Acute Kidney Injury – Scientific Evidence Driving Change in Patient Management Guest Editors
Rinaldo Bellomo, Heidelberg, Vic. Joseph Bonventre, Boston, Mass.
19 figures, 4 in color, and 12 tables, 2008
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Vol. 109, No. 4, 2008
Contents
c181 Introduction Bellomo, R. (Heidelberg, Vic.); Bonventre, J. (Boston, Mass.)
e109 Antioxidants. Do They Have a Place in the Prevention
or Therapy of Acute Kidney Injury?
c182 Definition and Classification of Acute Kidney Injury Kellum, J.A. (Pittsburgh, Pa.); Bellomo, R. (Melbourne, Vic.); Ronco, C. (Vicenza) c188 The Epidemiology of Severe Acute Kidney Injury:
p80 Distant-Organ Changes after Acute Kidney Injury Feltes, C.M.; Van Eyk, J.; Rabb, H. (Baltimore, Md.)
from BEST to PICARD, in Acute Kidney Injury: New Concepts
p85 Emerging Therapies for Extracorporeal Support Bouchard, J.; Khosla, N.; Mehta, R.L. (San Diego, Calif.)
Pisoni, R.; Wille, K.M.; Tolwani, A.J. (Birmingham, Ala.)
e118 The Bioartificial Kidney and Bioengineered Membranes in Acute Kidney Injury
c192 Biomarkers for the Diagnosis of Acute Kidney Injury Waikar, S.S.; Bonventre, J.V. (Boston, Mass.) c198 Imaging Techniques in Acute Kidney Injury Sharfuddin, A.A.; Sandoval, R.M.; Molitoris, B.A. (Indianapolis, Ind.)
Ding, F. (Ann Arbor, Mich./Shanghai); Humes, H.D. (Ann Arbor, Mich.) c217 Outcome Prediction for Patients with Acute Kidney
Injury Uchino, S. (Tokyo)
p55 Cardiac Surgery-Associated Acute Kidney Injury:
Putting Together the Pieces of the Puzzle Shaw, A.; Swaminathan, M.; Stafford-Smith, M. (Durham, N.C.) e95
Koyner, J.L. (Chicago, Ill.); Sher Ali, R. (New York, N.Y.); Murray, P.T. (Chicago, Ill.)
c224 Acute Kidney Injury: New Concepts, Renal Recovery Bell, M. (Solna/Stockholm)
Septic Acute Kidney Injury: New Concepts Bellomo, R.; Wan, L.; Langenberg, C.; May, C. (Melbourne, Vic.)
p61 Radiocontrast-Induced Acute Kidney Injury McCullough, P.A. (Royal Oak, Mich.) p73 Acute Kidney Injury: New Concepts. Hepatorenal
Syndrome: The Role of Vasopressors Moreau, R.; Lebrec, D. (Clichy) e102 Inflammation in Acute Kidney Injury Kinsey, G.R.; Li, L.; Okusa, M.D. (Charlottesville, Va.) c206 New Insights on Intravenous Fluids, Diuretics and
Acute Kidney Injury Townsend, D.R.; Bagshaw, S.M. (Edmonton, Alta.)
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c229 Author Index Vol. 109, No. 4, 2008 c230 Subject Index Vol. 109, No. 4, 2008
c231 Author Index Vol. 109, 2008 c234 Subject Index Vol. 109, 2008 after c236 Contents Vol. 109, 2008
Nephron Clin Pract 2008;109:c181 DOI: 10.1159/000142925
Published online: September 18, 2008
Introduction
The field of acute nephrology has seen significant changes in recent times. These changes go to the core of many significant clinical issues. They affect the definition and classification of acute kidney dysfunction, our understanding of its epidemiology, our ability to make earlier diagnoses, our ability to use novel imaging modalities to understand its pathogenesis, and our insight into why acute kidney injury (AKI) might occur under different clinical circumstances including cardiac surgery, septic shock, radiocontrast agent exposure, liver disease and various toxins. Advances in our understanding have affected our strategies for intervention which have been directed toward the modulation of inflammation, improvement in fluid therapy, administration of antioxidants, optimization of dialytic technique, and development of new dialytic paradigms with the introduction of bio-assist devices. Finally, new pathophysiological insights have enabled us to better appreciate how to predict outcome in these patients as well as understand the significance of renal recovery and the factors that modulate it. In this issue of Nephron, we have gathered experts in each of the above areas of acute nephrology to offer readers a condensation of many major advances in this field. The title itself summarizes an important change from the concept of acute renal failure to that of acute kidney injury. This is a key conceptual change [1] supported by consensus opinion [2, 3]. This term has been proposed and accepted because it deals with the full spectrum of the syndrome of kidney involvement in a variety of acute diseases and emphasizes that even minor changes in renal function which may be dismissed clinically carry an independent association with an increased risk of mortality [2, 3]. Using this conceptual framework, new definitions © 2008 S. Karger AG, Basel 1660–2110/08/1094–0181$24.50/0 Fax +41 61 306 12 34 E-Mail
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and classifications have been developed and one, the RIFLE classification, has now been studied and found robust in 1250,000 patients. Armed with a definition and a classification system and with the understanding that even minor subclinical injury to the kidney may matter, we have been able to emphasize the need to develop early biomarkers of such injury [4] and appreciate the role of inflammation [5] in inducing injury. Through sufficiently early diagnosis, a better classification system and a clearer understanding of the pathogenesis, these steps promise, for the first time in a long while, to deliver novel and effective therapies for patients. Clinicians need to keep abreast of these evolutions if they wish to continue to deliver the best care to their patients. We believe this issue of Nephron goes a long way in making this possible. Rinaldo Bellomo, Heidelberg, Vic. Joseph Bonventre, Boston, Mass.
