iradef

Arab Journal of Nephrology and Transplantation

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Arab Journal of Nephrology and Transplantation. 2013 Sep;6(3):145-52

Review AJNT

AbstractIntroduction: It is now evident that even minimal reductions in glomerular filtration rate (GFR) are associated with a dramatic increase in mortality. The term acute kidney injury (AKI) describes an acute fall of estimated GFR (eGFR) and allows patient stratification based on AKI severity.

Review: The Risk, Injury, Failure, Loss and End-stage kidney disease (RIFLE) system defines AKI by a change in serum creatinine (SCr) level or eGFR from a baseline value, and urine output per kilogram of body weight over a specified time period. The Acute Kidney Injury Network (AKIN) definition was based on the RIFLE system but added an absolute change in SCr of ≥0.3 mg/dL, omitted eGFR criteria and included a time constraint of 48 hours. The AKIN system also omitted the stages “Loss” and “End-stage” and allocated patients who needed acute dialysis to stage-3. The most recent Kidney Disease Improving Global Outcomes (KDIGO) guidelines retained the AKIN staging criteria but allowed a time frame of seven days for a 50% increase in SCr. The KDIGO criteria do not rely on changes in GFR for staging except in children under the age of 18 years. AKI misclassification may result from the lack of a uniform approach to estimate baseline SCr and the changes in SCr concentrations resulting from acute severe illness and altered fluid balance. In addition, exact data on urine output are not always available resulting in underutilization of the urine output criteria.

Conclusion: The existing definitions of AKI rely on imperfect markers of renal function rather than direct measures of kidney damage, but remain an important diagnostic and prognostic tool.

Keywords: Acute Kidney Injury; AKIN; KDIGO; RIFLE

The authors declared no conflict of interest

IntroductionBefore 2004, the generic term acute renal failure (ARF) was used for an abrupt and sustained decrease in glomerular filtration rate (GFR) resulting in retention of nitrogenous (urea and creatinine) and non-nitrogenous waste products. Depending on the severity and duration of the renal dysfunction, their accumulation is accompanied by metabolic disturbances, such as metabolic acidosis and hyperkalemia, changes in body fluid balance, and by effects on many other organ systems [1].

The lack of a precise biochemical definition of ARF resulted in at least 35 definitions in the medical literature [2], which gave rise to a wide variation in reported incidence and clinical significance of ARF, impeded a meaningful comparison of studies that assess preventive and therapeutic strategies and made generalization of data generated from single center studies difficult and, finally, prevented patient stratification based on acute kidney injury (AKI) severity.

Furthermore, the conventional term ARF was often used in reference to the subset of critically ill patients, often admitted to the ICU, with a need for acute dialysis support. Because of accumulating evidence in the years 2004 - 2006, that even minimal increases in serum creatinine (SCr) are associated with a dramatic impact on the risk for mortality [3-6], the Acute Kidney Injury Network (AKIN) proposed to replace the term ARF by that of AKI [7].

AKI is thus not limited to ARF and is independent of the presence of underlying histopathological alterations or of the pattern of functional recovery. It is a broad clinical

The Definitions and Staging Systems of Acute Kidney Injury and Their Limitations in Practice

Norbert Lameire*

Former Chief of the Renal Division, University Hospital, Belgium

* Corresponding author; University Hospital; 185, De Pintelaan; 9000 Gent, Belgium; E. mail: [email protected]


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syndrome, at present defined by an acute fall of GFR as reflected by an acute rise of serum creatinine (SCr) and/or decline in urine output over a given time interval.

A traditional classification of AKI is based on various etiologies including pre-renal AKI, acute post-renal obstructive nephropathy and intrinsic acute kidney diseases, i.e. acute tubular necrosis (ATN), acute interstitial nephritis (AIN), and acute glomerular and renal vasculitis diseases. Of these, only “intrinsic” renal AKI represents ‘true kidney disease’ while pre-renal and most cases of post-renal AKI are the consequence of extra-renal diseases, leading to the decreased GFR. If these pre- and/or post-renal conditions persist, they will eventually evolve to renal cellular damage and to intrinsic renal disease. Because the manifestations and clinical consequences of AKI can be quite similar (even indistinguishable) regardless of whether the etiology is predominantly within the kidney or predominantly from outside stresses on the kidney, the syndrome of AKI encompasses both direct injury to the kidney as well as acute impairment of function.

