Sclerostin and TNF-related weak inducer of apoptosis: can they be important in the patients with glomerulonephritis?

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dc.contributor.authorOzer, Hakan
dc.contributor.authorBaloglu, Ismail
dc.contributor.authorAykut, Talat
dc.contributor.authorDemirci, Mehmet Ali
dc.contributor.authorAydemir, Fatma Humeyra Yerlikaya
dc.contributor.authorTurkmen, Kultigin
dc.date.accessioned2024-02-23T14:30:09Z
dc.date.available2024-02-23T14:30:09Z
dc.date.issued2023
dc.departmentNEÜen_US
dc.description.abstractOBJECTIVE: 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 TNFrelated weak inducer of apoptosis in patients with glomerulonephritis, we think these mechanisms will be the target of both diagnosis and new therapies.en_US
dc.identifier.doi10.1590/1806-9282.20230239
dc.identifier.issn0104-4230
dc.identifier.issn1806-9282
dc.identifier.issue7en_US
dc.identifier.pmid37466605en_US
dc.identifier.scopus2-s2.0-85165520089en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.urihttps://doi.org/10.1590/1806-9282.20230239
dc.identifier.urihttps://hdl.handle.net/20.500.12452/15038
dc.identifier.volume69en_US
dc.identifier.wosWOS:001033719400015en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherAssoc Medica Brasileiraen_US
dc.relation.ispartofRevista Da Associacao Medica Brasileiraen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectGlomerulonephritisen_US
dc.subjectPulse Wave Velocityen_US
dc.subjectProteinuriaen_US
dc.subjectVascular Stiffnessen_US
dc.titleSclerostin and TNF-related weak inducer of apoptosis: can they be important in the patients with glomerulonephritis?en_US
dc.typeArticleen_US

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