Self-management intervention aims to facilitate an individual’s ability to make lifestyle changes. The effectiveness of this intervention in non-dialysis patients with chronic kidney disease (CKD) is limited. In this study, we applied a systematic review and meta-analysis to investigate whether self-management intervention improves renoprotection for non-dialysis chronic kidney disease. We conducted a comprehensive search for randomized controlled trials addressing our objective. We searched for studies up to May 12, 2018. Two reviewers independently evaluated study quality and extracted characteristics and outcomes among patients with CKD within the intervention phase for each trial. Meta-regression and subgroup analyses were conducted to explore heterogeneity. We identified 19 studies with a total of 2540 CKD patients and a mean follow-up of 13.44 months. Compared with usual care, self-management intervention did not show a significant difference for risk of all-cause mortality (5 studies, 1662 participants; RR 1.13; 95% CI 0.68 to 1.86; I2 = 0%), risk of dialysis (5 studies, 1565 participants; RR 1.35; 95% CI 0.84 to 2.19; I2 = 0%), or change in eGFR (8 studies, 1315 participants; SMD -0.01; 95% CI -0.23 to 0.21; I2 = 64%). Moreover, self-management interventions were associated with a lower 24 h urinary protein excretion (4 studies, 905 participants; MD − 0.12 g/24 h; 95% CI -0.21 to − 0.02; I2 = 3%), a lower blood pressure level (SBP: 7 studies, 1201 participants; MD − 5.68 mmHg; 95%CI − 9.68 to − 1.67; I2 = 60%; DBP: 7 studies, 1201 participants; MD − 2.64 mmHg, 95% CI -3.78 to − 1.50; I2 = 0%), a lower C-reactive Protein (CRP) level (3 studies, 123 participants; SMD -2.8; 95% CI -2.90 to − 2.70; I2 = 0%) and a longer distance on the 6-min walk (3 studies, 277 participants; SMD 0.70; 95% CI 0.45 to 0.94; I2 = 0%) when compared with the control group. We observed that self-management intervention was beneficial for urine protein decline, blood pressure level, exercise capacity and CRP level, compared with the standard treatment, during a follow-up of 13.44 months in patients with CKD non-dialysis. However, it did not provide additional benefits for renal outcomes and all-cause mortality.

Accumulating evidence reveals that both inflammation and lymphocyte dysfunction play a vital role in the development of diabetic nephropathy (DN). Hyperoside (HPS) or quercetin-3-O-galactoside is an active flavonoid glycoside mainly found in the Chinese herbal medicine Tu-Si-Zi. Although HPS has a variety of pharmacological effects, including anti-oxidative and anti-apoptotic activities as well as podocyte-protective effects, its underlying anti-inflammatory mechanisms remain unclear. Herein, we investigated the therapeutic effects of HPS on murine DN and the potential mechanisms responsible for its efficacy. We used C57BLKS/6J ^Lepdb/db mice and a high glucose (HG)-induced bone marrow-derived macrophage (BMDM) polarization system to investigate the potentially protective effects of HPS on DN. Our results showed that HPS markedly reduced diabetes-induced albuminuria and glomerular mesangial matrix expansion, accompanied with a significant improvement of fasting blood glucose level, hyperlipidaemia and body weight. Mechanistically, pretreatment with HPS effectively regulated macrophage polarization by shifting proinflammatory M1 macrophages (F4/80⁺CD11b⁺CD86⁺) to anti-inflammatory M2 ones (F4/80⁺CD11b⁺CD206⁺) in vivo and in bone marrow-derived macrophages (BMDMs) in vitro, resulting in the inhibition of renal proinflammatory macrophage infiltration and the reduction in expression of monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor (TNF-α) and inducible nitric oxide synthase (iNOS) while increasing expression of anti-inflammatory cytokine Arg-1 and CD163/CD206 surface molecules. Unexpectedly, pretreatment with HPS suppressed CD4⁺ T cell proliferation in a coculture model of IL-4-induced M2 macrophages and splenic CD4⁺ T cells while promoting their differentiation into CD4⁺IL-4⁺ Th2 and CD4⁺Foxp3⁺ Treg cells. Taken together, we demonstrate that HPS ameliorates murine DN via promoting macrophage polarization from an M1 to M2 phenotype and CD4⁺ T cell differentiation into Th2 and Treg populations. Our findings may be implicated for the treatment of DN in clinic.

Kidneys are one of the targets for SARS-CoV-2, it is reported that up to 36% of patients with SARS-CoV-2 infection would develop into acute kidney injury (AKI). AKI is associated with high mortality in the clinical setting and contributes to the transition of AKI to chronic kidney disease (CKD). Up to date, the underlying mechanisms are obscure and there is no effective and specific treatment for COVID-19-induced AKI. In the present study, we investigated the mechanisms and interactions between Quercetin and SARS-CoV-2 targets proteins by using network pharmacology and molecular docking. The renal protective effects of Quercetin on COVID-19-induced AKI may be associated with the blockade of the activation of inflammatory, cell apoptosis-related signaling pathways. Quercetin may also serve as SARS-CoV-2 inhibitor by binding with the active sites of SARS-CoV-2 main protease 3CL and ACE2, therefore suppressing the functions of the proteins to cut the viral life cycle. In conclusion, Quercetin may be a novel therapeutic agent for COVID-19-induced AKI. Inhibition of inflammatory, cell apoptosis-related signaling pathways may be the critical mechanisms by which Quercetin protects kidney from SARS-CoV-2 injury.