Definition and staging of acute kidney injury (AKI)

RIFLEA broad consensus of experts assembled in The Acute Dialysis Quality Initiative (ADQI) group developed the Risk, Injury, Failure, Loss and End-stage kidney disease (RIFLE) system for diagnosis and classification of a broad range of acute impairments of kidney function [8]. In RIFLE, renal dysfunction is assessed by two parameters: a change in SCr level or estimated glomerular filtration rate (eGFR) from a baseline value, and urine output per kilogram of body weight over a specified time period. AKI stage is determined on the basis of the parameter that places the patient in the worst disease category.

Not unexpectedly, many studies in populations [9], hospitalized patients [6] as well as in critically ill patients [4, 10-12], from around the world have shown that AKI defined by RIFLE is associated with decreased survival and that increasing RIFLE stage leads to increased risk of death, a longer ICU and hospital stay, and a more limited renal recovery.

There are some inherent limitations of the RIFLE definition and classification, which are reflected in some variation in how the criteria are interpreted and used in the literature, like including use/non-use of urine output criteria, use of change in estimated GFR rather than change in SCr, and choice of a baseline SCr [13]. Given these limitations, the Acute Kidney Injury Network

(AKIN) working group modified some of the RIFLE criteria.

AKIN Although the diagnostic criteria for AKI and the staging system were based on the RIFLE criteria [7], a number of important modifications were added. First, the addition of an absolute change in serum creatinine of ≥0.3 mg/dL (≥26.4 µmol/L) is based on epidemiologic data demonstrating an 80 percent increase in mortality risk associated with these small changes [3, 5]. Second, the eGFR criteria and the stages “Loss” and “End-stage” were omitted. Third, the inclusion of a time constraint of 48 hours is based upon data that showed that poorer outcomes were associated when the rise in creatinine was observed within 24 to 48 hours [5, 14]. It should be remembered that the AKIN diagnostic criteria include both an absolute and a percentage change in SCr, to accommodate variations related to age, gender, and body mass index and to reduce the need for a baseline creatinine; on the other hand, they do require at least two creatinine values within 48 hours.

Fourth, AKI patients who need acute dialysis were automatically allocated to stage-3, regardless of the severity of their AKI.

Two additional caveats were proposed: the first is that the diagnostic criteria should be applied only after volume status had been optimized, and the second is that urinary tract obstruction needed to be excluded if oliguria was used as the sole diagnostic criterion.

At first sight, it is not clear whether the AKIN modifications to RIFLE have substantively changed the classification of patients with AKI or improved its ability to predict hospital mortality [15]. However, although the modifications may appear small, Joannidis et al [16] calculated that they translate into potentially important changes in the diagnosis and classification of AKI. In the multicenter simplified acute Physiology score (SAPs) 3 data base, and using both SCr levels and 24 h urine output data, in critically ill patients, AKI was classified using the AKIN and RIFLE criteria [16]. According to the calculations of Bagshaw, the same results were translated into an absolute 7% difference in AKI diagnosis between AKIN and RIFLE criteria. In total, 10.5% classified as having AKI by RIFLE criteria were missed by AKIN criteria; by contrast, RIFLE criteria missed only 3.5% classified as having AKI by AKIN criteria [17].


