Document Type
Case Series
Abstract
Background: In individuals with chronic kidney disease (CKD) or end-stage renal disease, one of the leading causes of cardiovascular death is cardiovascular calcification (CVC) (ESRD). Serum sclerostin levels were shown to be elevated in individuals with CKD. Serum sclerostin levels in kidney illness patients are a reliable predictor of low-turnover bone disease, according to new research. Bone metabolism and osseous calcification are both regulated by several of these characteristics. The purpose of this study was to determine the relationship between CKD patients' serum sclerostin levels and coronary calcifications. Methods and subjects: CKD patients with GFR less than 60 ml/min who were on regular hemodialysis, as well as 20 CKD patients who were not on hemodialysis and a control group were compared in this case control comparative research. Results: Hemodialysis-dependent CKD patients have significantly higher CAC scores (agatston scores) and calcific plaque than non-hemodialysis-dependent patients, as well as those who have been on hemodialysis for more than a year compared to those who have been on it for less than a year. They also have significantly higher serum Sclerostin levels than healthy control subjects. A positive MSCT Scan for Coronaries in individuals with CKD is associated with a higher risk of developing coronary artery disease (CAD). Patients with CAC score (agatston units) that suggest vascular calcification had higher serum sclerostin levels.A high blood sclerostin level is linked to an increased risk of developing CAC.
Keywords
Coronary Artery Calcification; Chronic kidney Disease; End Stage Renal Disease.
How to Cite This Article
El Baz, Tarek Zakaria; Saad, Ahmed Alaa El Dein Ahmed; Emam, Emam Mohammed AbdElaziz; Mohammed, NagwaAbd El-Ghaffar; and Omar, Essam Yahya Ali
(2023)
"Assessment of serum Sclerostin level and its relationship to coronary calcifications in chronic kidney disease patients,"
Al-Azhar International Medical Journal: Vol. 4:
Iss.
1, Article 18.
DOI: https://doi.org/10.58675/2682-339X.1636