, F. Bass, M. Boyle, M. Campbell, N. Hammond. Victoria — Stockdale Royal North Shore Hospital: S. Finfer, S. Ankers, A. O'Connor, Julie Potter; Royal Prince Alfred Hospital: R. Totaro, D. Rajbhandari; St. George Hospital: J. Myburgh, V. Dhiacou, A. Jovanovska, F. Munster; St. Vincent's Hospital: P. Nair, J. Breeding, C. Burns; Westmead Hospital: A. Banerjee, M. Morrison, C. Pfeffercorn, A. Ritchie. New Zealand — Auckland City Hospital/Cardiovascular Intensive Care Unit: S. McGuinness, H. Buhr, M. Eccleston, R. Parke; Auckland City Hospital/Department of Critical Care Medicine: C. McArthur, J. Bell, L. Newby; Christchurch Hospital: S. Henderson, J. Mehrtens; Whangarei Hospital: M. Kalkoff, C. West. Queensland — Mater Adult and Mater Private Hospital: J. Morgan, L. Rudder, J. Sutton; Nambour General Hospital: P. Garrett, N. Groves, S. McDonald, J. Jaspers; Princess Alexandra Hospital: C. Joyce, M. Harwood, J. Helyar, B. Mackie; Royal Brisbane Hospital: J. Lipman, R. Boots, C. Bertenshaw, R. Deans, C. Fourie, M. Lassig-Smith, J. Stuart. South Australia — Royal Adelaide Hospital: A. Flabouris, J. Edwards, S. O'Connor, K. Lewis, J. Rivett. Tasmania — Royal Hobart Hospital: A. Turner, T. Field, R. McAllister, K. Marsden. Victoria — Austin Hospital: R. Bellomo, C. Mathlin, D. Goldsmith, I. Mercer, K. O'Sullivan; Bendigo Hospital: J. Edington, C. Boschert, J. Smith; Epworth Hospital: B. Ihle, M. Graan, S. Ho; Frankston Hospital: J. Botha, N. Fowler, J. McInness, N. Pratt; Geelong Hospital: N. Orford, T. Elderkin, M. Fraser, A. Kinmonth; Monash Medical Centre: C. Wright, J. Barrett, S. Wilson, P. Galt, S. Burton, C. Culhane, R. Ioannidis; Royal Melbourne Hospital: M. Roberston, D. Barge, T. Caf, B. Howe, P. Low; St. Vincent's Hospital Melbourne: A. Tobin, N. Groves, J. Holmes, R. Smith; Alfred Hospital: C. Scheinkestel, A. Davies, L. Murray, R. Nevill, S. Vallance, S. Varley, V. White; Western Hospital: C. French, L. Little, H. Raunow. Western Australia — Fremantle Hospital: D. Blythe, A. Palermo; Royal Perth Hospital: G. Dobb, M. Boardman, J. Chamberlain, A. Gould, G. McEntaggart, S. Perryman, L. Thomas.
