Background Diabetic nephropathy (DN) is a kidney damage caused by diabetes and the main cause of end-stage renal disease. However, the current treatment of DN has many limitations. Quercetin is a bioflavonoid compound with therapeutic benefits in metabolic diseases. This study aims to determine the therapeutic potentials and underlying mechanism of quercetin on DN. Methods We collected blood samples from DN patients and healthy controls and treated human mesangial cells (HMCs) with high glucose (HG) to establish an in vitro model of DN. Then we assessed the expression difference of miR-485-5p as well as YAP1 in serum of DN patients and healthy controls and between HG-induced HMCs and control cells. qRT-PCR and western blot were performed to assess miR-485-5p and YAP1 expression levels; CCK-8 and ELISAs were used to examine cell proliferation, inflammation, and oxidative stress. Dual luciferase reporter assay was implemented to detect the binding of miR-485-5p and YAP1 mRNA sequence. Results Quercetin suppressed proliferation, inflammation, and oxidative stress of HMCs induced by HG. As for mechanism, miR-485-5p directly bound to YAP1 and inhibited YAP1 expression. The downregulation of miR-485-5p and upregulation of YAP1 were also observed in the serum of DN patients. Quercetin modulated miR-485-5p/YAP1 axis to regulate HG-induced inflammation and oxidative stress. Conclusion: Quercetin inhibits the proliferation, inflammation, and oxidative stress of HMCs induced by HG through miR-485-5p/YAP1 axis, which might provide a novel treatment strategy for DN.

https://journals.sagepub.com/doi/pdf/10.1177/20587384211066440

Quercetin attenuates the proliferation, inflammation, and oxidative stress of high glucose-induced human mesangial cells by regulating the miR-485-5p/YAP1 pathway

β-N-Oxalyl-L-α,β-diaminopropionic acid from Panax notoginseng plays a major role in the treatment of type 2 diabetic nephropathy.

Background A very low protein diet (VLPD) with ketoacid analogs of essential amino acids (KA/EAA) administration can remarkably influence protein synthesis and metabolic disturbances of patients with advanced chronic kidney disease (CKD), and may also slow the decline in renal function. Methods A retrospective cohort study was carried out to monitor renal progression and metabolic and nutritional status among 140 patients with CKD stage III or IV. One group (n = 70) was on a low protein diet (LPD) with 0.6 g of protein intake, and another group (n = 70) was on a VLPD with 0.3 g of protein and KA/EAA supplementation of 100 mg/kg/day for 12 months. Results At 12-month follow-up, estimated glomerular filtration rate (GFR) significantly decreased from 41.6 ± 10.2 to 36.4 ± 8.8 mL/min/1.73 m2 (P 10% annually (adjusted hazard ratio, 0.42; 95% confidence interval, 0.23-0.79; P = 0.006) and significant correlations were found between using VLPD plus KA/EEA and increased GFR. Conclusion VLPD supplementation with KA/EAA is associated with delayed renal progression while preserving the nutritional status in the patients with CKD. Co-administration of VLPD and KA/EAA may prove an effective alternative to conservative management of CKD.

Very low protein diet plus ketoacid analogs of essential amino acids supplement to retard chronic kidney disease progression.

