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http://purl.uniprot.org/citations/37466605http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/37466605http://www.w3.org/2000/01/rdf-schema#comment"

Objective

Sclerostin is a protein produced by osteocytes, kidneys, and vascular cells and has many effects on kidney and vascular structures. Soluble TNF-related weak inducer of apoptosis is a proinflammatory cytokine that may cause glomerular and tubular injury and increase sclerostin expression. This study aimed to investigate serum sclerostin and soluble TNF-related weak inducer of apoptosis levels in patients with glomerulonephritis and the effects they may be associated with.

Methods

This cross-sectional study included 93 patients, 63 of whom were glomerulonephritis and 30 were healthy controls. Serum sclerostin, soluble TNF-related weak inducer of apoptosis, and 24-h urinary protein excretion were measured, and pulse wave velocity was calculated for arterial stiffness.

Results

Serum sclerostin and soluble TNF-related weak inducer of apoptosis were higher in glomerulonephritis patients than in the control group, and serum sclerostin and soluble TNF-related weak inducer of apoptosis levels were correlated with both proteinuria and pulse wave velocity. In addition, in the regression analysis, serum sclerostin and soluble TNF-related weak inducer of apoptosis levels were found to be independent predictors of proteinuria in patients with glomerulonephritis.

Conclusion

This is the first study to show that serum sclerostin and soluble TNF-related weak inducer of apoptosis are elevated in glomerulonephritis patients, and these two markers correlate with arterial stiffness and proteinuria in these patients. Considering the effects of sclerostin and soluble TNF-related weak inducer of apoptosis in patients with glomerulonephritis, we think these mechanisms will be the target of both diagnosis and new therapies."xsd:string
http://purl.uniprot.org/citations/37466605http://purl.org/dc/terms/identifier"doi:10.1590/1806-9282.20230239"xsd:string
http://purl.uniprot.org/citations/37466605http://purl.uniprot.org/core/author"Ozer H."xsd:string
http://purl.uniprot.org/citations/37466605http://purl.uniprot.org/core/author"Turkmen K."xsd:string
http://purl.uniprot.org/citations/37466605http://purl.uniprot.org/core/author"Baloglu I."xsd:string
http://purl.uniprot.org/citations/37466605http://purl.uniprot.org/core/author"Aydemir F.H.Y."xsd:string
http://purl.uniprot.org/citations/37466605http://purl.uniprot.org/core/author"Aykut T."xsd:string
http://purl.uniprot.org/citations/37466605http://purl.uniprot.org/core/author"Demirci M.A."xsd:string
http://purl.uniprot.org/citations/37466605http://purl.uniprot.org/core/date"2023"xsd:gYear
http://purl.uniprot.org/citations/37466605http://purl.uniprot.org/core/name"Rev Assoc Med Bras (1992)"xsd:string
http://purl.uniprot.org/citations/37466605http://purl.uniprot.org/core/pages"e20230239"xsd:string
http://purl.uniprot.org/citations/37466605http://purl.uniprot.org/core/title"Sclerostin and TNF-related weak inducer of apoptosis: can they be important in the patients with glomerulonephritis?"xsd:string
http://purl.uniprot.org/citations/37466605http://purl.uniprot.org/core/volume"69"xsd:string
http://purl.uniprot.org/citations/37466605http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/37466605
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