MCP-1 and soluble TWEAK levels are independently associated with coronary artery disease severity in patients with chronic kidney disease.

PURPOSE: Patients diagnosed with chronic kidney disease (CKD) have a greater rate of cardiovascular mortality when compared with the general population. The soluble form of TNF-like weak inducer of apoptosis (TWEAK) and monocyte chemoattractan protein 1 (MCP-1) play important roles in cellular proliferation, migration and apoptosis. The current study aimed to analyze whether soluble TWEAK (sTWEAK) and MCP-1 levels are associated with the severity of coronary arterial disease (CAD) in CKD patients. METHODS: Ninety-seven patients diagnosed with CKD stages 2-3 according to their estimated glomerular filtration rate and the presence of kidney injury were included in the study. Plasma sTWEAK and MCP-1 concentrations were determined using commercially available ELISA kits. Coronary angiographies were performed through femoral artery access using the Judkins technique. RESULTS: Correlation analysis of sTWEAK and Gensini scores showed significant association (p < 0.01, r(2) = 0.287). Also significant correlation has been found in MCP-1 levels and Gensini scores (p < 0.01, r(2) = 0.414). When patients were divided into two groups with a limit of 17 according to their Gensini score, sTWEAK levels indicated a statistically significant difference (p < 0.01). CONCLUSIONS: Our findings support a relationship between sTWEAK and MCP-1 levels and CAD in CKD stages 2-3 patients.

Soluble TWEAK levels are independently associated with coronary artery disease severity in patients with stage 2-3 kidney disease.

PURPOSE: Patients diagnosed with chronic kidney disease (CKD) have a greater rate of cardiovascular mortality compared with the general population. The soluble form of TNF-like weak inducer of apoptosis (TWEAK) plays a role in cellular proliferation, migration, and apoptosis. The current study aimed to analyze whether soluble TWEAK levels are associated with the severity of coronary arterial disease (CAD) in CKD patients. METHODS: Ninety-seven patients diagnosed with CKD stages 2-3 according to their estimated glomerular filtration rate and the presence of kidney injury were included in the study. Plasma sTWEAK concentrations were determined using commercially available ELISA kits. Coronary angiographies were performed through femoral artery access using the Judkins technique. RESULTS: Correlation analysis of sTWEAK and Gensini scores showed significant association (p < 0.01, r (2) = 0.287). When patients were divided into two groups with a limit of 17 according to their Gensini score, sTWEAK levels indicated a statistically significant difference (p < 0.01). CONCLUSIONS: Our results indicate a relationship between sTWEAK levels and CAD in CKD stages 2-3 patients.