Hemodialysis (HD) patients are highly susceptible to COVID-19 infection. However, comprehensive assessments of current evidence regarding COVID-19 in HD patients remain incomplete. We systematically searched PUBMED and EMBASE for articles published on incidence or mortality of COVID-19 infection in HD patients until September 2020. Two independent researchers extracted data and study-level risk of bias across studies. We conducted meta-analysis of proportions for incidence and mortality rate. Study heterogeneity and publication bias were assessed. A total of 29 articles with 3261 confirmed COVID-19 cases from a pool of 396,062 HD patients were identified. Incidence of COVID-19 in these HD patients was 7.7% (95% CI: 5.0–10.9%; study heterogeneity: I2 = 99.7%, p < 0.001; risk of publication bias, Egger’s test, p < 0.001). Overall mortality rate was 22.4% (95% CI: 17.9–27.1%; study heterogeneity: I2 = 87.1%, p < 0.001; risk of publication bias, Egger’s test: p = 0.197) in HD patients with COVID-19. Reported estimates were higher in non-Asian than Asian countries. Quality of study may affect the reported incidence but not the mortality among studies. Both incidence and mortality of COVID-19 infection were higher in HD patients. Available data may underestimate the real incidence of infection. International collaboration and standardized reporting of epidemiological data should be needed for further studies.

Background: Micronutrients are essential in maintaining normal human physiology. Data regarding the association between micronutrients and renal outcomes in chronic kidney disease (CKD) are lacking. Methods: This prospective observational cohort study enrolled 261 patients with CKD stages 1–5 and 30 subjects with normal renal function. Baseline serum zinc (Zn), selenium (Se), chromium, manganese, and copper, and laboratory tests were performed at enrolment. The primary endpoint was the presence of end-stage renal disease (ESRD) requiring long-term renal replacement therapy. Results: The median follow-up periods of renal and non-renal survivals were 67.78 and 29.03 months, respectively. Multiple linear regression showed that Zn and Se (β ± SE: 24.298 ± 8.616, p = 0.005; 60.316 ± 21.875, p = 0.006, respectively) levels were positively correlated with renal function. Time to ESRD was significantly longer for those with Zn levels ≥1287.24 ng/g and Se levels ≥189.28 ng/g (both p < 0.001). Cox regression analysis identified a higher Zn level as an independently negative predictor of ESRD after adjusting for renal function (hazard ratio, 0.450, p = 0.019). Conclusion: Serum Se and Zn concentrations are positively associated with renal function and better renal outcomes. A higher Zn concentration could independently predict better renal survival.

Background: Chronic kidney disease (CKD) is pathologically correlated with a sophisticated milieu of innate and adaptive immune dysregulation, but the underlying immunological disturbances remain poorly understood. Methods: To address this, we comprehensively interrogated cellular and soluble elements of the immune system by using high-dimensional flow cytometry to analyze peripheral blood mononuclear cells and performing cytokine/chemokine profiling of serum samples, respectively, in a cohort of 69 patients and 19 non-CKD controls. Results: Altered serum levels of several cytokines/chemokines were identified, among which concentrations of stem cell factor (SCF) were found to be elevated with the progression of CKD and inversely correlated with estimated glomerular filtration rate (eGFR). Deep immunophenotyping analyses reveal a global change in immune modulation associated with CKD severity. Specifically, a decrease in the subsets of CD56dim natural killer (NK) cells (KLRG-1+CD38+CD64+CD15+CD197+) and monocytes (KLRG-1+CD38+PD-1+) was detected in severe CKD compared with controls and mild CKD. In addition, comparisons between mild and severe CKD demonstrated a loss of a mature B cell population (PD-1+CD197+IgD+HLA-DR+) in the advanced stages of disease. Further, we identified immunophenotypic markers to discriminate mild CKD from the controls, among which the portion of CD38+ monocytes was of particular value in early diagnosis. Conclusions: Our data unveil severity-specific immunological signatures perturbed in CKD patients.

