International Criteria for Acute Kidney Injury: Advantages and Remaining Challenges


Nicholas Selby and colleagues describe how the definition of acute kidney injury brings opportunities and challenges in identifying patients at higher risk of adverse outcomes.


Published in the journal: . PLoS Med 13(9): e32767. doi:10.1371/journal.pmed.1002122
Category: Essay
doi: 10.1371/journal.pmed.1002122

Summary

Nicholas Selby and colleagues describe how the definition of acute kidney injury brings opportunities and challenges in identifying patients at higher risk of adverse outcomes.

Summary Points

  • Acute Kidney Injury (AKI) is defined using widely accepted international criteria that are based on changes in serum creatinine concentration and degree of oliguria.

  • AKI, when defined in this way, has a strong association with poor patient outcomes, including high mortality rates and longer hospital admissions with increased resource utilisation and subsequent chronic kidney disease.

  • The detection of AKI using current criteria can assist with AKI diagnosis and stratification of individual patient risk.

  • The diagnosis of AKI requires clinical judgement to integrate the definition of AKI with the clinical situation, to determine underlying cause of AKI, and to take account of factors that may affect performance of current definitions.

Introduction

Acute kidney injury (AKI), previously termed acute renal failure, has been the focus of increasing attention in the medical and popular press because of its high incidence and strong association with poor patient outcomes. Alarming figures include an incidence of between 5%–22% of hospital admissions and mortality rates that exceed 50% in those most severely affected [14]. The impact of AKI in low- and middle-income countries (LMICs) is equally stark: estimates of the global burden of AKI suggest that over 13 million people are affected annually and that AKI contributes to 1.7 million deaths per year [5]. There is also growing appreciation that renal function does not always recover following AKI and that AKI and chronic kidney disease (CKD) have a bidirectional relationship, with each increasing the risk of the other [6,7]. Such long-term health consequences coupled with prolonged hospital stays and considerable health care costs emphasise the huge societal impact of AKI [8,9]. These statistics have led to a number of calls to increase awareness of AKI and allocate more resources towards its prevention and treatment, including the International Society of Nephrology’s 0by25 campaign that aims to eliminate all preventable deaths related to AKI by 2025 [10,11].

Diagnosing Acute Kidney Injury

In part, increased awareness has sprung from the widespread adoption of international criteria for the definition of AKI that are based on changes in serum creatinine concentration and degree of oliguria (Table 1) [1214]. These criteria include small changes in serum creatinine alongside larger increments and receipt of renal replacement therapy (RRT). AKI therefore represents a wide spectrum of patients in comparison to historical concepts of acute renal failure. There is no doubt that this harmonisation in AKI definition has been a major step forward, replacing more than 35 previously used definitions in the medical literature [15] and focussing attention on opportunities of prevention and recognition that arise earlier in the natural history of AKI. A standardised definition is essential for robust epidemiological research to define the magnitude of the problem posed by AKI; a clear association between AKI defined in this way and patient outcomes has been consistently shown across a large number of studies [3,16]. The magnitude of this association is strong (e.g., odds ratios for mortality in the range of 5–10, [17]), is proportional to the severity of AKI, and remains remarkably consistent across every clinical condition and environment in which it has been studied. Similar high mortality and associations of AKI severity with outcomes are also seen in data from LMICs, despite the relative paucity of studies and the many differences in AKI epidemiology in these settings [18]. These findings have been extremely important in highlighting the challenges posed by AKI much more widely, as is necessary with the majority of AKI care delivered by non-nephrologists [1]. AKI has now become a term that is widely understood in clinical discussions, and the criteria provide a structure for education and guidelines, describing the severity of AKI as well as just its presence. Whilst a standardised definition brings advantages, it also brings challenges when applied to the syndrome of AKI to clinical practice. Although some may take these challenges as reason not to use current AKI classification outside of epidemiological research, we would argue that such an approach would restrict the benefits that a standardised definition of AKI brings. Here, we discuss the practical considerations that are essential to consider when doing so.

