Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury

For any condition, the clinician needs to know whether the disease is present and, if so, where and when the patient falls in the natural history of the disease. The former facilitates recognition whereas the latter defines time points for intervention. Unfortunately, there has been no uniformly accepted definition of AKI. Studies describe ARF or AKI based on serum creatinine changes, absolute levels of serum creatinine, changes in blood urea nitrogen or urine output, or the need for dialysis [ 1 , 11 , 20 , 29 – 36 ]. The wide variation in definitions has made it difficult to compare information across studies and populations [ 37 ].

Diagnostic criteria

Recognition of AKI requires the delineation of easily measured criteria that can be widely applied. Serum creatinine levels and changes in urine output are the most commonly applied measures of renal function; however, they are each influenced by factors other than the glomerular filtration rate (GFR) and do not provide any information about the nature or site of kidney injury. The proposed diagnostic criteria (Table ) were based on consideration of the following concepts:

Table 1

An abrupt (within 48 hours) reduction in kidney function currently defined as an absolute increase in serum creatinine of more than or equal to 0.3 mg/dl (≥ 26.4 μmol/l), a percentage increase in serum creatinine of more than or equal to 50% (1.5-fold from baseline), or a reduction in urine output (documented oliguria of less than 0.5 ml/kg per hour for more than six hours).Open in a separate window

1. The definition needs to be broad enough to accommodate variations in clinical presentation over age groups, locations, and clinical situations.

2. Sensitive and specific markers for kidney injury are not currently available in clinical practice. Several groups are working on developing and validating biomarkers of kidney injury and GFR which may be used in the future for diagnosis and prognosis.

3. There is accumulating evidence that small increments in serum creatinine are associated, in a variety of settings, with adverse outcomes [13-20] that are manifest in short-term morbidity and mortality and in longer-term outcomes, including 1-year mortality [15-17]. Current clinical practice does not focus much attention on small increments in serum creatinine, which are often attributed to lab variations. However, the coefficient of variation of serum creatinine with modern analyzers is relatively small and therefore increments of 0.3 mg/dl (25 μmol/l) are unlikely to be due to assay variation [38]. Changes in volume status can influence serum creatinine levels [39]. Because the amount of fluid resuscitation depends on the underlying clinical situation [40], the group agreed that application of the diagnostic criteria would be used only after an optimal state of hydration had been achieved.

4. A time constraint of 48 hours for diagnosis was selected based on the evidence that adverse outcomes with small changes in creatinine were observed when the creatinine elevation occurred within 24 to 48 hours [15,16] and to ensure that the process was acute and representative of events within a clinically relevant time period. In the two aforementioned studies, there was no distinction of underlying CKD or de novo AKI. However, in the study by Chertow and colleagues [13], the odds ratio for mortality with a change in creatinine of 0.3 mg/dl (25 μmol/l) was 4.1 (confidence interval 3.1 to 5.5) adjusting for CKD. There is no requirement to wait 48 hours to diagnose AKI or initiate appropriate measures to treat AKI. Instead, the time period is designed to eliminate situations in which the increase in serum creatinine by 0.3 is very slow and thus is not ‘acute.’

5. It was recognized that AKI is often superimposed on pre-existing CKD. Further validation will be required to determine whether the criterion of a creatinine elevation of 0.3 mg/dl (25 μmol/l) is applicable to these patients (that is, whether a creatinine increase of more than 0.3 mg/dl from an elevated baseline represents AKI and has the same risks as a creatinine increase from a normal baseline).

6. The need for including urine output as a diagnostic criterion is based on the knowledge of critically ill patients in whom this parameter often heralds renal dysfunction before serum creatinine increases.

A minority of group members, both intensivists and nephrologists, felt that a urine output reduction of less than 0.5 ml/kg per hour over the span of six hours was not specific enough to lead confidently to the designation of AKI. It was recognized that the hydration state, use of diuretics, and presence of obstruction could influence the urine volume, hence the need to consider the clinical context. Additionally, accurate measurements of urine output may not be easily available in all cases, particularly in patients in non-intensive care unit settings. Despite these limitations, it was felt that the use of changes in urine offers a sensitive and easily discernible means of identifying patients, but its value as an independent criterion for diagnosis of AKI will need to be validated.

The proposed diagnostic criteria for AKI are designed to facilitate acquisition of new knowledge and validate the emerging concept that small alterations in kidney function may contribute to adverse outcomes. The goal of adopting these explicit diagnostic criteria is to increase the clinical awareness and diagnosis of AKI. It is recognized that there may be an increase in false-positives, so that some patients labeled with AKI will not have the condition. There was consensus that adopting the more inclusive criteria is preferable to the current situation, in which the condition is under-recognized and many people are identified late in the course of their illness and potentially miss the opportunity for prevention or application of strategies to minimize further kidney damage.