BackgroundThe aim of this systematic review and meta-analysis was to summarize the association of obstructive sleep apnea (OSA) with renal outcome.MethodsOur study followed the PRISMA guidelines. Two independent reviewers searched for relevant articles in the databases of Pubmed, the Web of Science and CENTRAL, and conducted study selection and quality assessment. A random-effect model was used to estimate the effects.ResultsA total of 1240 articles were initially identified (Pubmed = 568, Web of Science = 640, CENTRAL = 32). After removal of duplicate articles (n = 415) and irrelevant articles (n = 788), 37 were selected for full-text review, and 18 were finally included in the analysis. Overall, patients diagnosed with OSA were found to have a higher odds ratio (OR) of a poorer renal outcome, with a pooled OR of 1.77 (95% C.I.: 1.37–2.29). The significant association between OSA and a poorer renal outcome was not affected by the medical condition of diabetes mellitus (DM). In addition, we found that OSA was consistently associated with higher albuminuria/proteinuria and a lower estimated glomerular filtration rate (eGFR), with a pooled OR of 1.84 (95% C.I.: 1.24–2.73) and 1.60 (95% C.I.: 1.19–2.16), respectively. A greater OSA severity was also found to be related to a higher OR, with a mild group OR of 1.45 (95% C.I.: 1.19–1.77) and a moderate and severe group OR of 2.39 (95% C.I.: 1.96–2.90).ConclusionsOur study demonstrated that OSA is significantly associated with poorer renal function.

Our study first showed that treatment with both pioglitazone and basal insulin improved glycemic control, while only pioglitazone treatment was observed to be advantageous in terms of preserving renal function when used as an add-on therapy for patients with type 2 DM in whom sulfonylurea and metformin regimens failed.

Background Serum cytokeratin-18 is believed to be a marker of hepatic cell damage. However, few studies have discussed about the serum cytokeratin-18 concentration in type 2 diabetes mellitus patients and investigated its association with non-alcoholic fatty liver disease as well as metabolic biomarkers. Methods Healthy participants and type 2 diabetes mellitus patients were enrolled. Physical and metabolic factors were recorded, and non-alcoholic fatty liver disease was screened by abdominal ultrasound and the fatty liver index. The cytokeratin-18 concentration was detected using two commercially available immunoassay kits (M30 and M65 ELISA kit, Previa AB, Sweden). Results Overall, 22.8% (29/127) and 35.9% (42/117) of the participants were diagnosed with non-alcoholic fatty liver disease in the non-diabetes mellitus group and type 2 diabetes mellitus group, respectively. In the non-diabetes mellitus group and type 2 diabetes mellitus group, our result showed that participants with non-alcoholic fatty liver disease had a higher serum cytokeratin-18 M30 and cytokeratin-18 M65 concentration as compared with participants without non-alcoholic fatty liver disease. Interestingly, as compared with healthy participants without non-alcoholic fatty liver disease, our result also demonstrated that type 2 diabetes mellitus patients without non-alcoholic fatty liver disease had a higher serum cytokeratin-18 M30 (108.4 ± 66.2 vs. 87.1 ± 34.6 U/L; P = 0.038) and cytokeratin-18 M65 concentration (285.4 ± 115.3 vs. 248.5 ± 111.3 U/L; P = 0.031). The independent relationship between type 2 diabetes mellitus and cytokeratin-18 was further strengthened by the significant positive association between fasting plasma glucose and serum cytokeratin-18 concentration via multivariate regression analyses (cytokeratin-18 M30: β = 0.034, P = 0.029; cytokeratin-18 M65: β = 0.044, P = 0.002). Conclusions Independent of non-alcoholic fatty liver disease, our results suggested that the cytokeratin-18 concentration is closely associated with the hyperglycaemic milieu. The association between serum cytokeratin-18 and type 2 diabetes mellitus may be worthy of further investigation.

he use of commercialized statins in the prevention of cardiovascular diseases (CVD) has commonly been accepted based on the informative results of the Cholesterol Treatment Trialists (CTT) reports [1] As an additional effort in the prevention of CVD, professional societies have issued practical recommendations for healthcare providers on the effective use of statins in lowering low-density-lipoprotein cholesterol (LDL-C) [2]. Among these statins, atorvastatin and rosuvastatin are regarded as the most effective as they can reduce more than 30% of LDL-C, even at low doses (i.e. atorvastatin 10 mg; rosuvastatin 5 mg) [2]. The results of the recent HOPE-3 study [3], in which 10 mg rosuvastatin was found to reduce the development of CVD by 24% in intermediate-risk persons, may reinforce the role of rosuvastatin in CVD prevention. However, there are some concerns regarding the use of rosuvastatin.Based on the CTT report [1] and our recent literature review [4], 6 atorvastatin and 4 rosuvastatin studies, characterized by their rigorous double-blind, randomized, placebo-controlled study designs, have been published in the past two decades. A meta-analysis using a random effect model showed that atorvastatin significantly reduced the risk of CVD, with an odds ratio (OR) of 0.82 (95% CI: 0.75-0.90, p <0.001, Figure 1). In contrast, the results of a meta-analysis including the 4 rosuvastatin trials failed to detect a significant reduction in CVD risk, with an OR of 0.86 (0.69-1.07, p = 0.163). Surprisingly, the effect of rosuvastatin in CVD risk prevention remained controversial, even after inclusion of the encouraging HOPE-3 study [3] in the analysis, which then yielded an overall OR of 0.84 (0.70-1

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