Tab. 1. KDIGO (Kidney Disease: Improving Global Outcomes) criteria for classification of acute kidney injury [14].
KDIGO (Kidney Disease: Improving Global Outcomes) criteria for classification of acute kidney injury [<em class=&quot;ref&quot;>14</em>].
Both serum creatinine and urine output criteria should be applied, and the AKI stage should be taken as whichever is the higher.

Challenges of Applying AKI Diagnostic Criteria in Clinical Practice

Aetiology, Baseline Creatinine, and Preexisting CKD

Classifying a patient with AKI should not detract from identification of the underlying cause; whilst it may be obvious that AKI is heterogeneous and that different aetiologies require distinct therapeutic approaches, AKI aetiology is not part of current AKI definitions. Use of a standard definition may therefore create the false impression that all cases of AKI are similar and can be managed in the same way, which must be avoided. This argument can be extended to include consideration of the clinical context in which AKI occurs and its relationship to outcomes: for example, AKI in the setting of sepsis worsens prognosis; urological AKI (with a higher proportion of obstructive causes) has the opposite effect [19].

As AKI is defined on an individual basis with respect to baseline serum creatinine value, choice of different baseline values can have a significant effect on the sensitivity and specificity of AKI criteria [20,21]. In addition, a baseline serum creatinine may not always be available in clinical practice. On a case-by-case basis, this can usually be resolved by clinician interpretation of serial creatinine results or an early repeat measurement to determine rate of change. The issue has more relevance to database studies or the development of electronic detection and alerting systems, where there is a need for greater standardisation of definitions for baseline creatinine [22,23].

Interpreting AKI criteria can also be more challenging in patients with preexisting CKD. Higher baseline creatinine values mean that small changes (e.g., rises of 26.5 μmol/l or 0.3 mg/dl) in serum creatinine concentration might represent laboratory or biological variation rather than a true change in renal function [24]; conversely, reduced renal reserve in individuals with CKD confers increased vulnerability [25]. Furthermore, the combination of a threshold value and percentage changes in serum creatinine to describe AKI stage 3 somewhat reduces the gradated association of AKI severity with mortality in those with higher baseline serum creatinine values [1,20]. Whilst some have advocated alternate classifications of AKI using only absolute changes in serum creatinine, there is insufficient evidence to recommend such approaches currently.

Should Small Creatinine Changes Be Included?

There have been concerns from some quarters that the inclusion of relatively small increases in serum creatinine may result in overdiagnosis, labelling patients with AKI who actually have clinically insignificant biochemical changes and risking exposure to at best unnecessary and at worst potentially harmful treatment [26]. It is true that small changes in serum creatinine concentration may not always represent clinically meaningful reductions in glomerular filtration rate (GFR). There is both biological and laboratory variation in serum creatinine measurements; the former may result from changes in diet, creatinine generation, volume status, tubular secretion, and actions of certain medications, whilst the latter is more pronounced in patients with CKD and high baseline creatinine values [24]. However, inclusion of these smaller serum creatinine changes reflects their strong epidemiological associations with adverse outcomes, including mortality and long-term risk of CKD that persist even after adjustment for age and comorbidities [17,2734]. There are also data to show that the inclusion of small creatinine changes improves early diagnosis of AKI compared to previous criteria [35], in combination with education programmes [36] or if used to generate electronic alerts [37]. Small creatinine changes should not be ignored but rather integrated with the clinical picture, not only for AKI diagnosis but also to help gauge overall patient risk. There are examples of the latter: combining clinical risk factors for AKI with small creatinine changes produced a good predictive model for more severe AKI (stages 2 or 3) and the need for RRT and mortality, at least in an ICU setting [38]. Crucially however, the negative predictive value of this model was extremely high, with a more modest positive predictive value; not everyone with small creatinine changes subsequently experienced more severe AKI, but those with no creatinine changes and fewer risk factors were extremely unlikely to do so. Such approaches allow targeting of early AKI intervention and/or risk prevention.