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Kidney Diseases: Improving Global Outcomes (KDIGO) Guidelines [18] Rationale for KDIGO AKI guidelines

In view of the universal importance of AKI, the absence of evidence-based clinical practice guidelines on this topic, and in accordance with its mission, Kidney Diseases - Improving Global Outcomes (KDIGO), realized that there is room for improving international cooperation in the development, dissemination, and implementation of clinical practice guidelines, also in the field of AKI. In addition, because two similar definitions based on SCr and urine output (RIFLE and AKIN) were proposed and validated, the KDIGO working group members concluded that there was a need for a single definition of AKI for practice, research, and public health. In addition, KDIGO felt that addressing the unique circumstances and needs of developing countries, especially in the detection of AKI in its early and potentially reversible stages to prevent its progression to end stage renal failure, is of paramount importance.

Brief discussion of the KDIGO guidelines

The KDIGO clinical practice guidelines included a revised definition of AKI while retaining the AKIN staging criteria (Table-1). In the KDIGO definition, the time frame for an absolute increase in SCr of 0.3 mg/dL (26.4 µmol/L) is retained from the AKIN definition (48 hours) while the time frame for a 50 percent increase in SCr is the seven days, as originally suggested by the RIFLE criteria. The KDIGO criteria only utilize changes in SCr and urine output, and not changes in GFR for staging, with the exception of children under the age of 18 years, for whom an acute decrease in estimated GFR to < 35 ml/min per 1.73m² is included in the criteria for stage-3 AKI [19]. As with the RIFLE and AKIN staging systems, patients should be classified according to criteria that result in the highest (i.e., most severe) stage of injury.

KDIGO made one additional change in the criteria for the sake of clarity and simplicity. For patients reaching Stage-3 by SCr >4.0 mg/dl (353.6 µmol/L), rather than require an acute increase of ≥0.5 mg/dl (44.2 µmol/L) over an unspecified time period, KDIGO instead requires that the patient first achieves the creatinine-based change specified in the definition, either ≥0.3 mg/dl (26.4 µmol/L) within a 48-hour time window or an increase of ≥1.5 times baseline. This change brings the definition and staging criteria to greater parity and simplifies the criteria. For example, if a patient shows an increase of SCr ≥0.3 mg/dl (26.4 µmol/L) within 48 hours and the absolute SCr increases to a level ≥4.0 mg/dl (354 µmol/L), this patient

should be classified a stage-3. It goes without saying that a patient developing acute on chronic kidney injury will more rapidly arrive in AKI stage-3 than a patient with AKI starting with normal kidney function.

Additional remarks on the KDIGO definitions

In applying the definitions and staging of AKI some important additional remarks should be made. Firstly, the purpose of setting a timeframe for diagnosis of AKI is to clarify the meaning of the word “acute”. A disease process that results in a change in SCr over many weeks is not AKI (though it may still be an important clinical entity). AKI is defined in terms of a process that results in a 50% increase in SCr within 1 week or a 0.3 mg/dl (26.5 µmol/l) increase within 48 hours. Importantly, there is no stipulation as to when the 1-week or 48-hour time periods can occur; it does not need to be the first week or first 48 hours of a hospital or ICU stay. Neither does the time window refer to duration of the inciting event. For example, a patient may have a 2-week course of sepsis but only develop AKI in the second week. Importantly, the 1-week or 48-hour timeframe is for diagnosis of AKI, not staging. Secondly, the AKIN recommendation that the criteria should be used following adequate fluid resuscitation, when applicable, has disappeared from the KDIGO definition.

Problems related to the different definition and classifications systemsThe baseline serum creatinine

Although all these consensus criteria (RIFLE, AKIN, and KDIGO) have helped standardize the approach to the diagnosis and staging of AKI, there still remain specificity limitations. One of the most discussed limitations is the importance of determining the baseline kidney function in patients admitted in AKI and in whom this baseline is not known. The lack of a uniform approach to estimate this baseline has recently been shown to compound the risk for AKI misclassification, hindering effective comparisons of this disease between settings [20-22].