Background: Animal studies have demonstrated that an oral absorbent AST-120 modulates gut environment. However, this phenomenon remains unclear in humans. This study aimed to assess the effects of AST-120 on the gut microbiota, related functional capability and metabolomic profiling in advanced chronic kidney diseases (CKD) patients. Methods: Eight advanced CKD patients with AST-120 (CKD+AST), 24 CKD patients (CKD), and 24 non-CKD controls were enrolled. We analyzed 16S rRNA pyrosequencing of feces and serum metabolomics profiling. Results: The CKD+AST group exhibited dispersed microbial community structure (β-diversity, p < 0.001) compared to other groups. The relative abundances of at least 16 genera were significantly different amongst the three groups. Increases of fatty acids-producing bacteria (Clostridium_sensu_stricto_1, Ruminococcus_2, Eubacterium_nodatum and Phascolarctobacterium) associated with elevated serum acetic acid and octanoic acid levels were found in CKD+AST group. Analysis of microbial gene function indicated that pathway modules relevant to metabolisms of lipids, amino acids and carbohydrates were differentially enriched between CKD+AST and CKD groups. Specifically, enrichments of gene markers of the biosynthesis of fatty acids were noted in the CKD+AST group. Conclusion: Advanced CKD patients exhibited significant gut dysbiosis. AST-120 can partially restore the gut microbiota and intervenes in a possible signature of short- and medium-chain fatty acids metabolism.

The mortality rate of patients on extracorporeal membrane oxygenation (ECMO), especially those patients that develop acute kidney injury (AKI) is high. Acute kidney disease (AKD) is a term used to describe the continuum from AKI to chronic kidney disease. However, the role of AKD in predicting the prognosis of patients on ECMO support is unclear. A total of 168 patients who received ECMO support and survived for more than 7 days at a single hospital from 2003 to 2008 were enrolled for this study and followed up for 10 years or till mortality. Kaplan-Meier analysis and Cox proportional hazards model were used to determine the prognostic factors associated with survival. The median survival times of patients with stage 0, stage 1, stage 2 and stage 3 AKD were ≥ 10 years, 43.9 months, 1 month, and half a month, respectively. There were statistically significant differences in cumulative survival rate between patients with stage 3 AKD and those with stage 0, 1, and 2 AKD (Cox-Mantel log rank test, p<0.001, p<0.001, p = 0.023), and between patients with stage 0 AKD and those with stage 1 and 2 AKD (Cox-Mantel log rank test, p = 0.012, p<0.001). Cox regression analysis revealed that AKD stage (hazard ratio [HR]: 2.576, 95% confidential interval [CI]: 1.268–5.234, p = 0.009 for stage 1; HR: 2.349; 95% CI: 1.101–5.512, p = 0.029 for stage 2; HR: 5.252; 95% CI: 2.715–10.163, p<0.001 for stage 3) was significant independent predictor of survival. AKD stage is an independent predictor of survival in patients on ECMO support.

Technique failure secondary to peritonitis is a grave impediment to remain in peritoneal dialysis (PD) therapy leading to high mortality. Multidisciplinary predialysis education (MPE) has shown improvement in outcomes of chronic kidney disease (CKD) patients. However, the legacy effects of MPE in PD patients remain unclear. All patients who started PD at single hospital in 2007–16 were enrolled. The incidences of peritonitis and peritonitis-related mortality were compared between MPE recipients and non-recipients. The content of the MPE was standardized in accordance with the NKF/DOQI guidelines. Kaplan-Meier analysis and Cox proportional hazards model were applied to identify the prognostic factors associated with peritonitis-free survival. Of 398 PD patients, 169 patients had received MPE before starting PD. The patients of MPE group had a lower peritonitis rate [median (IQR) 0 (0.29) versus 0.11 (0.69) episodes/person-year, P< 0.001] and a lower percentage of peritonitis-related deaths (3.6% versus 8.7%, P = 0.04) compared with the non-MPE group. The median time to the first episode of peritonitis in the non-MPE and MPE groups was 33.9 months and 46.7 months, respectively (Cox-Mantel log rank test, P = 0.003). Cox regression analysis revealed that MPE assignment (HR: 0.594; 95% CI: 0.434–0.813, P< 0.001) were significant independent predictors for peritonitis-free survival. An efficient standardized MPE program may prolong the time to the first episode of peritonitis and reduce peritonitis rate, independent of age, gender, diabetes, hypertension, educational status and PD modality. Subsequently, decreased peritonitis-related death.