Pre-Procedural N-Terminal Pro-B Type Natriuretic Peptide Predicts Contrast-Induced Acute Kidney Injury and Long-Term Outcome in Elderly Patients After Elective Percutaneous Coronary Intervention.

The aim of the study is to evaluate the association of pre-procedural N-terminal pro-B type natriuretic peptide (NT-proBNP) with contrast-induced acute kidney injury (CI-AKI) and long-term outcomes in elderly patients undergoing elective percutaneous coronary intervention (PCI).A total of 540 patients aged ≥ 75 years who had undergone elective PCI between January 2012 and December 2015 were enrolled in this study. Admission NT-proBNP levels were measured before PCI. CI-AKI was defined as a relative increase in serum creatinine (SCr) of ≥50%, or an absolute increase of ≥ 0.3 mg/dL, occurring within 48 hours after contrast medium exposure. The predictive value of NT-proBNP for predicting CI-AKI was assessed by receiver operating characteristic (ROC) and multivariable logistic regression analysis.A total of 54 (10.0%) patients developed CI-AKI. The best cutoff value of NT-pro-BNP for detecting CI-AKI was 1133 pg/mL with 66.7% sensitivity and 70.8% specificity according to the ROC analysis (C statistic = 0.719; 95% CI, 0.679-0.756). Multivariable analysis demonstrated that Lg-NT-proBNP is significantly related to CI-AKI (odds ratio [OR] = 3.892; 95% CI, 1.996-7.590; P < 0.001). Cox regression analysis showed that Lg-NT-proBNP is associated with long-term mortality (adjusted hazard ratio [HR] = 2.158; 95% CI, 1.246-3.740; P = 0.006) during follow-up.Pre-procedural NT-proBNP is a significant and independent predictor of CI-AKI and long-term mortality in elderly patients following elective PCI, and the best cutoff point for predicting CI-AKI was 1133 pg/mL.

Association of Preprocedural Hyperglycemia With Contrast-Induced Acute Kidney Injury and Poor Outcomes After Emergency Percutaneous Coronary Intervention.

We investigated whether preprocedural hyperglycemia was associated with contrast-induced acute kidney injury (CI-AKI) and long-term outcomes in patients with acute coronary syndrome (ACS) who underwent emergency percutaneous coronary intervention (PCI). Patients (n = 558) with ACS who underwent emergency PCI were consecutively enrolled. Preprocedural hyperglycemia was defined as glucose levels >198 mg/dL (11 mmol/L). The primary outcome was CI-AKI (≥0.3 mg/dL absolute or ≥50% relative serum creatinine increase 48 hours after contrast medium exposure). Overall, 103 (18.5%) patients had preprocedural hyperglycemia and 89 (15.9%) patients developed CI-AKI. The incidence of CI-AKI was significantly higher in patients with hyperglycemia than without (28.2% vs 13.2%; P < .01). Multivariate analysis indicated that preprocedural hyperglycemia was an independent predictor of CI-AKI (odds ratio = 1.971, 95% confidence interval [CI]: 1.129-3.441; P < .05). In addition, preprocedural hyperglycemia was associated with an increased risk of all-cause mortality during the 2-year follow-up (hazard ratio = 2.440, 95% CI: 1.394-4.273; P = .002). Preprocedural hyperglycemia is a significant and independent predictor of CI-AKI and long-term outcomes.

[Effects of human tissue kallikrein gene delivery on the proliferation of vascular smooth muscle cells].

OBJECTIVE: Tissue kallikrein cleaves kininogen substrate to produce vasoactive kinin peptides that have been implicated in the proliferation of vascular smooth muscle cells. We investigated the effects of adenovirus-mediated human tissue kallikrein (Ad-hKLK1) gene delivery on the proliferation of vascular smooth muscle cells of SHR (VSMCs(SHR)) induced by platelet derived growth factor-BB (PDGF-BB). METHODS: Primary VSMCs(SHR) were isolated and cultured from thoracic aorta of male SHR. The VSMCs(SHR) proliferation induced by PDGF-BB was accessed by cell counting and methyl thiazolyl tetrazolium (MTT). Western blot was used to determine the protein expression of hKLK1, the cycle-independent kinase inhibitors p27(Kip1) and p21(Cip1). The mRNA expressions of bradykinin B1 receptor and B2 receptor were detected by RT-PCR in VSMCs(SHR). RESULTS: Proliferation of VSMCs(SHR) induced by PDGF-BB was significantly inhibited post transfection of Ad-hKLK1 (20-100 MOI) in a MOI-dependent manner. The peak inhibition titer of Ad-hKLK1 was 100 MOI with peak inhibition rate of 39.3% (cell counting, n = 3, P < 0.01), 30.2% (MTT, n = 3, P < 0.01) and 36.4% (peak stunning rate of cell-cycle in phase G(0)/G(1)). The inhibitory effects of proliferation and cell-cycle caused by hKLK1 gene delivery could be abolished by Hoe140, a bradykinin B2 receptor antagonist. The protein expression of p27(Kip1) and p21(Cip1) increased significantly after the hKLK1 gene delivery, whereas Hoe140 nearly completely blocked these effects (n = 3, P < 0.001, respectively). PDGF-BB also significantly upregulated the mRNA expression of B2 receptor but not B1 receptor in VSMCs(SHR). CONCLUSION: The hKLK1 gene delivery could inhibit PDGF-BB induced proliferation in VSMCs(SHR) through Bradykinin B2 receptor and up-regulate expression of p27(Kip1) and p2l(Cip1).