Endostatin and vascular endothelial growth factor: potential regulators of endothelial progenitor cell number in chronic kidney disease

• Published in: Polskie archiwum medycyny wewne̦trznej Vol. 121; no. 9; pp. 296 - 302
• Main Authors: Wątorek, Ewa, Paprocka, Maria, Duś, Danuta, Kopeć, Wacław, Klinger, Marian
• Format: Journal Article
• Language: English
• Published: Poland 01.09.2011
• Subjects: Aged; Cell Count; Endostatins - blood; Female; Humans; Male; Middle Aged; Renal Insufficiency, Chronic - blood; Renal Insufficiency, Chronic - physiopathology; Risk Factors; Stem Cells - metabolism; Vascular Endothelial Growth Factor A - blood
• ISSN: 1897-9483; 1897-9483
• DOI: 10.20452/pamw.1079

Cardiovascular mortality is significantly increased in patients with chronic kidney disease (CKD). The number of circulating endothelial progenitor cells (EPCs) may affect vascular regenerative potential and thus influence cardiovascular mortality. The aim of the study was to assess the number of circulating EPCs and the factors that potentially affect these cells, including vascular endothelial growth factor (VEGF) and endostatin, in patients with CKD. The study involved 139 patients divided into groups depending on the severity of renal impairment: 67 predialysis patients with CKD, 46 patients on hemodialysis (HD), and 26 patients on peritoneal dialysis (PD). Plasma levels of VEGF and endostatin were measured by enzyme-linked immunosorbent assays. The number of circulating EPCs, defined as CD34+VEGFR2+, was assessed in the whole blood using flow cytometry. There was a positive correlation between VEGF and CD34+VEGFR2+ and the glomerular filtration rate. Endostatin levels increased with renal impairment. The highest endostatin levels were observed in HD and PD patients. The number of EPCs was significantly lower in predialysis patients with CKD and in HD patients, while in PD patients it was nonsignificantly lower compared with the control group. In patients with CKD, a decrease in circulating EPCs may impair vascular regenerative potential and thus contribute to a higher cardiovascular risk. The effect of significantly increased endostatin levels on the endothelial function and progenitors in patients with CKD requires further investigation.