Complanatoside A targeting NOX4 blocks renal fibrosis in diabetic mice by suppressing NLRP3 inflammasome activation and autophagy.

Сhronic kidney Disease (CKD) is the cause of both morbidity and mortality worldwide. In Ukraine, 12 % of the population is diagnosed with CKD. Significantly worsen the quality of life in patients with CKD progression of renal fibrosis and impaired mineral homeostasis. Early diagnosis and treatment are the main measures to prevent CKD progression and delay adverse effects. Deficiency of early, non-invasive biomarkers adversely affects the ability to rapidly detect and treat CKD. Proximal tubular lesions play an important role in the progression of CKD. There are new markers of kidney damage, such as uromodulin (UMOD), Klotho protein and post-translational modifications of fetuin A (FtA). Treatment of CKD in the early stages may improve renal function and/or slow the progression of CKD.

/pdf/the-value-of-proteomic-studies-of-the-latest-markers-of-2nyvho3n.pdf

The value of proteomic studies of the latest markers of kidney damage in the urine to assess the course, progression and complications in patients with CKD

Uromodulin is a nephrospecific protein that is most common in normal urine. And although it has been known for more than 70 years, the function of uromodulin remains unclear. Uromodulin is involved in regulating the transport of salts, protects against urinary tract infections, namely, the mucous membrane of the bladder, and prevents the formation of kidney stones, as well as plays a role in kidney damage and innate immunity. Serum uromodulin and uromodulin of urine, daily excretion and excretion of uromodulin per 1 milliliter of creatinine clearance are actively studied. Complete genome studies of the association have established a correlation between uromodulin gene mutations and autosomal dominant tubulointerstitial kidney disease. 

/pdf/uromodulin-as-a-potential-candidate-marker-for-predicting-2745n1y4.pdf

Uromodulin as a potential candidate marker for predicting the course of chronic kidney disease

Uromodulin is recognized as a protective factor during AKI-to-CKD progression, but the mechanism remains unclear. We previously reported that uromodulin interacts with complement factor H (CFH) in vitro, and currently aimed to study the expression and interaction evolution of uromodulin and CFH during AKI-to-CKD transition. We successfully established a rat model of AKI-to-CKD transition induced by a four-time cisplatin treatment. The blood levels of BUN, SCR, KIM-1 and NGAL increased significantly during the acute injury phase and exhibited an uptrend in chronic progression. PAS staining showed the nephrotoxic effects of four-time cisplatin injection on renal tubules, and Sirius red highlighted the increasing collagen fiber. Protein and mRNA levels of uromodulin decreased while urine levels increased in acute renal injury on chronic background. An extremely diminished level of uromodulin correlated with severe renal fibrosis. RNA sequencing revealed an upregulation of the alternative pathway in the acute stage. Renal CFH gene expression showed an upward tendency, while blood CFH localized less, decreasing the abundance of CFH in kidney and following sustained C3 deposition. A co-IP assay detected the linkage between uromodulin and CFH. In the model of AKI-to-CKD transition, the levels of uromodulin and CFH decreased, which correlated with kidney dysfunction and fibrosis. The interaction between uromodulin and CFH might participate in AKI-to-CKD transition.

/pdf/the-reduction-of-uromodulin-complement-factor-h-and-their-175v6jbm.pdf

The Reduction of Uromodulin, Complement Factor H, and Their Interaction Is Associated with Acute Kidney Injury to Chronic Kidney Disease Transition in a Four-Time Cisplatin-Injected Rat Model

Uromodulin (Umod) is the most abundant constituent of urine in humans and exclusively found in the kidney tubular epithelium. However, the specific role of Umod in renal tubulointerstitial injury is yet to be understood. The present study was conducted with aim of investigating the potential therapeutic mechanism of Umod in the regulation of renal tubulointerstitial injury. Protein expression of Umod in renal tubular epithelial cells was measured with the conduction of Western blot analysis. Enzyme-linked immunosorbent assay and immunofluorescence assay were performed to detect the complement activation products and the activation products of surface deposition. The expression of C1q, C2, C4, B factor, C3, C5, H factor, CD46, CD55, C3aR, and C5aR were determined with the use of reverse-transcription quantitative polymerase chain reaction and Western blot analyses. Subsequently, the unilateral ureteral obstruction (UUO) rat model was established. Renal tubulointerstitial injury was assessed with the application of hematoxylin-eosin staining and Masson staining in rats. UUO rats and normal rats were injected with si-NC or si-Umod and complement inhibitor. UUO rats were observed to have serious impairment of kidney tubule, renal tubular dilation, and epithelial atrophy, with downregulated Umod and activated complement pathway. Silencing of Umod resulted in the activation of complement system while promoting interstitial fibrosis in renal tubules. Moreover, addition of complement inhibitor significantly alleviated the renal tubule injury and fibrosis. Collectively, our study suggests that silencing of Umod mediates the complement pathway, exacerbating renal tubulointerstitial injury in rats, which provides insight into the development of novel therapeutic agents for renal tubulointerstitial injury.

Uromodulin aggravates renal tubulointerstitial injury through activation of the complement pathway in rats

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Uromodulin aggravates renal tubulointerstitial injury through activation of the complement pathway in rats