Urine Output Criteria

Although less often utilised in epidemiological research and clinical practice, current AKI definitions also include urine output criteria. The importance of oliguria is supported by epidemiological studies showing associations between AKI diagnosed on urine output criteria and adverse outcomes, although mainly in critical care settings [39]. Oliguria does not occur at the same time as changes in serum creatinine, so use of urine output criteria may identify AKI earlier but also may select a different (additional) patient cohort from those with changes in serum creatinine [40]. How best to employ urine output criteria for the diagnosis of AKI outside critical care requires further study, as does consideration of potential unintended consequences (e.g., iatrogenic urinary tract sepsis resulting from increased rates of catheterisation).

Does Improved Diagnosis of AKI Matter?

International guidelines, including those from the National Institute for Health and Care Excellence [41], advocate that management of AKI is based around supportive care (correction and avoidance of hypovolaemia, prompt treatment of sepsis and shock, avoidance of medications that may cause or worsen AKI, appropriate investigation to determine aetiology, and timely referral of patients with need of specialist input), although the evidence to support the specific recommendations within guidelines is currently incomplete. Along with the lack of specific pharmacotherapies for AKI, this has led some to question the value of applying diagnostic criteria in clinical care. However, if the utilisation of the diagnostic criteria enables better recognition and improves early diagnosis, then this is a strong argument for their use. Whilst evidence for current AKI management strategies needs expansion, there are clear signals that failure to deliver a good standard of supportive care leads to poor outcomes; despite recent advances, we know that this still occurs commonly across a variety of health care systems [4248]. Efforts to address standards of care that are below the minimum recommendation of currently acceptable practice should not be controversial, and if linked to data collection to measure their effect, they will add to the current evidence base. Testing new approaches is important, as there have been reports of both successes and failures of quality improvement initiatives [4951]. The requirement for consistent measurement of incidence and outcomes becomes a further argument for adoption of standardised AKI diagnostic criteria. We are beginning to see more sophisticated measurement approaches—such as a national AKI registry, as proposed by the National Health Service (England) “Think Kidneys” programme [52]—and at the same time, it is vital that the causes and risk factors for AKI in LMICs are better studied to inform preventative and public health strategies [53].

Diagnosis of AKI in LMICs

The challenges of applying current AKI criteria in LMICs are very different and much more fundamental. They include limited laboratory resources coupled with logistical issues, preventing timely serum creatinine concentration measurement or even measurement at all; lack of availability of previous creatinine results; financial constraints, meaning that some patients can’t afford serial creatinine tests (upon which current criteria are based); and late presentation of patients to health care services, thereby reducing opportunities for early detection and prevention. Work is accelerating to address this—for example, a recent description of key areas of need along with practical suggestions for quality improvement [54]. The 0by25 programme also discusses a number of strategies, such as educational campaigns (including the promotion of urine output criteria to diagnose AKI) and use of inexpensive point-of-care testing [11]. Even the latter may not be straightforward—for example, point-of-care creatinine equipment at present requires an electrical power source that may prevent use in certain contexts. It remains to be seen as to whether the current diagnostic criteria for AKI need refinement to improve suitability for settings that are far removed from the developed countries in which they were first conceived. The challenges of tackling AKI in LMICs extend to public health, resource, and organisational issues that at present must take priority.

Future Directions and Developments

At present, we believe the advantages of using the current diagnostic criteria for AKI outweigh perceived disadvantages. However, serum creatinine concentration has a number of limitations as a biomarker of AKI, not least that it is affected by a number of factors other than renal function, the delay before it rises after renal injury, and that as a functional marker it does not provide information about the nature or aetiology of renal damage. These obvious deficiencies have driven extensive research activity to identify novel biomarkers for AKI, although none have yet found a place in clinical practice. There is increasing realisation that a “single-shot” diagnostic biomarker will not be identified, in part reflecting the heterogeneous nature of AKI. Future directions may include: better clinical targeting of biomarkers to phenotypes and/or aetiologies of AKI; the combination of functional and damage biomarkers; or a two-step process, the first highly sensitive but relatively nonspecific, followed by a second, more specific test to rule in the diagnosis [55,56]. Future advances in other diagnostic modalities such as imaging may also support biomarker development.