Several strategies for estimating the basal SCr have been proposed [22-25], ranging from the use of an estimation of SCr by backward calculation from a presumed ‘standard GFR’ of 75 mL/min/1.73 m², use of the SCr value at admission, or the peak SCr in the AKI episode under consideration. Whereas RIFLE and KDIGO suggest the use of back calculation, AKIN recommends to use the evolution of SCr relative to the first observed value in that episode, while the European Renal Best Practice position statement and others [26] recommend the admission SCr [27].


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However, Siew et al [22] reported that the use of the admission SCr value as a baseline resulted in nearly 50% reduction in the detection of AKI compared with that using a known baseline SCr. The MDRD-estimated baseline SCr had a significantly higher sensitivity for “detecting” AKI than the 2 other methods. Although the use of SCr levels at admission resulted in the least amount of misclassification, this parameter also had the lowest sensitivity (38.9%) for diagnosis of AKI. When admission SCr levels were used, nearly half of the ‘true’ AKI cases were missed: 25.5% of the cohort had AKI when true baseline SCr levels were used, versus 13.7% with use of admission SCr levels. This decrease is perhaps best explained by the missed diagnosis of community-acquired AKI that improves or stabilizes during hospitalization [28]. Zavada et al [25] found that use of an MDRD-estimated baseline creatinine could result in either overestimation or underestimation of some mild (Risk) AKI cases but is unlikely to misclassify patients in Injury and Failure. Thus, it is important to consider the goal of AKI classification when selecting a baseline. For clinical purposes, it may be important ‘not to miss’ any case of potential AKI. Therefore, using the MDRD equation to estimate a baseline kidney function, at least provisionally, makes sense. The same may hold true for epidemiologic studies where some degree of overestimation or underestimation may average out and not affect overall rates. On the contrary, for research studies where precise case adjudication is critical, estimated creatinine should be used with caution, if at all, especially for defining mild (stage-1) AKI [28].

In a large hospitalized population with AKI the baseline kidney function was estimated by calculating the eGFR using a baseline SCr, which was derived from the nadir (or lowest) value recorded in the first 3 days of hospitalization [29]. Different thresholds of nadir-to-peak SCr were found to be independently associated with increased in-

hospital mortality according to baseline eGFR strata. A nadir-to-peak SCr minimum threshold of ≥0.2, ≥0.3, and ≥0.5 mg/dl was required to be independently associated with increased in-hospital mortality among patients with baseline eGFR ≥60 ml/min/1.73 m², 30 to 59 ml/min/1.73 m², and <30 ml/min/1.73 m², respectively. There was a significant interaction between the nadir-to-peak SCr and baseline eGFR for in-hospital mortality (P < 0.001). Using these thresholds, survivors of AKI episodes also had an increased hospital length of stay and were more likely to be discharged to a facility rather than home.

Limitations of the SCr

A first caveat illustrating the limitations of plasma creatinine concentrations for the diagnosis of AKI in the setting of critical illness comes from the recent data published by Pickering et al [30]. To examine the effect of acute severe illness on SCr concentrations, they applied a 2‑compartment, variable volume model of creatinine kinetics to serial creatinine measurements and fluid balance in 49 patients admitted to hospital after cardiac arrest. They found that in the majority of patients (n = 39), SCr concentrations decreased during the first 24 h after admission (median decrease of 32%). According to their kinetic model, hemodilution (see below) only partly accounted for this decrease, suggesting an acute reduction in the creatinine generation rate. Application of the kinetic model to patients who had unchanged creatinine levels 24 h after hospital admission (n = 6) suggested that their GFRs had declined to ~50% of baseline. The presence of clinically significant AKI in these patients was confirmed by increased levels of AKI biomarkers and increased mortality. The researchers conclude that diagnosis of AKI after cardiac arrest might be missed or delayed if changes in SCr concentrations are solely relied on as a marker of injury. As further illustrated in an accompanying editorial [31] such reductions in creatinine generation rate could have a major impact on the timing of AKI diagnosis and