This study aimed to investigate the association between the proportion of glomerulosclerosis (focal segmental glomerulosclerosis and/or global glomerulosclerosis) and renal prognosis in patients with idiopathic membranous nephropathy (IMN). A retrospective analysis performed from January 2008 to December 2017 in the First Affiliated Hospital of Shenzhen University by renal biopsy confirmed 200 patients with IMN, and their clinical pathology and prognosis were compared. Patients were divided into three groups on the basis of glomerular sclerosis proportion tertiles: low (Tertile1 group, proportion of glomerulosclerosis, 0–0%), middle (Tertile2 group, proportion of glomerulosclerosis, 0–5.5%) and high (Tertile3 group, proportion of glomerulosclerosis, 5.8–72.7%) tertiles. The follow-up endpoints were decreased estimated glomerular filtration rate (eGFR) by 20%, end-stage renal disease, and all-cause mortality. (1) Both, the Tertile1 and Tertile2, groups had significantly lower albumin level and higher 24-h urine protein level than that in the Tertile3 group. Regarding treatment, as the proportion of glomerulosclerosis increases, a more aggressive treatment with glucocorticoids and immunosuppressants should be provided. (2) Correlation analysis showed that the proportion of glomerulosclerosis was positively associated with age (P < 0.05). However, it was negatively associated with eGFR (P < 0.05). (3) Renal tubular atrophy and renal interstitial inflammatory cell infiltration were considered independent correlative factors for glomerulosclerosis. Kaplan–Meier analysis revealed that renal survival rate was significantly lower in patients with a proportion of glomerulosclerosis ≥ 6.45% than in patients with a proportion of glomerulosclerosis < 6.45%. Cox regression analysis revealed that as the proportion of glomerulosclerosis increases, the risk of renal outcomes increases gradually. Patients in the Tertile3 (higher proportion of glomerulosclerosis) group had more severe renal pathological damage compared to patients in the Tertile1 and Tertile2 groups. Glomerulosclerosis is a risk factor for renal function progression and poor renal prognosis in patients with IMN. As the proportion of glomerulosclerosis increases, the risk of renal endpoint events increases gradually.

Glomerulosclerosis predicts poor renal outcome in patients with idiopathic membranous nephropathy.

The prevalence of diabetes mellitus (DM) is increasing at a staggering rate around the world. In the United States, more than 30.3 million Americans have DM. Type 2 diabetes mellitus (T2DM) accounts for 91.2% of diabetic cases and disproportionately affects African Americans and Hispanics. T2DM is a major risk factor for cardiovascular disease (CVD) and is the leading cause of morbidity and mortality among diabetic patients. While significant advances in T2DM treatment have been made, intensive glucose control has failed to reduce the development of macro and microvascular related deaths in this group. This highlights the need to further elucidate the underlying molecular mechanisms contributing to CVD in the setting of T2DM. Endothelial dysfunction (ED) plays an important role in the development of diabetes-induced vascular complications, including CVD and diabetic nephropathy (DN). Thus, the endothelium provides a lucrative means to investigate the molecular events involved in the development of vascular complications associated with T2DM. microRNAs (miRNA) participate in numerous cellular responses, including mediating messages in vascular homeostasis. Exosomes are small extracellular vesicles (40-160 nanometers) that are abundant in circulation and can deliver various molecules, including miRNAs, from donor to recipient cells to facilitate cell-to-cell communication. Endothelial cells are in constant contact with exosomes (and exosomal content) that can induce a functional response. This review discusses the modulatory role of exosomal miRNAs and proteins in diabetes-induced endothelial dysfunction, highlighting the significance of miRNAs as markers, mediators, and potential therapeutic interventions to ameliorate ED in this patient group. 

/pdf/to-the-future-the-role-of-exosome-derived-micrornas-as-53mhcjp6.pdf

To the Future: The Role of Exosome-Derived microRNAs as Markers, Mediators, and Therapies for Endothelial Dysfunction in Type 2 Diabetes Mellitus

Idiopathic membranous nephropathy (IMN) is one of the most common causes of nephrotic syndrome (NS) in adults. The latest study of the chronic kidney disease-prognosis consortium showed that a 30% decrease in the estimated glomerular filtration rate (eGFR) within 2 years could cover more patients and showed a better correlation with end-stage renal disease (ESRD), as compared with serum creatinine (SCr). The aim of the present study was to analyze prognostic factors of ESRD using a 30% decrease in eGFR within 2 years as the end-point. The medical records of patients who were diagnosed as having IMN by clinical pathology between February 2011 and August 2012 and had been followed up for ≥24 months were analyzed retrospectively. A 30% decrease in eGFR or the occurrence of ESRD were the end-points. Factors affecting the prognosis were analyzed by the χ2 test and multivariate logistic regression analysis, and the cumulative risk of risk factors was analyzed by Kaplan-Meier curve. A total of 73 patients with IMN were confirmed by clinical pathology. Blood pressure, tubulointerstitial injury area (TIA), glomerular sclerosis ratio, SCr, blood urea nitrogen, cystatin C, serum albumin and 24-h urine protein. In total, 28 patients (38.4%) reached the observation end-point. Multivariate logistic regression analysis showed that only age ≥60 years, serum albumin 25% were independent risk factors for predicting the occurrence of end-point events in the two groups (P 25% (log-rank P=0.004, P=0.024 and P=0.001). The results of the present study revealed that age ≥60 years, low serum albumin concentrations and severe tubulointerstitial injury are independent risk factors for the occurrence of ESRD in IMN patients.

