Sir, The paper by Kimmel et al. [1] concludes that cystatin C blood level variations are a more reliable parameter than serum creatinine increments for the diagnosis of contrastinduced nephropathy (CIN). However, this conclusion does not seem sufficiently supported by the data to us. Since the definition of CIN is based on serum creatinine variations, it is not clear what the meaning is of the cystatin C increase when the former does not occur. Does it reflect a true GFR reduction or some other condition, i.e. the release of cystatin C from atherosclerotic vascular lesions during arterial catheterization [2] or the biological variability of the parameter [3]? We are also puzzled with the variability of cystatin C in the period d-1/d0. Looking at Figure 1, our feeling is that it is quite large. As a matter of fact, it was reported that the critical difference for sequential values is 37% for serum cystatin C—a value that includes the cystatin C levels plotted in Figure 1—and only 14% for serum creatinine [3]. The authors state that the temporary increase in GFR possibly due to the peri-procedural hydration does not translate into a cystatin C decrement because of its slower kinetics vis-a-vis serum creatinine. However, what is the evidence for such a statement? Is it just speculation to explain the dichotomic trends between serum cystatin C and creatinine levels? The issue is very important, since if cystatin C really has a delayed progression with respect to serum creatinine, we might suspect that the interval d0/d2, 48 h, is too long to grasp mild, transient serum creatinine variations occurring inbetween. We think that, although cystatin C is an attractive biomarker of GFR, before concluding that it should be the preferred biomarker for the development of CIN, an experimental design with a more strict timing in sampling and a much larger case population is necessary.