Stage Serum creatinine Urine output

1 1.5-1.9 times baseline OR ≥0.3 mg/dl (≥26.5 µmol/l) increase

<0.5 ml/kg/h for 6-12 hours

2 2.0-2.9 times baseline <0.5 ml/kg/h for ≥12 hours

3 3.0 times baseline ORIncrease in serum creatinine to ≥4.0 mg/dl (≥353.6 µmol/l) OR Initiation of renal replacement therapy OR In patients <18 years, decrease in eGFR to <35 ml/min per 1.73 m2

<0.3 ml/kg/h for ≥24 hours OR Anuria for ≥12 hours

Table 1: Summary of the classification of AKI according to KDIGO [18]


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the assessment of its severity, in particular in critically ill, septic patients. The study by Pickering et al [30] suggests that a reduction in GFR can occur in critically ill patients with unchanged creatinine levels. Importantly, the magnitude of the decrease in creatinine generation rate might correlate with illness severity [32]; thus in sicker patients, increases in creatinine concentration could be smaller and occur more slowly than in less-sick patients with the same AKI severity.

Adding further to the uncertainty is the identification of changes in the patient’s fluid balance as additional confounder impacting the SCr. Liu et al [33] examined the occurrence of AKI in critically ill patients with the acute respiratory distress syndrome randomized to a fluid conservative versus fluid liberal management strategy in the ARDS Network Fluid and Catheter Treatment study. After adjusting SCr measurements for fluid balance, notable increases in the incidence of stage-1 AKI were noted in each study arm [(conservative, 57 vs. 51% ) (liberal 66 vs. 58%)]. No impact of the different fluid management strategies on the incidence of AKI in AKI stages 2 or 3 was noted. Comparable mortality rates between those patients in whom the AKI diagnosis was ‘masked’ versus those with known AKI before fluid correction were also observed (31 vs. 38%). These findings suggest that in addition to being an important prognostic factor [34, 35], variations in fluid balance can cause the diagnosis of AKI to be missed or delayed in high-risk patients when using SCr-based definitions alone. As further iterations of these definitions are refined, these limitations continue to underscore the need to effectively segregate evolving aspects of injury from changes in function.

Estimation of the basal SCr

A standard definition for baseline SCr does not exist, leading to heterogeneity across research studies [36] and the potential for misinterpreting the true nature of perturbed kidney function in hospitalised patients [21]. The baseline SCr value has been estimated in various ways, such as the level on hospital admission [16, 37], the minimum SCr level (nadir value) during the hospital stay [37, 38], the value back-estimated from the MDRD equation [6, 15] or the lowest value among these. The choice of estimation technique used to obtain the baseline SCr value has an effect on the prevalence of AKI, the severity (or stage) of disease, and on the mortality risk associated with various stages of AKI [36, 39].

The accuracy of commonly used methods for estimating baseline SCr was compared with that of a reference standard adjudicated by a panel of board-certified nephrologists in 379 patients with AKI or CKD admitted to a tertiary referral center [22]. It was found that

agreement between estimating methods and the reference standard was highest when using SCr values measured 7–365 days before admission, suggesting that the mean outpatient SCr measured within a year of hospitalisation most closely approximates nephrologist-adjudicated basal SCr values. A follow-up study confirmed that the use of these averaged outpatient SCr values also yields a reliable value among high-risk patients, already suffering from pre-existing CKD [40].

The urine output RIFLE, AKIN and KDIGO use the same urine output criteria to define AKI and to determine its severity. Since exact data on urine output are not always available, only a minority of retrospective studies have included urinary output criteria. Theoretically, measuring the urine output per hour in 6 or 12 h intervals as proposed by RIFLE, AKIN and KDIGO requires continuous monitoring of the diuresis which is practically limited to critically ill patients admitted in an Intensive Care Unit (ICU). However, the finding of “acute oliguria”, even crudely measured in a 24 hour urine collection can be an important and early diagnostic tool of kidney dysfunction. Since many cases of AKI occur in patients hospitalized in clinical wards it could be recommended to instruct the patients to collect the urine over 8 hours’ intervals in parallel with the normal nursing shifts. When defined in these “6-8 hour blocks”, urinary output is independently associated with mortality, morbidity, and renal outcomes [41, 42].