Objective: Diabetic kidney disease (DKD) has become the major cause of end-stage renal disease (ESRD) associated with the progression of renal fibrosis. As gut microbiota dysbiosis is closely related to renal damage and fibrosis, we investigated the role of gut microbiota and microbiota-related serum metabolites in DKD progression in this study.Methods: Fecal and serum samples obtained from predialysis DKD patients from January 2017 to December 2019 were detected using 16S rRNA gene sequencing and liquid chromatography-mass spectrometry, respectively. Forty-one predialysis patients were divided into two groups according to their estimated glomerular filtration rate (eGFR): the DKD non-ESRD group (eGFR ≥ 15 ml/min/1.73 m²) (n = 22), and the DKD ESRD group (eGFR < 15 ml/min/1.73 m²) (n = 19). The metabolic pathways related to differential serum metabolites were obtained by the KEGG pathway analysis. Differences between the two groups relative to gut microbiota profiles and serum metabolites were investigated, and associations between gut microbiota and metabolite concentrations were assessed. Correlations between clinical indicators and both microbiota-related metabolites and gut microbiota were calculated by Spearman rank correlation coefficient and visualized by heatmap.Results: Eleven different intestinal floras and 239 different serum metabolites were identified between the two groups. Of 239 serum metabolites, 192 related to the 11 different intestinal flora were mainly enriched in six metabolic pathways, among which, phenylalanine and tryptophan metabolic pathways were most associated with DKD progression. Four microbiota-related metabolites in the phenylalanine metabolic pathway [hippuric acid (HA), L-(−)-3-phenylactic acid, trans-3-hydroxy-cinnamate, and dihydro-3-coumaric acid] and indole-3 acetic acid (IAA) in the tryptophan metabolic pathway positively correlated with DKD progression, whereas L-tryptophan in the tryptophan metabolic pathway had a negative correlation. Intestinal flora g_Abiotrophia and g_norank_f_Peptococcaceae were positively correlated with the increase in renal function indicators and serum metabolite HA. G_Lachnospiraceae_NC2004_Group was negatively correlated with the increase in renal function indicators and serum metabolites [L-(−)-3-phenyllactic acid and IAA].Conclusions: This study highlights the interaction among gut microbiota, serum metabolites, and clinical indicators in predialysis DKD patients, and provides new insights into the role of gut microbiota and microbiota-related serum metabolites that were enriched in the phenylalanine and tryptophan metabolic pathways, which correlated with the progression of DKD.

Chronic wounds are a major health problem with increasing global prevalence, which endangers the physical and mental health of those affected and is a heavy burden to healthcare providers. Artemisia argyi extract (AE) has excellent antibacterial and anti-inflammatory properties. In this research, we developed AE loaded composite hydrogel scaffold based on methacrylate gelatin (GelMA)/methacrylate hyaluronic acid (HAMA) and mesoporous silica nanoparticle (MSN) as sustained-release drug carrier vehicles for the treatment of chronic wounds. The presented GelMA/1%HAMA hydrogel possessed stable rheological properties, suitable mechanical properties, appropriate biodegradability, swelling, sustained-release AE capacity. In vitro antibacterial and cell experiments showed that the GelMA/HAMA/MSN@AE hydrogel had excellent antibacterial activity and biocompatibility and induced macrophages to differentiate into M2 phenotype. In vivo wound healing of rat full-thickness cutaneous wounds further demonstrated that the prepared GelMA/HAMA/MSN@AE hydrogel could significantly promote chronic wound healing by upregulating the expression of IL-4, TGF-β1, CD31, and α-SMA but downregulating the expression of TNF-α and IFN-γ and promoting M1-M2 macrophages polarization. Altogether, we believe that the GelMA/HAMA/MSN@AE hydrogel will have wide application prospects in healing chronic wounds.

Diabetic kidney disease (DKD) is the most common diabetic complication and is a leading cause of end-stage kidney disease. Increasing evidence shows that DKD is regulated not only by many classical signaling pathways but also by epigenetic mechanisms involving chromatin histone modifications, DNA methylation, and non-coding RNA (ncRNAs). In this review, we focus on our current understanding of the role and mechanisms of ncRNAs, including microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) in the pathogenesis of DKD. Of them, the regulatory role of TGF-β/Smad3-dependent miRNAs and lncRNAs in DKD is highlighted. Importantly, miRNAs and lncRNAs as biomarkers and therapeutic targets for DKD are also described, and the perspective of ncRNAs as a novel therapeutic approach for combating diabetic nephropathy is also discussed.