Thank you Frank, this is most helpful. A couple of other considerations:
- The definition of AKI is a rapid loss of renal function - this means the SCr & UO definitions are mere surrogates (& not great ones). So even before we get to model them we have lost a lot of information (eg about the true extent of loss of GFR & about the individual’s renal reserve). I’ve bemoaned in the literature that after the RIFLE defintion the nephrology community dropped a delta GFR from the AKI definition & stuck with SCr and UO only (I expect because it is so darn difficult to measure).
- In addition to the use of SCr as a continuous variable I think what is needed is to include a measure of the rate of change. Physiologically two people with identical baseline SCr and identical elevated SCr will have had a different loss of GFR & quite possibly a different risk of death, if the elevated SCr is measured at a different time post onset of injury.
- An elevated SCr in population studies suggests poor outcomes, but even if it and the rate of change is identical between individuals it does not imply that at the time of measurement they have identical GFR. This is because SCr changes are always delayed following GFR changes. I’ve found a crude way to predict if SCr will fall or continue to rise (using UO + urinary Cr), but think more could be done. Nephrologists making decisions about fluid loading, dialysis etc may find predictions of where SCr is heading helpful. Any ideas?