Aim: Renal replacement therapy was primary treatment for end stage kidney (ESRD) patients. Numbers of studies comparing peritoneal dialysis (PD) and hemodialysis (HD) yielded inconsistent results. The aim of this study was to assess the mortality risk between diabetic PD patients and those in HD. Methods: We included cohort studies comparing the risk of death among diabetic ESRD patients who receiving peritoneal dialysis or hemodialysis by searching Medline and Embase. Overall estimates were calculated using the random-effects model. Results: Seventeen studies were included in the meta-analyses. Mortality comparison between PD and HD in the diabetic ESRD patients showed PD significantly increased mortality rate (hazard ratio (HR) 1.20; 95% confidence interval (CI) 1.10-1.30; I 2 ¼ 89.1%). The overall HR using an intention-to-treat analysis was 1.23 with 95% CI (1.13 to 1.34). Meta-regression demonstrated PD patients from Asian country were associated with increase in mortality risk (coefficient ¼ 0.270, SE ¼ 0.112, p ¼ .033). Limitation: The high heterogeneity in our meta-analyses undermined the robustness of the findings. Conclusion: ESRD patients with diabetes may benefit more from HD than PD.
The combined use of Foley catheter and misoprostol results in a reduced time to delivery, a reduced frequency tachysystole with fetal heart rate changes, and an increased incidence of chorioamnionitis.
Purpose: Morbidity associated with and mortality from acute kidney injury (AKI) is gradually increasing, and no efficient drug is available. We explored whether neferine, a bisbenzylisoquinoline alkaloid, attenuated AKI, and the possible mechanisms in play in vivo and in vitro.
Methods: We induced AKI using ischemia-reperfusion (I/R) or lipopolysaccharide (LPS) in vivo. C57 BL/6 male mice were randomized into two groups each containing four subgroups: control, neferine, I/R or LPS, and I/R or LPS + neferine. Mice were sacrificed 24 h after AKI induction and kidneys and sera were collected. NRK-52E cells were exposed to hypoxia/reoxygenation (H/R) or LPS in vitro.
Results: Neferine pretreatment significantly alleviated kidney functional loss and pathological damage. In the AKI mouse models induced by I/R or LPS, neferine inhibited the infiltration of inflammatory cells, including granulocytes and macrophages. Both in vivo and in vitro, neferine attenuated apoptosis, suppressed inflammatory cytokine production, decreased degradation of IκB-α, and inhibited nuclear translocation of NF-κB. Furthermore, it also upregulated Klotho expression in AKI.
Conclusion: Neferine mitigated renal injury in AKI models, perhaps by suppressing the activation of NF-κB and upregulating the expression of Klotho.
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