Effect of nutritional supplementation on mortality in peritoneal dialysis patients: A meta-analysis.

BACKGROUND: Malnutrition is a common clinical problem in peritoneal dialysis (PD) patients and is a predictor of mortality. This work analyzes the effect of nutritional supplementation for PD patients on all-cause and cardiovascular disease (CVD)-related deaths by meta-analysis. METHODS: A study about nutritional interventions for PD patients on all-cause or CVD-related mortality is included. RESULTS: Eight studies were included. The results showed that nutritional intervention can reduce all-cause mortality in PD patients (HR, 0.71; 95% confidence interval (CI), 0.64-0.79; p < 0.01). In CVD-related mortality, the results also showed that nutritional interventions significantly reduce CVD-related mortality (HR, 0.75; 95% CI, 0.64-0.87; p < 0.01). In exploratory analysis, vitamin D, folic acid, and high-plant-protein ratio intake have relative advantages. CONCLUSION: Appropriate nutritional supplementation to PD patients can effectively reduce all-cause and CVD- related mortality in clinical practice, especially for vitamin D, folic acid, sodium supplements, and a high proportion of plant protein.

Bacterial IgA protease-mediated degradation of agIgA1 and agIgA1 immune complexes as a potential therapy for IgA Nephropathy.

Mesangial deposition of aberrantly glycosylated IgA1 (agIgA1) and its immune complexes is a key pathogenic mechanism of IgA nephropathy (IgAN). However, treatment of IgAN remains ineffective. We report here that bacteria-derived IgA proteases are capable of degrading these pathogenic agIgA1 and derived immune complexes in vitro and in vivo. By screening 14 different bacterial strains (6 species), we found that 4 bacterial IgA proteases from H. influenzae, N. gonorrhoeae and N. meningitidis exhibited high cleaving activities on serum agIgA1 and artificial galactose-depleted IgA1 in vitro and the deposited agIgA1-containing immune complexes in the mesangium of renal biopsy from IgAN patients and in a passive mouse model of IgAN in vitro. In the modified mouse model of passive IgAN with abundant in situ mesangial deposition of the agIgA-IgG immune complexes, a single intravenous delivery of IgA protease from H. influenzae was able to effectively degrade the deposited agIgA-IgG immune complexes within the glomerulus, demonstrating a therapeutic potential for IgAN. In conclusion, the bacteria-derived IgA proteases are biologically active enzymes capable of cleaving the circulating agIgA and the deposited agIgA-IgG immune complexes within the kidney of IgAN. Thus, the use of such IgA proteases may represent a novel therapy for IgAN.

[Cordycepin protects podocytes from injury mediated by complements complex C5b-9].

OBJECTIVE: To explore the protective effect of Cordycepin (3'-deoxyadenosine), a bioactive compound of Cordyceps Sinensis, on injury of podocytes. METHODS: C5b-9-induced podocyte injury was used as a model of membranous nephropathy in vitro. This model was established using mouse podocyte cell line--MPC5. Cordycepin was given as an intervention. Ultra-micro morphological changes were observed by electron microscope. F-actin cytoskeleton and expression of nephrin were observed by fluorescence microscope. The phosphorylation of mitogen-activated protein kinase (MAPK) was measured by Western blot. RESULTS: Stimulated by C5b-9 for 3 h, MPC5 showed secondary foot processes, with cytoskeleton structure damaged, nephrin relocated from the cell surface to the cytoplasm, and cell signal pathway-p38, JNK and ERK activated. Cordycepin protected foot processes and cytoskeleton structures of podocytes, suppressed the redistribution of nephrin, and inhibited p38/JNK action. CONCLUSION: Cordycepin can protect podocyte from C5b-9-induced injury partly through inhibiting the activation of p38/JNK signaling pathway.