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CrossRef | Web of Science | Medline
- Citing Articles (84)
Citing Articles
1
C. RIMES-STIGARE, A. AWAD, J. MÅRTENSSON, C.-R. MARTLING, M. BELL. (2012) Long-term outcome after acute renal replacement therapy: a narrative review. Acta Anaesthesiologica Scandinavica 56:2, 138-146
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S. VAARA, V. PETTILA, K.-M. KAUKONEN. (2012) Quality of pharmacokinetic studies in critically ill patients receiving continuous renal replacement therapy. Acta Anaesthesiologica Scandinavica 56:2, 147-157
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Hoi-Ping Shum, King-Chung Chan, Wing-Wa Yan. (2012) Regional Citrate Anticoagulation in Predilution Continuous Venovenous Hemofiltration Using Prismocitrate 10/2 Solution. Therapeutic Apheresis and Dialysis 16:1, 81-86
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M. Ostermann, H. Dickie, N. A. Barrett. (2012) Renal replacement therapy in critically ill patients with acute kidney injury--when to start. Nephrology Dialysis Transplantation
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Helmut Schiffl, Susanne M. Lang. (2012) Severe acute hypophosphatemia during renal replacement therapy adversely affects outcome of critically ill patients with acute kidney injury. International Urology and Nephrology
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P.M. Honoré, R. Jacobs, W. Boer, O. Joannes-Boyau, J. De Regt, E. De Waele, V. Van Gorp, V. Collin, H.D. Spapen. (2012) New Insights Regarding Rationale, Therapeutic Target and Dose of Hemofiltration and Hybrid Therapies in Septic Acute Kidney Injury. Blood Purification 33:1-3, 44-51
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M. Haase, R. Bellomo, D. Story, A. Letis, K. Klemz, G. Matalanis, S. Seevanayagam, D. Dragun, E. Seeliger, P. R. Mertens, A. Haase-Fielitz. (2012) Effect of mean arterial pressure, haemoglobin and blood transfusion during cardiopulmonary bypass on post-operative acute kidney injury. Nephrology Dialysis Transplantation 27:1, 153-160
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Santosh Varughese. (2012) Renal replacement therapy in acute kidney injury. Clinical Queries: Nephrology 1:1, 76-84
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Eun Kyoung Lee, Jai Won Chang. (2012) Renal Replacement Therapy in Acute Kidney Injury: Indication, Proper Initiation, and Prescription. Korean Journal of Medicine 82:1, 17
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Glenn M. Eastwood, Leah Peck, Helen Young, Michael Bailey, Michael C. Reade, Ian Baldwin, Rinaldo Bellomo. (2012) Haemodynamic Impact of a Slower Pump Speed at Start of Continuous Renal Replacement Therapy in Critically Ill Adults with Acute Kidney Injury: A Prospective Before-and-After Study. Blood Purification 33:1-3, 52-58
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Anitha Vijayan, Paul M. Palevsky. (2012) Dosing of Renal Replacement Therapy in Acute Kidney Injury. American Journal of Kidney Diseases
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J. Kron, S. Kron, R. Wenkel, H.-U. Schuhmacher, U. Thieme, T. Leimbach, H. Kern, H.-H. Neumayer, T. Slowinski. (2012) Extended daily on-line high-volume haemodiafiltration in septic multiple organ failure: a well-tolerated and feasible procedure. Nephrology Dialysis Transplantation 27:1, 146-152
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Sandeep Mahajan, Yasir Rizvi. (2012) Quantification of acute renal replacement therapy. Clinical Queries: Nephrology 1:1, 85-88
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Rolando Claure-Del Granado, Etienne Macedo, Ravindra L. Mehta. 2012. Management options: continuous renal replacement therapy. , 51-61.
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E. Clark, R. Wald, M. Walsh, S. M. Bagshaw, . (2011) Timing of initiation of renal replacement therapy for acute kidney injury: a survey of nephrologists and intensivists in Canada. Nephrology Dialysis Transplantation
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Neil J. Glassford, Rinaldo Bellomo. (2011) Acute kidney injury. Current Opinion in Critical Care 17:6, 562-568
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Zaccaria Ricci, Claudio Ronco. (2011) Timing, dose and mode of dialysis in acute kidney injury. Current Opinion in Critical Care 17:6, 556-561
