Metabolic syndrome (MetS) includes visceral obesity, hyperglycemia, dyslipidemia, and hypertension. The prevalence of MetS is 20-25%, which is an important risk factor for chronic kidney disease (CKD). MetS causes effects on renal pathophysiology, including glomerular hyperfiltration, RAAS, microalbuminuria, profibrotic factors and podocyte injury. This review compares several criteria of MetS and analyzes their differences. MetS and the pathogenesis of CKD includes insulin resistance, obesity, dyslipidemia, inflammation, oxidative stress, and endothelial dysfunction. The intervention of MetS-related renal damage is the focus of this article and includes controlling body weight, hypertension, hyperglycemia, and hyperlipidemia, requiring all components to meet the criteria. In addition, interventions such as endoplasmic reticulum stress, oxidative stress, gut microbiota, body metabolism, appetite inhibition, podocyte apoptosis, and mesenchymal stem cells are reviewed.

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Abstract. Numerous studies have reported that high-dose statin loading therapy prior to primary percutaneous coronary intervention (PPCI) improves the clinical outcomes of patients following acute myocardial infarction (AMI). However, little is known about the effects of long-term statin use prior to PPCI on such outcomes. Therefore, the aim of the present analysis was to clarify the effects of long-term statin use before PPCI on the treatment outcomes of patients following AMI. The records of 213 patients who had AMI and met the inclusion criteria were retrospectively reviewed. Patients were divided into two groups: A control group (n=178) who had received no statin pretreatment before AMI onset, and a statin group (n=35) who had received statin treatment for ≥1 month before AMI onset. All patients received a standard treatment regimen for the secondary prevention of coronary artery disease after PPCI. Baseline clinical variables, details of the PPCI procedure and clinical outcomes within 3 months after treatment were reviewed. Patients in the statin group were significantly older than those in the control group (P=0.003). Compared with the control group, there was a greater proportion of patients with hyperlipidemia and previous angina pectoris in the statin group. There were no differences in the use of other drugs (aspirin, β-blockers and angiotensin-converting enzyme inhibitors) prior to PPCI between the two groups. The corrected TIMI frame count (cTFC) was significantly lower in the statin group than in the control group (24.1±12.8 vs. 29.4±14.3, respectively; P=0.043). Multivariable linear regression analysis showed that long-term statin use before AMI was a significant predictor of cTFC after PPCI (P=0.012).Furthermore, the incidence of major adverse cardiac events within 3 months after PPCI was higher in the control group than in the statin group (16.8 vs. 2.9%, respectively; P=0.032). Logistic regression analysis showed that previous statin use was associated with the incidence of major adverse cardiac events within 3 months after treatment (P=0.012). The results of the present study demonstrate that long-term statin use prior to PPCI improved treatment outcomes after AMI in actual clinical practice.

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