Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01034 (cystatin C)
 3,397 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the study was to assess whether NGAL and cystatin C could predict contrast-induced nephropathy in non-diabetic patients (n=60, mean age 60+/-11 years) with normal serum creatinine undergoing elective PCI. We found a significant rise in serum NGAL after 2, 4 and 8 h, and in urinary NGAL after 4, 8 and 24 h after PCI. Cystatin C rose significantly 8 and 24 h after the procedure. Prevalence of CIN was 10%. We found 90% sensitivity and 74% specificity of serum and 76% sensitivity and 80% specificity of urinary NGAL increase. NGAL may represent a sensitive early biomarkers of renal impairment after PCI.
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PMID:NGAL (neutrophil gelatinase-associated lipocalin) and cystatin C: are they good predictors of contrast nephropathy after percutaneous coronary interventions in patients with stable angina and normal serum creatinine? 1756 73

We tested the hypothesis whether midkine could represent an early biomarker of contrast-induced acute kidney injury (CIAKI) in 89 patients with normal serum creatinine undergoing PCI. Midkine, serum and urinary NGAL, and cystatin C were evaluated before and 2, 4, 8, 24, and 48 hours after PCI using commercially available kits. Serum creatinine was assessed before and 24 and 48 hours after PCI. We found a significant rise in serum midkine as early as after 2 hours (P < 0.001) when compared to the baseline values. It was also significantly higher 4 hours after PCI and then returned to the baseline values after 24 hours and started to decrease after 48 hours. When contrast nephropathy was defined as an increase in serum creatinine by >25% of the baseline level 48 hours after PCI, the prevalence of CIN was 10%. Patients with CIN received significantly more contrast agent (P < 0.05), but durations of PCI were similar. Midkine was significantly higher 2, 4, and 8 hours after PCI in patients with CIN. Since the "window of opportunity" is narrow in CIAKI and time is limited to introduce proper treatment after initiating insult, particularly when patients are discharged within 24 hours after the procedure, midkine needs to be investigated as a potential early marker for renal ischemia and/or nephrotoxicity.
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PMID:Midkine: a novel and early biomarker of contrast-induced acute kidney injury in patients undergoing percutaneous coronary interventions. 2562 54

BACKGROUND Contrast-induced nephropathy is acute kidney injury caused by contrast medium exposure. Serum creatinine is the clinical diagnostic standard, but it does not yield quick results. The serum level of cystatin C is stable and it can reflect renal function sensitively. The study aimed to assess the usefulness of cystatin C for early diagnosis of contrast-induced nephropathy in patients undergoing coronary angiography. MATERIAL AND METHODS We included 300 patients who underwent CAG. According to the sCr at 48 h, patients were divided into 2 groups: CIN group and non-CIN group. Their demographics and basal renal function were recorded. Changes in sCr, Cys C, and e GFR were compared at the same time. ROC analysis was used to assess the sensitivity and specificity of Cys C in the early diagnosis of CIN. RESULTS Comparison of basal renal function and serum level of Cys C showed no significant differences between the 2 groups. Serum level of Cys C increased significantly at 24 h (p<0.001), and sCr increased significantly at 48 h. ROC analysis showed that the AUC of the change in Cys C between baseline and 24 h was 0.936 (95% CI: 0.879-0.992, p=0.000) and the optimum cut-off level was 0.26 mg/L (sensitivity=89.7% and specificity=95.6%). CONCLUSIONS The concentration change of Cys C is better than sCr as a biomarker in the early detection of CIN.
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PMID:Significance of Cystatin C for Early Diagnosis of Contrast-Induced Nephropathy in Patients Undergoing Coronary Angiography. 2754 57