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S. Demirjian, B. W. Teo, J. A. Guzman, R. J. Heyka, E. P. Paganini, W. H. Fissell, J. D. Schold, M. J. Schreiber. (2011) Hypophosphatemia during continuous hemodialysis is associated with prolonged respiratory failure in patients with acute kidney injury. Nephrology Dialysis Transplantation 26:11, 3508-3514
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Sarah Faubel, Charles L. Edelstein. (2011) Acute kidney injury: Severity of illness scoring systems in acute kidney injury. Nature Reviews Nephrology 8:1, 8-10
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Etienne Macedo, Rolando Claure-Del Granado, Ravindra L. Mehta. (2011) Effluent volume and dialysis dose in CRRT: time for reappraisal. Nature Reviews Nephrology 8:1, 57-60
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Kai Singbartl, John A Kellum. (2011) AKI in the ICU: definition, epidemiology, risk stratification, and outcomes. Kidney International
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Mei Tran, Denise Tam, Amit Bardia, Manoj Bhasin, Glenn C. Rowe, Ajay Kher, Zsuzsanna K. Zsengeller, M. Reza Akhavan-Sharif, Eliyahu V. Khankin, Magali Saintgeniez, Sascha David, Deborah Burstein, S. Ananth Karumanchi, Isaac E. Stillman, Zoltan Arany, Samir M. Parikh. (2011) PGC-1α promotes recovery after acute kidney injury during systemic inflammation in mice. Journal of Clinical Investigation 121:10, 4003-4014
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M. Haase, R. Bellomo, A. Haase-Fielitz. (2011) Time for an eGFR equivalent in AKI recognition?. Nephrology Dialysis Transplantation 26:10, 3075-3076
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A. G. Schneider, S. Uchino, R. Bellomo. (2011) Severe acute kidney injury not treated with renal replacement therapy: characteristics and outcome. Nephrology Dialysis Transplantation
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W. D. Lyndon, K. M. Wille, A. J. Tolwani. (2011) Solute clearance in CRRT: prescribed dose versus actual delivered dose. Nephrology Dialysis Transplantation
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P. Zhang, Y. Yang, R. Lv, Y. Zhang, W. Xie, J. h. Chen. (2011) Effect of the intensity of continuous renal replacement therapy in patients with sepsis and acute kidney injury: single-center randomized clinical trial. Nephrology Dialysis Transplantation
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H. Schmid, H. Schiffl, S.R. Lederer. (2011) Die akute Nierenschädigung. Intensivmedizin und Notfallmedizin 48:6, 468-473
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Robert F. Johnson, Jillian Gustin. (2011) Acute Renal Failure Requiring Renal Replacement Therapy in the Intensive Care Unit: Impact on Prognostic Assessment for Shared Decision Making. Journal of Palliative Medicine 14:7, 883-889
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Jean-Louis Vincent, Elena Carrasco Serrano, Aikaterina Dimoula. (2011) Current management of sepsis in critically ill adult patients. Expert Review of Anti-infective Therapy 9:7, 847-856
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Didier Journois. (2011) Dix pièges à éviter en hémofiltration continue. Le Praticien en Anesthésie Réanimation 15:3, 194-199
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Martial Moonen, Vincent Fraipont, Luc Radermacher, Catherine Masset, Éric Firre, Xavier Warling. (2011) L’insuffisance rénale aiguë : du concept à la pratique. Néphrologie & Thérapeutique 7:3, 172-177
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Niklas Nielsen, Hans Friberg. (2011) Insights from the evidence evaluation process – Do we have the answers for therapeutic hypothermia?. Resuscitation 82:5, 501-502
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M. Joannidis. (2011) Nierenersatztherapie: Wann? Wie? Wie lange?. Intensivmedizin und Notfallmedizin 48:4, 264-269
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Shaikh A. Nurmohamed, Mark V. Koning, Marc G. Vervloet, A.B. Johan Groeneveld. (2011) Delivered dose of continuous venovenous hemofiltration predicts outcome in septic patients with acute kidney injury: A retrospective study. Journal of Critical Care 26:2, 213-220
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Zaccaria Ricci, Andrea Polito, Angelo Polito, Claudio Ronco. (2011) The implications and management of septic acute kidney injury. Nature Reviews Nephrology 7:4, 218-225
