Predictive Value of Peripheral Blood Neutrophil-To-Lymphocyte Ratio and Platelet-To-Lymphocyte Ratio on Patient Survival with Peritoneal Dialysis.

BACKGROUND: This study is to explore the predictive value of peripheral blood neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) on the prognosis of patients with peritoneal dialysis (PD). METHODS: A total of 378 patients who underwent PD from July 2004 to November 2019 were selected as the research subjects. According to whether death occurred during the follow-up period, they were divided into death group (86 cases) and survival group (292 cases). The differences in clinical indicators between the two groups were compared, and the multivariate Cox regression model and receiver operating characteristic curve (ROC) were used to analyze and summarize the factors affecting the prognosis of PD patients. RESULTS: Compared with the survival group, there were significant differences in age, lymphocytes, NLR, PLR, and combined cerebrovascular disease between the death group and the survival group (p < 0.05). Multivariate Cox regression analysis showed that advanced age (HR = 1.055, 95% CI: 1.038 - 1.072), increased NLR (HR = 1.136, 95% CI: 1.067 - 1.210), and increased PLR (HR = 1.184, 95% CI: 1.018 - 3.026) were risk factors for all-cause death in PD patients. The results showed that the area under the ROC curve (AUC) of NLR and PLR for predicting all-cause death of PD patients were 0.698 and 0.659, respectively, the sensitivity was 69.77%, and the specificity was 66.78% and 58.56%, respectively. The optimal critical values were NLR ≥ 3.71 and PLR ≥ 149.28. Taking the best cutoff value of the ROC curve as the threshold, it showed that the cumulative survival rate of patients with NLR ≥ 3.71 was significantly lower than that of patients with NLR < 3.71 (Log rank 2 = 37.551, p = 0.000). It also showed that the cumulative survival rate of patients with PLR ≥ 149.28 was lower than that of patients with PLR < 149.28 (Log rank 2 =23.686, p = 0.000). CONCLUSIONS: NLR and PLR have a good predictive effect on the prognosis of PD patients.

Perilipin2 inhibits diabetic nephropathy-induced podocyte apoptosis by activating the PPARγ signaling pathway.

Podocyte apoptosis plays a pivotal role in the pathogenesis of diabetic nephropathy (DN). The main purpose of this study was to investigate the effects of perilipin2 on high glucose (HG)-induced podocyte apoptosis and associated mechanisms. Differentially expressed genes (DEGs) in BTBR ob/ob mice vs. nondiabetic mice kidneys were obtained from GSE106841 dataset and picked out using the 'limma' package. The protein-protein interaction (PPI) network was constructed using the Search Tool for the Retrieval of Interacting Genes (STRING) and was visualized by Cytoscape. Perilipin2 was a hub gene using the cytoHubba plug-in from Cytoscape. Gene ontology (GO) analysis revealed that the 126 overlapping DEGs were mainly enriched in 'oxidation reduction' [biological process, (BP)], metal ion binding' [molecular function, (MF)] and 'extracellular region' [cellular component, (CC)]. KEGG pathway analysis revealed that perilipin2 was mainly involved in 'PPAR signaling pathway'. DN inhibited perilipin2 expression and PPARγ expression, as by both in vitro and in vivo studies. In vitro experiments demonstrated that perilipin2 inhibition could not only reduced PPARγ expression in podocytes, it could also promote the apoptosis, and inhibit the viability in HG treated podocytes using western blot, CCK8 and flow cytometry assays. Perilipin2 overexpression reversed the effects of HG on inhibiting podocalyxin, nephrin, precursor (pro)-caspase-3/-9 and PPARγ protein expression and increasing cleaved caspase-3/-9 protein expression. Furthermore, the functions of perilipin2 overexpression reversing HG-induced podocyte apoptosis were inhibited by PPARγ inhibitor. In conclusion, the functions of DN-induced podocyte apoptosis were inhibited by activation of the PPARγ signaling pathway caused by perilipin2 overexpression.

Successful application of roxadustat in the treatment of patients with anti-erythropoietin antibody-mediated renal anaemia: a case report and literature review.

