We developed a risk score for contrast-induced nephropathy (CIN) in elderly patients (n = 668) before percutaneous coronary intervention (PCI). Another 277 elderly patients were studied for validation. Based on the odds ratio, risk factors were assigned a weighted integer; the sum of the integers was the risk score. Among the 668 elderly patients, 105 (15.7%) experienced CIN. There were 9 risk factors for CIN (with weighted integer): estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m(2) (4), diabetes (3), left ventricular ejection fraction <45% (3), hypotension (2), age >70 years (2), myocardial infarction (2), emergency PCI (2), anemia (2), and contrast agent volume >200 mL (2). The incidence of CIN was 3.4%, 11.9%, 36.9%, and 69.8% in the low-risk (≤4), moderate risk (5-8), high-risk (9-12), and very-high-risk groups (≥13). The model demonstrated good discriminative power in the validation population (c statistic = 0.79). This score can be used to plan preventative measures.
Risk classification based on the most significantly correlated parameters is useful for predicting CI-AKI before contrast exposure. The simple preprocedural score showed excellent predictive ability for identifying patients at high risk of nephropathy and those with deteriorative prognosis after PCI.
Background:The prophylactic efficacy of statin pretreatment for the prevention of contrast-induced nephropathy (CIN) in patients undergoing coronary angiography (CAG) or percutaneous coronary intervention (PCI) remains controversial. The aim of the study was to perform a meta-analysis of randomized controlled trials (RCTs) to assess the effectiveness of short-term moderate or high-dose rosuvastatin pretreatment in preventing CIN.Methods:We included RCTs comparing short-term moderate or high-dose rosuvastatin treatment versus low-dose rosuvastatin treatment or placebo for preventing CIN. The primary endpoint was the incidence of CIN within 2 to 5 days after contrast administration, and related-parameters including serum creatinine (SCr), cystatin C (CysC), hypersensitive C-reactive protein (hs-CRP), urine microalbumin (mALB) were also extracted.Results:Fifteen RCTs with a total of 2673 patients were identified and analyzed. Patients who received moderate or high-dose rosuvastatin pretreatment had a 55% lower risk of CIN compared with low-dose rosuvastatin pretreatment or placebo group based on a fixed effect model (RR = 0.45, 95% CI 0.35–0.58, P < .0001). The benefit of moderate or high-dose rosuvastatin was consistent in both comparisons with low-dose rosuvastatin (RR = 0.40, 95% CI 0.27–0.59, P < .0001) or placebo (RR = 0.45, 95% CI 0.35–0.58, P < .0001). And moderate (20 mg) or high dose (≥40 mg) rosuvastatin significantly reduced the incidence of CIN compared with the control (RR = 0.39, 95% CI 0.29–0.54, P < .0001, RR = 0.56, 95% CI 0.37–0.85, P = .006, respectively). Subgroup analysis showed that moderate or high-dose rosuvastatin pretreatment could decrease the incidence of CIN in patients with chronic kidney disease (CKD) (RR = 0.53, 95% CI 0.30–0.93, P = .03) or diabetes mellitus (DM) (RR = 0.51, 95% CI 0.31–0.86, P = .01) or acute coronary syndrome (ACS) patients undergoing PCI (RR = 0.52, 95% CI 0.35–0.76, P = .0009) or in studies which received mean contrast volume ≥110 mL (RR = 0.43, 95% CI 0.32–0.58, P < .0001). The SCr, CysC, hs-CRP, and mALB after the operation in the moderate or high-dose rosuvastatin group were lower than those of low-dose rosuvastatin group.Conclusion:This meta-analysis demonstrated that moderate or high-dose rosuvastatin treatment could reduce the incidence of CIN in patients undergoing CAG or PCI. Moreover, moderate or high-dose rosuvastatin would be beneficial in high-risk patients with CKD or DM or undergoing PCI.
IL-27, a heterodimeric cytokine of the IL-12 family, has diverse influences on the development of multiple inflammatory diseases. In this study, we identified the protective role of IL-27/IL-27R in host defense against Chlamydia muridarum respiratory infection and further investigated the immunological mechanism. Our results showed that IL-27 was involved in C. muridarum infection and that IL-27R knockout mice (WSX-1–/– mice) suffered more severe disease, with greater body weight loss, higher chlamydial loads, and more severe inflammatory reactions in the lungs than C57BL/6 wild-type mice. There were excessive IL-17–producing CD4+ T cells and many more neutrophils, neutrophil-related proteins, cytokines, and chemokines in the lungs of WSX-1–/– mice than in wild-type mice following C. muridarum infection. In addition, IL-17/IL-17A–blocking Ab treatment improved disease after C. muridarum infection in WSX-1–/– mice. Overall, we conclude that IL-27/IL-27R mediates protective immunity during chlamydial respiratory infection in mice by suppressing excessive Th17 responses and reducing neutrophil inflammation.
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