Valuable Markers for Contrast-Induced Nephropathy in Patients Undergoing Cardiac Catheterization

Abstract

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

The Role of Serum Cystatin C in the Early Detection of Contrast-Induced Nephropathy after Coronary Intervention

“…The results of the present study are in agreement with the most results obtained by others reports Kato et al and Mehran et al [19][20][21][22][23][24][25][26][27]. In present study was found a highly significant increment in serum creatinine and cystatin C while decrease in eGFR 24 hours after angiography (p<0.001, 0.01) when compared between two groups (CIN+, CIN-).…”

“…In present study was found a highly significant increment in serum creatinine and cystatin C while decrease in eGFR 24 hours after angiography (p<0.001, 0.01) when compared between two groups (CIN+, CIN-). This result is consistent with Wang et al, Liu et al and Nozue et al founded serum level of cystatin C is a reliable marker for CIN at 24 hours p<0.001 and serum creatinine increased significantly at 48 hours, also study carried by Wacker-Gussmann et al [16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31] found that cystatin C level and the cystatin C/creatinine ratio independently predict the risk of CIN in patients undergoing coronary angiography, but another study by Ribichini et al [32] found a significant increase in serum cystatin C concentrations 12 hours earlier than serum creatinine, therefore a rise of serum cystatin C at 12 hours from baseline was the earliest predictor of CIN than serum creatinine [18].…”

“…He found that CIN occurred in 30 patients (18%) [18]. A prospective study of consecutive 87 patients who underwent elective PCI and CAG, 31 patients had a moderate kidney disease, CIN occurred in 18 patients and was more frequent 42.0% [19]. The reason for the difference in incidence rates of CIN among different studies including this study may be due to differences in the definitions of CIN (absolute or relative) [20,21].…”

“…Although several studies have revealed that serum cystatin C cut off level >1.2 or >1.18 or >1.3 mg/l, 94% sensitivity and 48% specificity is more accurate for diagnostic CIN than serum creatinine [19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36]. While study obtained by Ribichini et al found that absolute changes in serum creatinine proved more accurate than serum cystatin C for predicting CIN at an early stage 12 hours after angiography [18].…”

Urinary Liver Type-Fatty Acid Binding Protein and Plasma Cystatin C as Early Predictors of Contrast Induced Acute Kidney Injury

“…These results are similar to those of Kato et al, (2008) [27]; who found that urinary L-FABP levels were significantly increased after coronary angiography, suggesting transient proximal tubular damage by contrast medium, although the classical markers were not useful for predicting or detecting CIN. Another study carried out by BachorzewskaGajewska et al, (2009) [28]; supported this finding, where the 25 included patients underwent PCI; none of them fulfilled the criteria of contrast nephropathy, despite there was highly significant elevation of urinary L-FABP as early as 4 hours after contrast administration (25.90±21.93 pg/ml) and at 24 hours (33.49±26.41 pg/ml) compared to a baseline value of 3.76±1.52 pg/ml.…”