| Background：The treatment in patients who underwent percutaneous coronary intervention (PCI)was a milestone in cardiovascular diseases treatment history. A lot of evidence stands thatthis approach has improved the prognosis of patients. As this technique gets established asa powerful weapon in the medical arsenal, the number of patients with CAD booms inrecent years, while the ratio of patients with complex lesions increase as well. A big intakeof contrast agents carries more risk, especially for those who are co-diagnosed with theCIN related to cardiovascular disease, renal dysfunction. This significantly reduces theeffectiveness of this approach..Few molecules can predict CIN or MACE after PCI, it is critical to select a markerwith high specificity and sensitivity. Plasma adiponectin is closely related to CAD. Mostpeople have accepted that low plasma adiponectin is a risk factor for CAD, but that the level of plasma adiponectin can effectively predict MACE is still controversial. Thepossibility of the CIN is closely related to MACE. The incidence of CIN is associated withmany factors, among which Scr is a golden and well-accepted one. But the increase of Scrtends to emerge after the beginning of renal dysfunctional changes, so dependence on Scrfor the diagnosis delays our treatment unpredictably. It has been suggested that UAPN canreflect the early renal dysfunction, and as a new marker of endothelial injury it can predictcardiovascular risk. Until now, there is no report about the power of UAPN to predict CINor MACE. Our research will discuss the relationship between them.Objective:1. To study the incidence of contrast-induced nephropathy (CIN) and the risk factorsof CIN after percutaneous coronary intervention (PCI) in patients with CAD. To explorethe relationship between UAPN and the risk factors of CIN in patients after PCI.2. To study the relations between UAPN and major adverse cardiac event (MACE) inpatients who underwent PCI; To explore UAPN levels for predicting the MACE andclinical outcomes after PCI.Methods:1. A total of208hospitalized patients from February2011to May2012withcoronary heart disease（diagnosed by coronary angiography）,who underwent PCI inDepartment of cardiology of Xijing Hospital, were admitted as subjects of my experiment.The individual information listed below was collected from each patient：①Medicalhistory and physical examination②blood pressure, fasting blood glucose, triglyceride,total cholesterol, HDL, LDL, base serum creatinine,24-Hour urine protein, hemoglobin,serum total protein, albumin, hs-CRP, Pro-BNP, Cardiac ultrasound parameters such asLVEF were recorded before the treatment.③5ml of middle-segmented urine wascollected in the morning，and immediately stored in the refrigerator at-80℃degree forfollowing measurement of UAPN levels by ELISA(Enzyme linked immunosorbent assay).2. UAPN were detected by ELISA,thus patients with high UAPN(the uppest quartile of UAPN level,UAPN≥12.36ng/ml, n=52) as Higher UAPN group, Patients with lowerUAPN(the lower quartile of UAPN level:UAPN＜12.36ng/ml, n=156) as Lower UAPNgroup.3. After admitted in hostipal, all patients have to wait at least24hours before thetreatment procedure (CAG+PCI). Three days of continuous detection of serum creatinine(Scr) to determine the occurrence of CIN will be taken postoperatively. MACE (includingany cause of death, reinfarction, repeat coronary revascularization, heart failurereadmissions) will be tracked for patients after discharged from the hospital by means oftelephone, outpatient or hospitalization. All follow-up information will be recored and themean follow-up peried is10.5months (18months the longest and3months the shortest).Results:1.①The overall incidence of CIN after PCI in patients with coronary heart diseaseswas9.1%(19/208).②One factor analysis presented that WHR(waist-hips ratio),base serumcreatinine,type2diabetes, fasting blood glucose,hemoglobin, serum total protein, alumin,pro-BNP, hs-CRP,contrast agents dose(contrast agents dose＞300ml) and UAPN arecorrelated to CIN occurrence (P＜0.05).③Age, type2diabetes, fasting blood glucose,basic renal function (serum creatinine,24-Hour urine protein), Pro-BNP and hs-CRPshowed statistically significant difference between high UAPN group and lower UAPNgroup(P＜0.05).④The group with high UAPN has higher incidence of CIN(P＜0.05).⑤When the cut-off value predicting CIN by UAPN was set at12.24ng/ml, the diagnosticvalue were high(the area under the ROC curve was0.72, standard error：0.069, P=0.002，95％CI：0.585～0.855).⑥Multi-factor(Logistic) analysis indicated that the high level ofUAPN before PCI, fasting blood glucose, basic renal function(serum creatinine), basiccardiac function (LVEF) were risk factors of CIN.2.①MACE, Age, type2diabetes, basic renal function(serum creatinine,24-Hoururine protein), Pro-BNP and hs-CRP showed statistically significant difference betweenhigh UAPN group and lower UAPN group(P＜0.05).②The diameter of the stent, theseverity of coronary artery disease (the Grading of the Gensini scoring system) showed statistically significant difference between high UAPN group and lower UAPN group (P＜0.05).③Basic renal function(serum creatinine), basic cardiac function (Pro-BNP,LVEF),hs-CRP, the level of UAPN showed statistical significance to the group withMACE and the non-MACE group (P＜0.05).④The number of the stents, the cumulativelength of the stent, the severity of coronary artery disease (the Gensini scoring system)showed statistical significant difference between MACE group and the non-MACE group(P＜0.05).⑤The group with high UAPN has higher incidence of MACE (40.39%vs14.74%； P＜0.05).⑥Multiple analyses showed that the upper quartile of UAPNlevel(UAPN≥12.36ng/ml) was independently correlated with MACE；Kaplan-Meieranalysis demonstrated a higher MACE rate in the group with high UAPN than in thatGroup lower UAPN (Log-rank=14.859，P＜0.001).Conclusion:The group with the higher levels of UAPN has a higher risk of CIN and MACE. TheUAPN level may be helpful for predicting the incidence of CIN, MACE and clinicaloutcomes after PCI. |
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