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David Askenazi. (2011) Evaluation and management of critically ill children with acute kidney injury. Current Opinion in Pediatrics 23:2, 201-207
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Raghavan Murugan, John A. Kellum. (2011) Acute kidney injury: what's the prognosis?. Nature Reviews Nephrology 7:4, 209-217
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Zaccaria Ricci, Stefano Romagnoli. (2011) Underdosing continuous venovenous hemofiltration predicts outcome in septic patients with acute kidney injury. Journal of Critical Care 26:2, 221
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Shaikh A. Nurmohamed, Mark V. Koning, Marc G. Vervloet, A.B. Johan Groeneveld. (2011) Underdosing continuous venovenous hemofiltration predicts outcome in septic patients with acute kidney injury. Journal of Critical Care 26:2, 222
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Edward L. Korn, Boris Freidlin. (2011) Inefficacy Interim Monitoring Procedures in Randomized Clinical Trials: The Need to Report. The American Journal of Bioethics 11:3, 2-10
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Jason A. Roberts, Ravindra L. Mehta, Jeffrey Lipman. (2011) Sustained low efficiency dialysis allows rational renal replacement therapy, but does it allow rational drug dosing?*. Critical Care Medicine 39:3, 602-603
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H.P. Kierdorf. (2011) Nierenersatztherapie in der Intensivmedizin. Der Nephrologe 6:2, 135-142
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Rolando Claure-Del Granado, Ravindra L. Mehta. (2011) Assessing and Delivering Dialysis Dose in Acute Kidney Injury. Seminars in Dialysis 24:2, 157-163
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Jorge Cerdá, Ashita Tolwani, Noel Gibney, Khajohn Tiranathanagul. (2011) Renal Replacement Therapy in Special Settings: Extracorporeal Support Devices in Liver Failure. Seminars in Dialysis 24:2, 197-202
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J. A. Roberts, C. M. J. Kirkpatrick, J. Lipman. (2011) Monte Carlo simulations: maximizing antibiotic pharmacokinetic data to optimize clinical practice for critically ill patients. Journal of Antimicrobial Chemotherapy 66:2, 227-231
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Andrew Lewington, Suren Kanagasundaram. (2011) Renal Association Clinical Practice Guidelines on Acute Kidney Injury. Nephron Clinical Practice 118:s1, c349-c390
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B. Agarwal, F. Kovari, R. Saha, S. Shaw, A. Davenport. (2011) Do Bicarbonate-Based Solutions for Continuous Renal Replacement Therapy Offer Better Control of Metabolic Acidosis than Lactate-Containing Fluids?. Nephron Clinical Practice 118:4, c392-c398
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John R Prowle, Antoine Schneider, Rinaldo Bellomo. (2011) Clinical review: Optimal dose of continuous renal replacement therapy in acute kidney injury. Critical Care 15:2, 207
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G. R. Hetzel, M. Schmitz, H. Wissing, W. Ries, G. Schott, P. J. Heering, F. Isgro, A. Kribben, R. Himmele, B. Grabensee, L. C. Rump. (2011) Regional citrate versus systemic heparin for anticoagulation in critically ill patients on continuous venovenous haemofiltration: a prospective randomized multicentre trial. Nephrology Dialysis Transplantation 26:1, 232-239
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Shaikh A. Nurmohamed, Borefore P. Jallah, Marc G. Vervloet, Albertus Beishuizen, A. B. Johan Groeneveld. (2011) Predilution versus Postdilution Continuous Venovenous Hemofiltration: No Effect on Filter Life and Azotemic Control in Critically Ill Patients on Heparin. ASAIO Journal 57:1, 48-52
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Graeme MacLaren. (2011) Distinction between induction and maintenance dosing in continuous renal replacement therapy. Critical Care 15:2, 419
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Se Jin Park, Jae Il Shin. (2011) Overview of Pediatric Continuous Renal Replacement Therapy in Acute Kidney Injury. Journal of the Korean Society of Pediatric Nephrology 15:2, 107
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Jordan M. Symons, Stuart L. Goldstein. 2011. Pediatric Renal Replacement Therapy in the Intensive Care Unit. , 1036-1042.
