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Our recent studies demonstrated that both nintedanib, an FDA-approved quadruple kinase inhibitor, and gefitinib, an epidermal growth factor receptor (EGFR) inhibitor, protect against obstructive kidney disease. It remains unknown whether they have a synergistic effect. In this study, we investigated the effect of combined administration of nintedanib and gefitinib on renal fibrosis in a murine model of renal fibrosis induced by unilateral ureteral obstruction (UUO). Combined treatment with nintedanib and gefitinib after UUO resulted in a greater antifibrotic effect compared with their individual application. Mechanistically, administration of nintedanib blocked UUO-induced phosphorylation of multiple kinase receptors associated renal fibrosis, including platelet-derived growth factor receptors, fibroblast growth factor receptors, vascular endothelial growth factor receptors, and Src family kinase, while gefitinib inhibited EGFR phosphorylation. Their combination also exhibited a more pronounced effect iand may hold translational potential for the treatment of chronic kidney disease. Previous studies have reported that serum magnesium (Mg) deficiency is involved in the development of heart failure, particularly in patients with end-stage kidney disease. The association between serum Mg levels and mortality risk in patients receiving hemodialysis is controversial. We aimed to estimate the prognostic value of serum Mg concentration on all-cause mortality and cardiovascular mortality in patients receiving hemodialysis. We did a systematic literature search in PubMed, EMBASE, Cochrane Library, and Web of Science to identify eligible studies that reported the prognostic value of serum Mg levels in mortality risk among patients on hemodialysis. We performed a meta-analysis by pooling and analyzing hazard ratios (HRs) and 95% confidence intervals (CIs). We identified 13 observational studies with an overall sample of 42,967 hemodialysis patients. Higher all-cause mortality (adjusted HR 1.58 [95% CI 1.31-1.91]) and higher cardiovascular mortality (adjusted HR 3.08 [95% CI 1.27-7.50]) were found in patients with lower serum Mg levels after multivariable adjustment. There was marked heterogeneity ( = 79.6%, < 0.001) that was partly explained by differences in age stratification and study area. In addition, subgroup analysis showed that a serum Mg concentration of ≤1.1 mmol/L might be the vigilant cutoff value. A lower serum Mg level was associated with higher all-cause mortality and cardiovascular mortality in patients receiving hemodialysis. A lower serum Mg level was associated with higher all-cause mortality and cardiovascular mortality in patients receiving hemodialysis. Stimulated by both microbial and endogenous ligands, toll-like receptors (TLRs) play an important role in the development and progression of renal diseases. As a highly conserved large family, TLRs have 11 members in humans (TLR1∼TLR11) and 13 members in mouse (TLR1∼TLR13). It has been widely reported that TLR2 and TLR4 signaling, activated by both exogenous and endogenous ligands, promote disease progression in both renal ischemia-reperfusion injury and diabetic nephropathy. TLR4 also vitally functions in CKD and infection-associated renal diseases such as pyelonephritis induced by urinary tract infection. Stimulation of intracellular TLR7/8 and TLR9 by host-derived nucleic acids also plays a key role in systemic lupus erythematosus. Given that certain microRNAs with GU-rich sequence have recently been found to be able to serve as TLR7/8 ligands, these microRNAs may initiate pro-inflammatory signal via activating TLR signal. Moreover, as microRNAs can be transferred across different organs via cell-secreted exosomes or protein-RNA complex, the TLR signaling activated by the miRNAs released by other injured organs may also result in renal dysfunction. In this review, we sum up the recent progress in the role of TLRs in various forms of glomerulonephritis and discuss the possible prevention or therapeutic strategies for clinic treatment to renal diseases. In this review, we sum up the recent progress in the role of TLRs in various forms of glomerulonephritis and discuss the possible prevention or therapeutic strategies for clinic treatment to renal diseases. Both acute kidney injury (AKI) and CKD are complex syndromes caused by multiple etiologies and presented with various degrees of severity. Studies on adults provide strong evidence that AKI is an independent risk factor for both the initiation and progression of CKD, and the severity, frequency, and duration of AKI are crucial factors in the subsequent development of CKD. https://www.selleckchem.com/products/sulfopin.html However, without consensus definitions of AKI and CKD and long-term follow-up studies using predictive biomarkers, it is difficult to clarify the potential for transition from AKI to CKD in pediatric populations. The goal of this review is to describe the most recent studies in epidemiology of pediatric AKI and biomarkers aiding in the earlier detection of AKI and CKD. KDIGO criteria for AKI have been widely applied for pediatric AKI studies. AKI in critically ill and non-critically ill children is common. CKD is highly prevalent in pediatric AKI survivors. Compared with traditional biomarkers such as serum Cr, proteinuria, and estimated glomerular filtration rate, urinary biomarkers earlier identifying AKI may also detect CKD earlier, but additional studies are required to determine their clinical utility. The use of consensus AKI criteria has improved our understanding of pediatric AKI epidemiology, and an association between AKI and CKD in pediatric populations has been endorsed. However, further studies are needed to better answer a definitive causal relationship between pediatric AKI and the subsequent development of CKD. The use of consensus AKI criteria has improved our understanding of pediatric AKI epidemiology, and an association between AKI and CKD in pediatric populations has been endorsed. However, further studies are needed to better answer a definitive causal relationship between pediatric AKI and the subsequent development of CKD.
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