We may hypothesize that the increase in BTP associated with the development of AKI is less dynamic in such patients as compared with the increase in cystatin C. However, this interpretation needs to be tested in larger study as the numbers of patients with AKI in our study is low, adversely affecting the power of multiple statistical models, and the number of patients with prediagnosed renal disease in our study is very low. This evidence concerns the gene CST3 and acute kidney injury.