References 1 Kellum JA: Acute kidney injury. Crit Care Med 2008; 36(suppl):S141– S145. 2 Bellomo R, Ronco C, Kellum JA, et al: Acute renal failure: definition, outcome measures, animal models, fluid therapy and information technology needs. The Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Crit Care 2004; 8: R204–R212. 3 Mehta RL, Kellum JA, Shah SV, et al: Acute kidney injury network: report of an initiative to improve outcome in acute kidney injury. Crit Care 2007;11:R31. 4 Vaidya VS, Ferguson MA, Bonventre JV: Biomarkers of acute kidney injury. Annu Rev Pharmacol Toxicol 2008;48:463–493. 5 Bonventre JV: Pathophysiology of acute kidney injury: roles of potential inhibitors of inflammation. Contrib Nephrol. Basel, Karger, 2007, vol 156, pp 39–46.
Prof. Rinaldo Bellomo Department of Intensive Care Austin Hospital Heidelberg, Vic. 3084 (Australia) Tel. +61 3 9496 5992, Fax +61 3 9496 3932, E-Mail
[email protected] Nephron Clin Pract 2008;109:c182–c187 DOI: 10.1159/000142926
Published online: September 18, 2008
Definition and Classification of Acute Kidney Injury John A. Kellum a Rinaldo Bellomo b Claudio Ronco c a
The Clinical Research, Investigation, and Systems Modeling of Acute illness (CRISMA) Laboratory, Department of Critical Care Medicine, University of Pittsburgh, Pittsburgh, Pa., USA; b Department of Intensive Care and Department of Medicine, Austin Hospital and University of Melbourne, Heidelberg, Melbourne, Vic., Australia; c Department of Nephrology, Ospedale San Bortolo, Vicenza, Italy
Key Words Acute kidney injury ⴢ Acute renal failure ⴢ RIFLE criteria ⴢ Epidemiology ⴢ Hemodialysis ⴢ Hemofiltration ⴢ Kidney disease ⴢ Critical illness
Abstract Changes in urine output and glomerular filtration rate are neither necessary nor sufficient for the diagnosis of renal pathology. Yet no simple alternative for the diagnosis currently exists. Until recently, there has been no consensus as to diagnostic criteria or clinical definition of acute renal failure. Depending on the definition used, acute renal failure has been reported to affect from 1 to 25% of ICU patients and has led to mortality rates from 15 to 60%. The RIFLE criteria were developed to standardize the diagnosis of acute renal failure and in the process the term acute kidney injury (AKI) has been proposed to encompass the entire spectrum of the syndrome from minor changes in renal function to requirement for renal replacement therapy. Thus, AKI is not acute renal failure but a more general description. Small changes in kidney function in hospitalized patients are important and are associated with significant changes in short and possibly long-term outcomes. The RIFLE criteria provide a uniform definition of AKI and have now been validated in numerous studies. Copyright © 2008 S. Karger AG, Basel
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Acute Organ Distress
The presence of, or risk for, acute dysfunction of vital organs is a defining aspect of critical illness. Indeed, the purpose of critical care is to provide life-sustaining organ support (e.g. mechanical ventilation) and to rapidly intervene to save organ function (e.g. opening of coronary arteries). For most vital organs, injury and reduced function are tightly correlated. For some organs injury can be severe before decreased function is apparent – for example as much as 80% of the liver can be damaged be before clinical symptoms are manifest. For other organs dysfunction may be greater than what is produced by irreversible injury (e.g. stunned or hibernating myocardium). However, the kidney may be unique in that the earliest clinical manifestations of injury are also consistent with ‘perfect’ function. Under stress, for example that occurs with acute hemorrhage, a perfectly functioning kidney responds to the fall in blood pressure and rise in vasopressin by reducing urine output and glomerular filtration rate (GFR). Indeed, a ‘normal’ urine output and GFR in the face of volume depletion could only be viewed as renal dysfunction. Thus, changes in urine output and GFR, while they are the hallmarks of kidney failure, are neither necessary nor sufficient for the diagnosis of renal pathology [1, 2]. John A. Kellum, MD Department of Critical Care Medicine, University of Pittsburgh, School of Medicine Room 608 Scaife Hall, 3550 Terrace Street Pittsburgh, PA 15261 (USA) Tel. +1 412 647 6966, Fax +1 412 647 8060, E-Mail
[email protected] Screat criteria* Risk
Urine output criteria
Increased creatinine ×1.5 x1.5 (Or (or increase Increasecreatine creatineof of ≥0.3mg/dl) ≥0.3 mg/dl)
UO