There are significant challenges to improving the recognition of AKI in resource-poor settings, and research is needed to not only to test the effectiveness of new approaches but also their feasibility and sustainability. Of relevance to all settings is the need to raise the awareness of AKI. This is not limited to health care workers but also must incorporate the public and patients, whose understanding of the role of kidneys and implications of kidney damage are currently low [11].

Conclusion

AKI is a major challenge to health care providers and clinicians. Current diagnostic criteria bring opportunities to identify patients at higher risk of adverse outcomes as well as providing a standardised and evidence-based approach to AKI recognition but require clinical interpretation for individual patient management. Whilst approaches to AKI are hugely different between developed and developing countries, the principles of AKI detection underpin efforts to improve delivery of AKI care as well methods to measure its impact and outcomes.


Zdroje

1. Selby NM, Crowley L, Fluck RJ, McIntyre CW, Monaghan J, Lawson N, et al. Use of electronic results reporting to diagnose and monitor AKI in hospitalized patients. Clin J Am Soc Nephrol. 2012;7(4):533–40. doi: 10.2215/CJN.08970911 22362062

2. Wang HE, Muntner P, Chertow GM, Warnock DG. Acute Kidney Injury and Mortality in Hospitalized Patients. Am J Nephrol. 2012;35(4):349–55. doi: 10.1159/000337487 22473149

3. Uchino S, Bellomo R, Goldsmith D, Bates S, Ronco C. An assessment of the RIFLE criteria for acute renal failure in hospitalized patients. Crit Care Med. 2006;34(7):1913–7. 16715038

4. Bagshaw SM, Uchino S, Bellomo R, Morimatsu H, Morgera S, Schetz M, et al. Septic Acute Kidney Injury in Critically Ill Patients: Clinical Characteristics and Outcomes. Clin J Am Soc Nephrol. 2007;2(3):431–9. 17699448

5. Lewington AJ, Cerda J, Mehta RL. Raising awareness of acute kidney injury: a global perspective of a silent killer. Kidney Int. 2013;84(3):457–67. doi: 10.1038/ki.2013.153 23636171

6. Coca SG, Yusuf B, Shlipak MG, Garg AX, Parikh CR. Long-term risk of mortality and other adverse outcomes after acute kidney injury: a systematic review and meta-analysis. Am J Kidney Dis. 2009;53(6):961–73. doi: 10.1053/j.ajkd.2008.11.034 19346042

7. Chawla LS, Eggers PW, Star RA, Kimmel PL. Acute kidney injury and chronic kidney disease as interconnected syndromes. N Engl J Med. 2014;371(1):58–66. doi: 10.1056/NEJMra1214243 24988558

8. Kerr M, Bedford M, Matthews B, O'Donoghue D. The economic impact of acute kidney injury in England. Nephrol Dial Transplant. 2014;29(7):1362–8. doi: 10.1093/ndt/gfu016 24753459

9. Kolhe NV, Eldehni MT, Selby NM, McIntyre CW. The reimbursement and cost of acute kidney injury: a UK hospital perspective. Nephron Clinical practice. 2014;126(1):51–6. doi: 10.1159/000358435 24514003

10. Li PK, Burdmann EA, Mehta RL, World Kidney Day Steering C. Acute kidney injury: global health alert. Curr Opin Nephrol Hypertens. 2013;22(3):253–8. doi: 10.1097/MNH.0b013e32836060be 24469006

11. Mehta RL, Cerda J, Burdmann EA, Tonelli M, Garcia-Garcia G, Jha V, et al. International Society of Nephrology's 0by25 initiative for acute kidney injury (zero preventable deaths by 2025): a human rights case for nephrology. Lancet. 2015;385(9987):2616–43. doi: 10.1016/S0140-6736(15)60126-X 25777661

12. Bellomo R, Ronco C, Kellum JA, Mehta RL, Palevsky P, Acute Dialysis Quality Initiative w. 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. Critical care. 2004;8(4):R204–12. 15312219

