- If you went to a national nephrology meeting in the 2000’s and walked into a lecture on clinical AKI there were two obligatory sections that would be part of the talk.
- The first would be how poor creatinine was as a marker for AKI. The expert at the front of the room would explain that creatinine was a lagging indicator and that by the time the creatinine had begun to climb the injury was yesterday’s news. Identifying AKI by a bump in the creatinine would force you to always be reactive rather than proactive. This discussion would then lead to a plea for better markers of AKI, followed by descriptions of NGAL, KIM-1, and other promising AKI assays of the future.The second would be a complaint about the lack of a consensus definition of AKI. The speaker would point to 35 different definitions of AKI in the literature, from highly sensitive (25% bumps in serum creatinine) to perfectly specific (need for acute dialysis during the hospitalization).
Depending on the exact year of the talk, they would then talk about the RIFLE criteria, or to the AKIN modifications to the RIFLE criteria, or to KDIGO’s modifications to AKIN. The speaker would always point to a future where we had a consensus definition of acute kidney injury so that we could start to move forward with a cohesive literature where one paper could be compared to another. What was always odd about these talks was that the second part of the lecture, about the emerging creatinine-based consensus definitions of AKI must have been browsing Facebook during the earlier part of the lecture about the futility of creatinine-based definitions of AKI.
But the consensus did emerge. Despite all the experts warning us about the problems with small changes in creatinine defining AKI, that is the world we live in. One problem with this definition recently emerged in a discussion of cardiorenal syndrome. This article by Testani et al found that:
The group experiencing hemoconcentration received higher doses of loop diuretics, lost more weight/fluid, and had greater reductions in filling pressures (p<0.05 for all). Hemoconcentration was strongly associated with WRF (OR=5.3, p<0.001) whereas change in right atrial pressure (p=0.36) and change in pulmonary capillary wedge pressure (p=0.53) were not. Patients with hemoconcentration had significantly lower 180 day mortality (HR=0.31, p=0.013). This relationship persisted after adjustment for baseline
We should not have a situation where increased risk of AKI (yes, I know the definition of worsening renal function, WRF, does not perfectly overlap with Stage 1 AKI, but work with me) is also associated with improved 180 day mortality. By defining AKI around changes in AKI we have deputized nephrologists to be the creatinine police and make decisions on treating patients based on what effect it has on short-term changes in GFR which may or may not have anything to do with long-term outcomes. In the above study, using serum creatinine to guide therapy leads to insufficient diuresis, poor fluid removal, and poor 180 day outcomes.
The Twitter discussion about this was particularly enlightening. Take a look.