Renovascular disease (RVD) is emerging as a common and frequently unsuspected cause of chronic renal failure and end-stage renal disease (1); moreover, it is frequently associated with renovascular hypertension, which generally carries a worse cardiovascular prognosis than other hypertensive conditions (2)(3). RVD and its associated hypertension are often not readily distinguishable from essential hypertension with renal damage, and the currently accepted diagnostic workup strategy is largely based on early clinical suspicion of the disease (4). Among the main elements contributing to an increased clinical suspicion of RVD is a decreased glomerular filtration rate (GFR), often detected by an increase in serum creatinine concentration. The creatinine concentration is indeed convenient and inexpensive to determine, but it is not ideal because of its sensitivity to changes in muscle mass, dietary protein intake, tubular secretion, and extrarenal metabolism. In addition, it is a relatively poor index of the function of individual kidneys and renal mass because unilateral renal artery stenosis >70% is often associated with decreased GFR in one kidney but no change in the creatinine concentration until 50% of the total renal mass is lost (“creatinine blinded area”) (1)(5). Recent evidence suggests that serum cystatin C is a reliable marker of GFR (5)(6)(7)(8). Moreover, cystatin C may more readily detect subtle decrements of GFR than does serum creatinine (5)(9)(10). We therefore investigated whether cystatin C can serve as a more sensitive indicator than creatinine in a rule-out strategy for the diagnostic workup for RVD. We studied 128 free-living individuals (64 males/64 females) who were normotensive and free of any drugs. No renal or other significant diseases were recorded in the history. The participant selection strategy was also aimed at having five age classes (<30, 31–40, 41–50, …