A European Renal Best Practice (ERBP) position statement on the Kidney Disease Improving Global Outcomes (KDIGO) Clinical Practice Guidelines on Acute Kidney Injury: Part 1: definitions, conservative management and contrast-induced nephropathy

Abstract

The broad clinical syndrome of acute kidney injury (AKI) encompasses various aetiologies, including specific kidney diseases (e.g. acute interstitial nephritis), non-specific conditions (e.g. renal ischaemia) as well as extrarenal pathology (e.g. post-renal obstruction). AKI is a serious condition that affects kidney structure and function acutely, but also in the long term. Recent epidemiological evidence supports the notion that even mild, reversible AKI conveys the risk of persistent tissue damage, and severe AKI can be accompanied by an irreversible decline of kidney function and progression to end-stage kidney failure [1–3]. The Kidney Disease Improving Global Outcomes (KDIGO) Clinical Practice Guidelines for AKI [4] were designed to systematically compile information on this topic by experts in the field. These guidelines are based on the systematic review of relevant trials published before February 2011. Nevertheless, for many sections of the guidelines, appropriate supporting evidence is lacking in the literature. As a consequence, variations in practice will inevitably occur when clinicians take into account the needs of individual patients, available resources and limitations unique to a region, an institution or type of practice. Therefore, in line with its philosophy [5], the European Renal Best Practice (ERBP) wanted to issue a position statement on these guidelines. A working group was established to produce guidance from the European nephrology perspective, based on the compiled evidence as presented, with an update of the literature up to March 2012, following the methodology as explained in the ERBP instructions to authors [6]. The present document will deal with the diagnosis and prevention of AKI, and contrast-induced nephropathy (CIN) (Sections 1–4 of the KDIGO document), and other chapters will be discussed in a separate position statement. As a general rule, we will only mention those guideline statements of the KDIGO document that we have amended, even when the change is small. If a KDIGO recommendation is not repeated, it can be considered as endorsed by ERBP as is, unless specifically stated otherwise. 1.1.1 We recommend using a uniform definition of AKI, based on urinary output and on changes in serum creatinine (SCr) level. It is important that both criteria are taken into account. (1C) 1.1.2 We recommend diagnosing and indicating the severity of AKI according to the criteria in the table below: (ungraded statement) Serum creatinine increased 1.5–1.9 times baseline Serum creatinine increase >0.3mg/dl (26.5 µmol/l) Urinary ouotput < 0.5ml/kg/h during a 6 hour block Serum creatinine increase 2.0–2.9 times baseline Urinary output <0.5ml/kg/h during two 6 hour blocks Serum creatinine increase >3 times baseline Serum creatinine increases to >4.0mg/dl (353 µmol/l) Initiation of renal replacement therapy Urinary output <0.3ml/kg/h during more than 24 hours Anuria for more than 12 hours The ERBP workgroup stresses that this classification should be considered as a severity scoring rather than a nosological definition 1.1.2a We recommend using the first documented serum creatinine value of the episode as ‘baseline’, rather than historical creatinines or a calculated value based on a presumed glomerular filtration rate (GFR) of 75 mL/min. (1C) 1.1.2b We suggest using ‘shift-based’ calculation of the urinary output criteria, especially in patients without a bladder catheter (1C). We recommend to use the ideal weight rather than the true weight in calculating the diuresis in mL/min/kg. (Ungraded statement) 1.1.3 The cause of AKI should be determined whenever possible. As a minimal work-up, the presence of hypovolaemia, post-renal causes, low cardiac output, use of nephrotoxic agents, acute glomerulonephritis and renal micro-angiopathy as underlying contributors to AKI should be evaluated. (Ungraded statement) In the past, a myriad of definitions for acute renal failure and AKI existed in parallel, making comparison of results difficult. In the KDIGO Clinical Practice Guidelines for AKI, definition and staging of AKI is based on a combination of the Risk, Injury, Failure; Loss, End-Stage Renal Disease (RIFLE) [7] and Acute Kidney Injury Network (AKIN) criteria [8]. Both criteria rely on GFR, and its proxy serum creatinine, and urinary output as the most useful overall indices of acute changes of kidney function. Changes in serum creatinine concentration and/or urine output are used as surrogates for acute changes in kidney function. The recommended diagnostic criteria establish a solid ground for standardized AKI assessment and classification in everyday clinical practice as well as in research conditions [9, 10]. As such, ERBP considers them as a good starting point towards a more standardized approach to AKI definition and particularly for the assessment of the predictive power of AKI with respect to overall and renal outcome (staging of severity) [11]. However, ERBP wants to update and fin