13. Mehta RL, Kellum JA, Shah SV, Molitoris BA, Ronco C, Warnock DG, et al. Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury. Crit Care. 2007;11(2):R31. 17331245

14. KDIGO AKI Work Group. Clinical Practice Guideline for Acute Kidney Injury. Kidney inter, Suppl. 2012;2(1):1–141.

15. Mehta RL, Chertow GM. Acute renal failure definitions and classification: time for change? J Am Soc Nephrol. 2003;14(8):2178–87. 12874474

16. Mehta RL, Pascual MT, Soroko S, Savage BR, Himmelfarb J, Ikizler TA, et al. Spectrum of acute renal failure in the intensive care unit: the PICARD experience. Kidney Int. 2004;66(4):1613–21. 15458458

17. Chertow GM, Burdick E, Honour M, Bonventre JV, Bates DW. Acute kidney injury, mortality, length of stay, and costs in hospitalized patients. J Am Soc Nephrol. 2005;16(11):3365–70. 16177006

18. Bagasha P, Nakwagala F, Kwizera A, Ssekasanvu E, Kalyesubula R. Acute kidney injury among adult patients with sepsis in a low-income country: clinical patterns and short-term outcomes. BMC Nephrol. 2015;16:4. doi: 10.1186/1471-2369-16-4 25592556

19. Caddeo G, Williams ST, McIntyre CW, Selby NM. Acute Kidney Injury in Urology Patients: Incidence, Causes and Outcomes. Nephro Urol Mon. 2013;5(5):955–61.

20. Lafrance JP, Miller DR. Defining acute kidney injury in database studies: the effects of varying the baseline kidney function assessment period and considering CKD status. Am J Kidney Dis. 2010;56(4):651–60. doi: 10.1053/j.ajkd.2010.05.011 20673605

21. Siew ED, Matheny ME, Ikizler TA, Lewis JB, Miller RA, Waitman LR, et al. Commonly used surrogates for baseline renal function affect the classification and prognosis of acute kidney injury. Kidney Int. 2010;77(6):536–42. doi: 10.1038/ki.2009.479 20042998

22. Selby NM. Electronic alerts for acute kidney injury. Curr Opin Nephrol Hypertens. 2013;22(6):637–42. doi: 10.1097/MNH.0b013e328365ae84 24100217

23. Selby NM, Hill R, Fluck RJ. Standardizing the Early Identification of AKI: The NHS England National Patient Safety Alert. Nephron. 2015;131(2):113–7. doi: 10.1159/000439146 26351847

24. Lin J, Fernandez H, Shashaty MG, Negoianu D, Testani JM, Berns JS, et al. False-Positive Rate of AKI Using Consensus Creatinine-Based Criteria. Clin J Am Soc Nephrol. 2015;10(10):1723–31. doi: 10.2215/CJN.02430315 26336912

25. Ishani A, Xue JL, Himmelfarb J, Eggers PW, Kimmel PL, Molitoris BA, et al. Acute Kidney Injury Increases Risk of ESRD among Elderly. J Am Soc Nephrol. 2009;20(1):223–8. doi: 10.1681/ASN.2007080837 19020007

26. Palevsky PM, Liu KD, Brophy PD, Chawla LS, Parikh CR, Thakar CV, et al. KDOQI US Commentary on the 2012 KDIGO Clinical Practice Guideline for Acute Kidney Injury. American Journal of Kidney Diseases. 2013;61(5):649–72. doi: 10.1053/j.ajkd.2013.02.349 23499048

27. Heung M, Steffick DE, Zivin K, Gillespie BW, Banerjee T, Hsu CY, et al. Acute Kidney Injury Recovery Pattern and Subsequent Risk of CKD: An Analysis of Veterans Health Administration Data. Am J Kidney Dis. 2016;67(5):742–52. doi: 10.1053/j.ajkd.2015.10.019 26690912

28. Uchino S, Bellomo R, Bagshaw SM, Goldsmith D. Transient azotaemia is associated with a high risk of death in hospitalized patients. Nephrol Dial Transplant. 2010;25(6):1833–9. doi: 10.1093/ndt/gfp624 20054022

