Sclerostin is an osteocyte-secreted protein that inhibits bone growth by inhibiting the Wnt/-catenin signaling pathway. Sclerostin can be triggered by inflammation, and significant amounts have been seen in individuals with proteinuria and kidney disease. Only a few studies have looked at the role of sclerostin in SLE patients. To better understand lupus nephritis and arthritis, researchers are measuring SLE patients’ serum sclerostin levels and correlating them with bone biomarkers and disease activity. Finally, researchers looked into possible predictors of sclerostin levels. From May 2017 to April 2018, this cross-sectional, case-control research was carried out. Serum sclerostin levels were determined using an enzyme-linked immunosorbent assay in 100 SLE patients, including 50 with active lupus nephritis and 27 with active arthritis, as well as 50 healthy controls. In SLE patients, serum sclerostin was correlated with demographics, bone biomarkers, and disease activity. Sclerostin levels in SLE patients, particularly those with lupus nephritis, were substantially higher than in healthy controls. Patients without arthritis showed higher levels than those with; nevertheless, the former group had greater proteinuria and renal impairment. Sclerostin levels were shown to have significant relationships with serum creatinine, proteinuria, ingested C3, and C4 complement, and corrected Ca. Proteinuria was the sole significant predictor of serum sclerostin in SLE patients using multiple linear regression.
This is the first study to show that serum sclerostin is linked to proteinuria in SLE patients and might be utilized as a biomarker for lupus nephritis.