ontrast-induced nephropathy (CIN) is a recognized complication of both coronary angiography (CAG) and percutaneous coronary intervention (PCI), and is associated with prolonged hospitalization and adverse clinical outcomes. [1][2][3][4][5] Several risk factors for CIN have been identified: chronic kidney disease (CKD), diabetes mellitus (DM), congestive heart failure, intravascular volume depletion, and using a large amount of contrast media are important predisposing factors. 2-4 CKD is also a risk factor of mortality in patients with cardiovascular disease. [6][7][8] The development of CIN is low in patients with normal renal function, varying from 0% to 10%, but its incidence is increased to 20% in patients with baseline serum creatinine (Cr) between 1.5 and 2.0 mg/dl. 9 In the patient with renal insufficiency, we make every effort to prevent CIN, but it can be difficult to distinguish patients with borderline serum Cr from whose renal function can not be preserved. There are several new renal markers; that is, serum cystatin C and urinary human liver-type fatty acid-binding protein (L-FABP). Serum cystatin C is a cysteine protease inhibitor produced by nearly all human cells and excreted into the Circulation Journal Vol.72, September 2008 bloodstream. It has 120 amino acids with a molecular weight of 13 kDa. The protein is freely filtrated by the renal glomerulus and then metabolized by the proximal tubule, so it is an improved marker of the glomerular filtration rate (GFR) compared with the serum Cr level. 10,11 Urinary L-FABP is expressed in human proximal tubules and engaged in free fatty acid metabolism, and its excretion reflects stress on the proximal tubules. It has been reported that there is a significant correlation of urinary L-FABP with the extent of tubulointestinal damage. 12 The goals of present study were to (1) investigate whether or not the serum cystatin C level before cardiac catheterization is a more useful marker of CIN than the serum Cr level, and establish a cut-off level for the determination of CIN, and (2) examine the differences in the changes of the new markers, serum cystatin C and urinary L-FABP, compared with those of the classical markers, urinary 1 and 2 microglobulins (MGs), N-acetyl--D-glucosaminidase (NAG), and microalbumin (Alb) in patients who underwent elective CAG with and without developing CIN.
MethodsThe study was performed from