29. Gottlieb SS, Abraham W, Butler J, Forman DE, Loh E, Massie BM, et al. The prognostic importance of different definitions of worsening renal function in congestive heart failure. J Card Fail. 2002;8(3):136–41. 12140805

30. Kork F, Balzer F, Spies CD, Wernecke KD, Ginde AA, Jankowski J, et al. Minor Postoperative Increases of Creatinine Are Associated with Higher Mortality and Longer Hospital Length of Stay in Surgical Patients. Anesthesiology. 2015;123(6):1301–11. doi: 10.1097/ALN.0000000000000891 26492475

31. Lassnigg A, Schmidlin D, Mouhieddine M, Bachmann LM, Druml W, Bauer P, et al. Minimal changes of serum creatinine predict prognosis in patients after cardiothoracic surgery: a prospective cohort study. J Am Soc Nephrol. 2004;15(6):1597–605. 15153571

32. Loef BG, Epema AH, Smilde TD, Henning RH, Ebels T, Navis G, et al. Immediate postoperative renal function deterioration in cardiac surgical patients predicts in-hospital mortality and long-term survival. J Am Soc Nephrol. 2005;16(1):195–200. 15563558

33. Newsome BB, Warnock DG, McClellan WM, Herzog CA, Kiefe CI, Eggers PW, et al. Long-term risk of mortality and end-stage renal disease among the elderly after small increases in serum creatinine level during hospitalization for acute myocardial infarction. Arch Intern Med. 2008;168(6):609–16. doi: 10.1001/archinte.168.6.609 18362253

34. Smith GL, Vaccarino V, Kosiborod M, Lichtman JH, Cheng S, Watnick SG, et al. Worsening renal function: what is a clinically meaningful change in creatinine during hospitalization with heart failure? J Card Fail. 2003;9(1):13–25. 12612868

35. Mallhi TH, Khan AH, Sarriff A, Adnan AS, Khan YH, Jummaat F. Defining acute kidney injury in dengue viral infection by conventional and novel classification systems (AKIN and RIFLE): a comparative analysis. Postgrad Med J. 2016;92(1084):78–86. doi: 10.1136/postgradmedj-2015-133582 26729887

36. Brady P, Gorham J, Kosti A, Seligman W, Courtney A, Mazan K, et al. "SHOUT" to improve the quality of care delivered to patients with acute kidney injury at Great Western Hospital. BMJ Qual Improv Rep. 2015;4(1).

37. Colpaert K, Hoste EA, Steurbaut K, Benoit D, Hoecke SV, Turck FD, et al. Impact of real-time electronic alerting of acute kidney injury on therapeutic intervention and progression of RIFLE class*. Crit Care Med. 2012;40(4):1164–70. doi: 10.1097/CCM.0b013e3182387a6b 22067631

38. Cruz DN, Ferrer-Nadal A, Piccinni P, Goldstein SL, Chawla LS, Alessandri E, et al. Utilization of small changes in serum creatinine with clinical risk factors to assess the risk of AKI in critically lll adults. Clin J Am Soc Nephrol. 2014;9(4):663–72. doi: 10.2215/CJN.05190513 24677553

39. Kellum JA. Diagnostic Criteria for Acute Kidney Injury: Present and Future. Crit Care Clin. 2015;31(4):621–32. doi: 10.1016/j.ccc.2015.06.001 26410133

40. Macedo E, Malhotra R, Bouchard J, Wynn SK, Mehta RL. Oliguria is an early predictor of higher mortality in critically ill patients. Kidney Int. 2011;80(7):760–7. doi: 10.1038/ki.2011.150 21716258

41. Ftouh S, Thomas M, Acute Kidney Injury Guideline Development G. Acute kidney injury: summary of NICE guidance. BMJ. 2013;347:f4930. doi: 10.1136/bmj.f4930 23985310

42. NCEPOD. Acute Kidney Injury: Adding Insult to Injury. National Confidential Enquiry into Patient Outcomes and Death, 2009. http://www.ncepod.org.uk/2009aki.html