/pdf/analysis-of-the-prognostic-risk-factors-of-idiopathic-3qfb09xggt.pdf

Analysis of the prognostic risk factors of idiopathic membranous nephropathy using a new surrogate end-point.

OBJECTIVE Diabetic nephropathy (DN) is a serious kidney-based complication of diabetes, wherein podocyte injury is deemed crucial in the development of early stage. Various miRNAs, as report goes, is involved in the pathogenesis of varieties of kidney diseases including DN. In this study, we found a target relationship between miR-30a-5p and Becn1, of which there are few studies about the role in podocyte injury. We therefore used immortalized rat podocyte cell line to explore the role and molecular mechanism of miR-30a-5p targeting Becn1 gene in high-glucose-induced glomerular podocyte injury. METHODS The mRNA and protein expressions of miR-30a-5p and Becn1 were detected respectively by quantitative reverse transcriptase PCR and western blotting. The proliferation, apoptosis, and the levels of interleukin (IL)-6 and tumor necrosis factor (TNF)-α were detected by MTT assay, flow cytometry, and enzyme-linked immuno sorbent assay, respectively. Intracellular reactive oxygen species (ROS), superoxide dismutase (SOD) and malondialdehyde (MDA) levels were also determined. RESULTS Compared with normal group, miR-30a-5p in model groups were down-regulated, while Becn1 expression was significantly up-regulated, with slower proliferation, higher apoptosis rate, lower SOD level, and significantly higher ROS, MDA, IL-6, and TNF-α levels (all P<0.05). Overexpression of miR-30a-5p or Becn1 knock-out could lower Becn1 expression, apoptosis rate, promote proliferation, with relatively higher SOD level and lower ROS, MDA, Il-6, and TNF-α levels of model cells (all P<0.05). CONCLUSION Up-regulation of miR-30a-5p can suppress the expression of Becn1 to increase the growth and inhibit the apoptosis of immortalized rat podocyte cell line, therefore ameliorating podocyte injury induced by high glucose in vitro.

miR-30a-5p targets Becn1 to ameliorate high-glucose-induced glomerular podocyte injury in immortalized rat podocyte cell line.

TGF-β1 has been recognized as a key mediator in DN. This study aimed to observe the effects of low-protein diets supplemented with ketoacid on mRNA and protein expression of TGF-β and TβRI and t TβRII receptors in the renal tissue of diabetic rats. A diabetes model was established in 72 male SD rats. They were then equally randomized to three groups: NPD group, LPD group, and LPD + KA group. Additional 24 male SD rats receiving normal protein diets were used as the control. Eight rats from each group were sacrificed at weeks 4, 8, and 12 after treatment, from which SCr, BUN, serum albumin, and 24 h urinary protein excretion were collected. The expressions of TGF-β1, TβRI, and TβRII in LPD and LPD + KA groups were significantly lower than those in NPD group and lower in LPD + KA group than those in LPD group. Low-protein diets supplemented with ketoacid have been demonstrated to provide a protective effect on the renal function as represented by reduced SCr, BUN, and urinary protein excretion, probably through downregulating the gene expression of TGF-β1 and its receptors in LPD + KA group.

/pdf/effects-of-low-protein-diets-supplemented-with-ketoacid-on-348jn7hbc8.pdf

Effects of Low-Protein Diets Supplemented with Ketoacid on Expression of TGF-β and Its Receptors in Diabetic Rats

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Analysis of the prognostic risk factors of idiopathic membranous nephropathy using a new surrogate end-point.

miR-30a-5p targets Becn1 to ameliorate high-glucose-induced glomerular podocyte injury in immortalized rat podocyte cell line.

Effects of Low-Protein Diets Supplemented with Ketoacid on Expression of TGF-β and Its Receptors in Diabetic Rats