Recombinant human erythropoietin (rHuEPO) has been used worldwide for treatment of renal anaemia due to its good curative effect. However, rHuEPO treatment is associated with a rare but severe complication because of the development of anti-EPO antibodies, which are difficult to treat. Currently, the main treatments for the anti-EPO antibodies include withdrawing the rHuEPO, providing blood transfusions and administrating steroid-based immunosuppressive agents. Although the above methods can alleviate anti-EPO-related anaemia, there are obvious side-effects such as decreased immunity and an increased risk of infection. Therefore, accurately identifying anti-EPO-related anaemia and effectively treating this complication is worth exploring. This current case report describes a 49-year-old female patient with chronic kidney disease that received rHuEPO subcutaneously and then developed anti-EPO antibody-mediated renal anaemia with her haemoglobin levels dropping to 37 g/l. The patient refused to be treated with steroids, so she received 120 mg roxadustat administered orally every 72 h and her Hb level increased to 110 g/l over a few months. This current case report demonstrates that roxadustat can be used to successfully treat anti-EPO antibody-mediated renal anaemia without the use of steroid-based immunosuppressants.

The Correlation Between Low Serum T3 Levels and All-Cause and Cardiovascular Mortality in Peritoneal Dialysis Patients.

OBJECTIVE: This study is to investigate the correlation between serum triiodothyronine (T3) levels and all-cause and cardiovascular mortality in PD patients. METHODS: A total of 376 end-stage renal disease (ESRD) patients who started maintenance PD treatment in the Department of Nephrology in our hospital and stable treatment for ≥3 months were selected, and the total T3 (TT3) and free T3 (FT3) levels were determined. Among them, 168 cases with FT3 <3.5 pmol/L and/or TT3 <0.92 nmol/L were divided into the low serum T3 level group, and the remaining 208 cases were divided into normal serum T3 level group. The Cox survival analysis method was used to analyze the correlation between low serum T3 levels and all-cause and cardiovascular mortality in PD patient. RESULTS: Compared with the normal serum T3 level group, patients with low serum T3 levels had higher systolic blood pressure and a higher proportion of heart disease, and lower levels of total T4, free T4, hemoglobin, serum albumin, blood calcium, serum total bilirubin, alanine aminotransferase, and 24-h urine volume (all P < 0.05). Binary Logistic regression analysis showed that heart disease (P = 0.003, OR: 2.628, 95% CI: 1.382-4.997) and high TT4 level (P < 0.001, OR: 0.968, 95% CI: 0.956-0.979) were related to low serum T3 levels in PD patients. Multivariate Cox regression analysis showed that low serum FT3 level was an independent risk factor for all-cause death in PD patients (HR = 0.633, 95% CI = 0.431-0.930; P < 0.020). CONCLUSION: Low serum T3 levels in PD patients were associated with heart disease and TT4 levels. Low serum FT3 levels were associated with the risk of all-cause death in PD patients.

Association between coffee consumption and risk of bladder cancer in a meta-analysis of 16 prospective studies.

BACKGROUND: Current evidence remains equivocal as to whether and how consumption of coffee may be associated with risk of bladder cancer, and potential influence of confounding by smoking on this association is yet to be elucidated. We conducted an updated meta-analysis of prospective studies to address these issues. METHODS: Relevant studies were identified by searching PubMed and EMBASE databases from inception to April 2019. A random-effects model was used to estimate summary relative risk (RR) with corresponding 95% confidence interval (CI) of bladder cancer associated with coffee consumption. RESULTS: The final analysis included 16 prospective studies comprising 2,122,816 participants and 11,848 bladder cancer cases. Overall, coffee consumption was not associated with risk of bladder cancer (RR high-vs-low = 1.07, 95% CI: 0.96-1.20). The lack of association persisted in the strata defined by sex or participants' smoking status. Meta-regression analyses identified the number cases (P difference = 0.06) and the degree of adjustment for smoking (P difference = 0.04) as potential sources of heterogeneity. There was an increased risk of bladder cancer related to higher coffee consumption among studies with fewer cases (RR high-vs-low = 1.38, 95% CI: 1.05-1.81) and among those with poorer adjustment for smoking (RR high-vs-low = 1.48, 95% CI: 1.14-1.93). Results were similar in the dose-response analyses (RR 1 cup/d = 1.01, 95% CI: 0.98-1.03). CONCLUSION: Best evidence available to date does not support an independent association between coffee consumption and bladder cancer risk. Some direct associations observed in individual studies may be a result of residual confounding by smoking. SUPPLEMENTARY INFORMATION: Supplementary information accompanies this paper at 10.1186/s12986-019-0390-3.