43. James MT, Wald R, Bell CM, Tonelli M, Hemmelgarn BR, Waikar SS, et al. Weekend hospital admission, acute kidney injury, and mortality. J Am Soc Nephrol. 2010;21(5):845–51. doi: 10.1681/ASN.2009070682 20395373

44. Mehta RL, McDonald B, Gabbai F, Pahl M, Farkas A, Pascual MT, et al. Nephrology consultation in acute renal failure: does timing matter? Am J Med. 2002;113(6):456–61. 12427493

45. Stevens PE, Tamimi NA, Al-Hasani MK, Mikhail AI, Kearney E, Lapworth R, et al. Non-specialist management of acute renal failure. QJM. 2001;94(10):533–40. 11588212

46. Cox ZL, McCoy AB, Matheny ME, Bhave G, Peterson NB, Siew ED, et al. Adverse Drug Events during AKI and Its Recovery. Clin J Am Soc Nephrol. 2013;8(7):1070–8 doi: 10.2215/CJN.11921112 23539228

47. Aitken E, Carruthers C, Gall L, Kerr L, Geddes C, Kingsmore D. Acute kidney injury: outcomes and quality of care. QJM. 2013;106(4):323–32. doi: 10.1093/qjmed/hcs237 23345468

48. Meran S, Wonnacott A, Amphlett B, Phillips A. How good are we at managing acute kidney injury in hospital? Clin Kidney J. 2014;7(2):144–50. doi: 10.1093/ckj/sfu010 25852863

49. Goldstein SL, Kirkendall E, Nguyen H, Schaffzin JK, Bucuvalas J, Bracke T, et al. Electronic Health Record Identification of Nephrotoxin Exposure and Associated Acute Kidney Injury. Pediatrics. 2013;132(3):e756–e67. doi: 10.1542/peds.2013-0794 23940245

50. Selby NM, Kolhe NV. Care Bundles for Acute Kidney Injury: Do They Work? Nephron. 2016. E-pub ahead of print. doi: 10.1159/000447758

51. Wilson FP, Shashaty M, Testani J, Aqeel I, Borovskiy Y, Ellenberg SS, et al. Automated, electronic alerts for acute kidney injury: a single-blind, parallel-group, randomised controlled trial. Lancet. 2015;385(9981):1966–1974. doi: 10.1016/S0140-6736(15)60266-5 25726515

52. NHS England. Acute Kidney Injury (AKI) Programme, www.thinkkidneys.nhs.uk 2014. http://www.england.nhs.uk/ourwork/patientsafety/akiprogramme/.

53. Susantitaphong P, Cruz DN, Cerda J, Abulfaraj M, Alqahtani F, Koulouridis I, et al. World incidence of AKI: a meta-analysis. Clin J Am Soc Nephrol. 2013;8(9):1482–93. doi: 10.2215/CJN.00710113 23744003

54. Lunyera J, Kilonzo K, Lewington A, Yeates K, Finkelstein FO. Acute Kidney Injury in Low-Resource Settings: Barriers to Diagnosis, Awareness, and Treatment and Strategies to Overcome These Barriers. Am J Kidney Dis. 2016;67(6):834–40. doi: 10.1053/j.ajkd.2015.12.018 26830256

55. Menon S, Goldstein SL, Mottes T, Fei L, Kaddourah A, Terrell T, et al. Urinary biomarker incorporation into the renal angina index early in intensive care unit admission optimizes acute kidney injury prediction in critically ill children: a prospective cohort study. Nephrol Dial Transplant. 2016;31(4):586–94. doi: 10.1093/ndt/gfv457 26908772

56. McCullough PA, Bouchard J, Waikar SS, Siew ED, Endre ZH, Goldstein SL, et al. Implementation of novel biomarkers in the diagnosis, prognosis, and management of acute kidney injury: executive summary from the tenth consensus conference of the Acute Dialysis Quality Initiative (ADQI). Contrib Nephrol. 2013;182:5–12. doi: 10.1159/000349962 23689652

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