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Hector R. Wong, Jeffrey E. Nowak, Stephen W. Standage, Cláudio Flauzino de Oliveira. 2011. Sepsis. , 1413-1429.
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Andrew Davenport. (2011) Dialytic Treatment for Septic Patients with Acute Kidney Injury. Kidney and Blood Pressure Research 34:4, 218-224
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Constantine J Karvellas, Maha R Farhat, Imran Sajjad, Simon S Mogensen, Alexander A Leung, Ron Wald, Sean M Bagshaw. (2011) A comparison of early versus late initiation of renal replacement therapy in critically ill patients with acute kidney injury: a systematic review and meta-analysis. Critical Care 15:1, R72
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Hiroyuki Hirasawa. (2011) Recent Progress in the Elucidation of Pathophysiology and Countermeasure with CHDF on Severe Sepsis / Septic Shock. Nihon Kyukyu Igakukai Zasshi 22:3, 85-116
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R. Jacobs, P.M. Honore, O. Joannes-Boyau, W. Boer, J. De Regt, E. De Waele, V. Collin, H.D. Spapen. (2011) Septic Acute Kidney Injury: The Culprit Is Inflammatory Apoptosis rather than Ischemic Necrosis. Blood Purification 32:4, 262-265
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Zhang Zhongheng, Xu Xiao, Zhu Hongyang. (2010) Intensive- vs less-intensive-dose continuous renal replacement therapy for the intensive care unit–related acute kidney injury: A meta-analysis and systematic review. Journal of Critical Care 25:4, 595-600
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A. Al-Chalabi, B. Kreymann, W. Huber. (2010) Leberunterstützungstherapien 2010. Intensivmedizin und Notfallmedizin 47:8, 576-581
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Pamela Fall, Harold M. Szerlip. (2010) Continuous Renal Replacement Therapy: Cause and Treatment of Electrolyte Complications. Seminars in Dialysis 23:6, 581-585
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Sean M. Bagshaw, Rinaldo Bellomo, Prasad Devarajan, Curtis Johnson, C. J. Karvellas, D. James Kutsiogiannis, Ravindra Mehta, Neesh Pannu, Adam Romanovsky, Geoffrey Sheinfeld, Samantha Taylor, Michael Zappitelli, R. T. Noel Gibney. (2010) Review article: Renal support in critical illness. Canadian Journal of Anesthesia/Journal canadien d'anesthésie 57:11, 999-1013
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C. Y. Chionh, C. Ronco, F. O. Finkelstein, S. S. Soni, D. N. Cruz. (2010) Acute peritoneal dialysis: what is the 'adequate' dose for acute kidney injury?. Nephrology Dialysis Transplantation 25:10, 3155-3160
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P.J. Heering, M. Schmitz. (2010) Akutes Nierenversagen auf der Intensivstation. Intensivmedizin und Notfallmedizin 47:6, 429-433
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N. Lameire, J. Floege, D. C. Wheeler. (2010) The five most cited NDT papers from 2005 to 2009. Nephrology Dialysis Transplantation 25:9, 2825-2831
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John R. Prowle, Rinaldo Bellomo. (2010) Continuous renal replacement therapy: recent advances and future research. Nature Reviews Nephrology 6:9, 521-529
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Steven G. Coca. (2010) Acute Kidney Injury in Elderly Persons. American Journal of Kidney Diseases 56:1, 122-131
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Edward T. Casey, Bhanu P. Gupta, Patricia J. Erwin, Victor M. Montori, M. Hassan Murad. (2010) The dose of continuous renal replacement therapy for acute renal failure: a systematic review and meta-analysis. Renal Failure 32:5, 555-561
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Helmut Schiffl. (2010) The dark side of high-intensity renal replacement therapy of acute kidney injury in critically ill patients. International Urology and Nephrology 42:2, 435-440