The importance of the urine volume output as parameter of the AKI definition particularly in critically ill ICU patients is illustrated by the study of Wlodzimirow and colleagues [43], who prospectively studied the Risk Injury Failure Loss End-stage renal disease (RIFLE) classification with SCr and urine output (UO) (RIFLESCr+UO) and without UO criteria (RIFLESCr) for AKI in 260 critically ill patients. RIFLESCr significantly underestimated the presence of AKI on admission and during the first week in the ICU and significantly delayed AKI diagnosis.

In addition, using a large cohort of unselected critically ill patients, another recent study [44] investigated the empirical relationships among SCr, urine output, observation period, in-hospital mortality, and renal replacement therapy (RRT). To visualize the dependence of adjusted mortality and RRT rate on SCr, the urine output, and the observation period, contour plots were generated that provide physicians with more complete pictures of AKI with respect to in-hospital mortality risk and anticipated need for RRT. In general, the severity of AKI was high when (1) absolute SCr increase was high regardless of observation period, (2) percentage SCr increase was high and the observation period was long,


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and (3) oliguria was sustained for a long period of time. Similar contour patterns emerged for both in-hospital mortality and RRT rates. Also this study illustrates the importance of considering the duration of oliguria as one of the parameters determining the outcome of critically ill patients with AKI.

Validation of the KDIGO definition proposals

Not many studies have validated the definitions and classification proposed by the KDIGO guidelines; some critical remarks on the KDIGO proposal have been formulated by other guideline making bodies such as the ad-hoc working group of the European Renal Best Practice working party [27], the Canadian Society of Nephrology [45], the KDOQI US Commentary [46] and the reader is referred to this literature. Most of the concerns on the definitions of AKI as formulated by KDIGO are focusing on the clinical application in the individual patient of small increases in absolute SCr values, the added value of considering urine output, the determination of the baseline SCr, and the suggestion of stage-based diagnostic and therapeutic interventions. A recent study [26] proposed a “novel” approach to classification and staging of AKI using ‘absolute’ rather than relative increases in SCr. Compared with the current KDIGO consensus AKI staging, Delta-Creatinine staging was found to be relatively simple and of better utility for large-scale epidemiologic studies.

In this proposal, using delta-SCr allows for use of an index SCr derived from samples mostly obtained on admission of the patient rather than referring to pre hospitalization baseline values, which are indeed not always readily available. Of course, making a classification simpler not necessarily means that it is more exact. As explained above the use of an admission SCr is less sensitive for diagnosing AKI and the admission index SCr is even more susceptible to the same potential confounding influences such as fluid overload and eventually decreased creatinine production.

To the best of our knowledge there is only one study where the 3 classical definitions and classifications for AKI (RIFLE, AKIN, KDIGO) have been compared with a more traditional worsening renal function (WRF) definition, as used in the particular case of acute cardio-renal syndrome [47]. The comparison revealed that there was a stepwise increase in primary outcome with increasing stages of AKI severity using RIFLE, KDIGO, or AKIN (p < 0.001). In direct comparison, there were only small differences in predictive abilities between RIFLE and KDIGO and WRF concerning clinical

outcomes at 30 days (AUC 0.76 and 0.74 vs. 0.72) as well as for KDIGO and WRF at 1 year (AUC 0.67 vs. 0.65).

ConclusionThe existing criteria proposed by RIFLE, AKIN, and their adaptation by KDIGO are certainly useful and have already been widely validated. As pointed out in this paper, existing definitions of AKI are far from perfect in that they rely on imperfect markers of renal function rather than direct measures of kidney damage. However, there is hope that in the future these considerations may be made obsolete [28]. Novel biomarkers probably assessing directly kidney injury are under intense investigation [48]. However, kidney function will still remain a valid and important parameter and it is likely that the next generation of AKI criteria, besides functional parameters will also include one or multiple injury biomarkers [49].

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