KDIGO Clinical Practice Guideline for Acute Kidney Injury
Timeframe for diagnosis and staging

Timeframe for diagnosis and staging

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: see Appendix B). For the purpose of this guideline, 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 (Recommendation 2.1.1). Importantly, there is no stipulation as to when the 1-week or 48-hour time periods can occur. It is stated unequivocally that it does not need to be the first week or 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. A patient can be staged over the entire episode of AKI such that, if a patient develops a 50% increase in SCr in 5 days but ultimately has a three-fold increase over 3 weeks, he or she would be diagnosed with AKI and ultimately staged as Stage 3.

As with any clinical criteria, the timeframe for AKI is somewhat arbitrary. For example, a disease process that results in a 50% increase in SCr over 2 weeks would not fulfill diagnostic criteria for AKI even if it ultimately resulted in complete loss of kidney function. Similarly, a slow process that resulted in a steady rise in SCr over 2 weeks, and then a sudden increase of 0.3 mg/dl ( 26.5 µmol/l) in a 48-hour period, would be classified as AKI. Such are the inevitable vagaries of any disease classification. However, one scenario deserves specific mention, and that is the case of the patient with an increased SCr at presentation. As already discussed, the diagnosis of AKI requires a second SCr value for comparison. This SCr could be a second measured SCr obtained within 48 hours, and if it is ≥ 0.3 mg/dl ( ≥ 26.5 µmol/l) greater than the first SCr, AKI can be diagnosed. Alternatively, the second SCr can be a baseline value that was obtained previously or estimated from the MDRD equation (see Table 9). However, this poses two dilemmas. First, how far back can a baseline value be retrieved and still expected to be ‘‘valid’’; second, how can we infer acuity when we are seeing the patient for the first time?

Both of these problems will require an integrated approach as well as clinical judgment. In general, it is reasonable in patients without CKD to assume that SCr will be stable over several months or even years, so that a SCr obtained 6 months or even 1 year previously would reasonable reflect the patient’s premorbid baseline. However, in a patient with CKD and a slow increasing SCr over several months, it may be necessary to extrapolate the baseline SCr based on prior data. In terms of inferring acuity it is most reasonable to determine the course of the disease process thought to be causing the episode of AKI. For example, for a patient with a 5-day history of fever and cough, and chest radiograph showing an infiltrate, it would be reasonable to infer that the clinical condition is acute. If SCr is found to be ≥ 50% increased from baseline, this fits the definition of AKI. Conversely, a patient presenting with an increased SCr in the absence of any acute disease or nephrotoxic exposure will require evidence of an acute process before a diagnosis can be made. Evidence that the SCr is changing is helpful in establishing acuity.