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M. Bernhard, G. Marx, K. Weismüller, C. Lichtenstern, K. Mayer, F.M. Brunkhorst, M.A. Weigand. (2010) Ergebnisse intensivmedizinischer Studien des Jahres 2009. Der Anaesthesist 59:5, 453-476
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John A. Kellum, Claudio Ronco. (2010) Dialysis: Results of RENAL—what is the optimal CRRT target dose?. Nature Reviews Nephrology 6:4, 191-192
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K. Reinhart, F.M. Brunkhorst, H.-G. Bone, J. Bardutzky, C.-E. Dempfle, H. Forst, P. Gastmeier, H. Gerlach, M. Gründling, S. John, W. Kern, G. Kreymann, W. Krüger, P. Kujath, G. Marggraf, J. Martin, K. Mayer, A. Meier-Hellmann, M. Oppert, C. Putensen, M. Quintel, M. Ragaller, R. Rossaint, H. Seifert, C. Spies, F. Stüber, N. Weiler, A. Weimann, K. Werdan, T. Welte. (2010) Prävention, Diagnose, Therapie und Nachsorge der Sepsis. Der Anaesthesist 59:4, 347-370
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K. Reinhart, F.M. Brunkhorst, H.-G. Bone, J. Bardutzky, C.-E. Dempfle, H. Forst, P. Gastmeier, H. Gerlach, M. Gründling, S. John, W. Kern, G. Kreymann, W. Krüger, P. Kujath, G. Marggraf, J. Martin, K. Mayer, A. Meier-Hellmann, M. Oppert, C. Putensen, M. Quintel, M. Ragaller, R. Rossaint, H. Seifert, C. Spies, F. Stüber, N. Weiler, A. Weimann, K. Werdan, T. Welte. (2010) Prävention, Diagnose, Therapie und Nachsorge der Sepsis. Intensivmedizin und Notfallmedizin 47:3, 185-207
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Z. Ricci, D. N. Cruz, C. Ronco. (2010) Intensive care. Nephrology Dialysis Transplantation 25:3, 678-683
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Ryan Van Wert, Jan O. Friedrich, Damon C. Scales, Ron Wald, Neill K. J. Adhikari. (2010) High-dose renal replacement therapy for acute kidney injury: Systematic review and meta-analysis. Critical Care Medicine1
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Josée Bouchard, Etienne Macedo, Ravindra L. Mehta. (2010) Dosing of Renal Replacement Therapy in Acute Kidney Injury: Lessons Learned From Clinical Trials. American Journal of Kidney Diseases 55:3, 570-579
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Olivier Joannes-Boyau, Patrick M. Honoré, Willem Boer, Thomas Rose. (2010) Septic acute kidney injury and tubular apoptosis: never a Lone Ranger. Intensive Care Medicine 36:3, 385-388
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(2010) Intensity of Continuous Renal-Replacement Therapy. New England Journal of Medicine 362:5, 466-468
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John R. Prowle, Jorge E. Echeverri, E. Valentina Ligabo, Claudio Ronco, Rinaldo Bellomo. (2010) Fluid balance and acute kidney injury. Nature Reviews Nephrology 6:2, 107-115
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Andrew Davenport, Ken Farrington. (2010) Dialysis dose in acute kidney injury and chronic dialysis. The Lancet 375:9716, 705-706
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(2010) Journal Club. Kidney International 77:2, 81-82
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Hiromi Ono, Akira Takada, Makoto Sasaki, Yukie Nakatsuji, Ken Ishikawa, Mikiya Endo, Shoichi Chida. (2010) Pediatric cases of severe hemophagocytic lymphohistiocytosis improved by continuous hemodiafiltration. Nihon Shoni Jinzobyo Gakkai Zasshi 23:2, 214-218
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Kenichi Matsuda, Takeshi Moriguchi, Norikazu Harii. (2010) Nihon Shuchu Chiryo Igakukai zasshi 17:4, 479-489
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Palevsky, Paul M., . (2009) Renal Support in Acute Kidney Injury — How Much Is Enough?. New England Journal of Medicine 361:17, 1699-1701
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