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Updated: Aug 10, 2026

Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Microvascular disease and endothelial dysfunction in chronic kidney diseases: therapeutic implication
Narisa Futrakul1, Punnee Butthep, Suthiluk Patumraj
1King Chulalongkorn Memorial Hospital and Ramathibody Hospital, Bangkok, Thailand. fmednft@md.chula.ac.th
Insights
Biomarkers for endothelial injury in chronic kidney disease (CKD) were studied. Increased circulating endothelial cells and depleted vascular endothelial growth factor (VEGF) indicate injury, which can be treated with vasodilators.
Area of Science:
- Nephrology
- Cardiovascular Biology
- Endothelial Biology
Background:
- Endothelial injury is implicated in chronic kidney disease (CKD) pathogenesis.
- Identifying reliable biomarkers for endothelial dysfunction in CKD is crucial for effective treatment.
Purpose of the Study:
- To investigate biomarkers of endothelial injury in patients with chronic kidney disease.
- To explore the relationship between endothelial cell markers, growth factors, and intrarenal hemodynamics in CKD.
Main Methods:
- Assessment of circulating endothelial cells (CECs) and soluble VCAM-1 (sVCAM).
- Measurement of transforming growth factor beta (TGFB) and vascular endothelial growth factor (VEGF).
- Evaluation of intrarenal hemodynamics in 50 CKD patients.
Main Results:
- Significantly increased CECs and depleted VEGF/TGFB ratio observed in CKD patients.
- No significant difference in sVCAM compared to controls.
- Intrarenal hemodynamics showed characteristic maladjustment, with reduced peritubular capillary flow.
Conclusions:
- Elevated CECs are sensitive biomarkers for endothelial cell injury in CKD.
- VEGF depletion supports endothelial injury, correlating with glomerular and peritubular capillary dysfunction.
- Correcting hemodynamic maladjustment with vasodilators may restore renal function in CKD.
Abstract:
This paper was aimed to study biomarkers of endothelial injury in chronic kidney diseases. Fifty chronic kidney disease patients were subject to the following determinations: (i) circulating endothelial cells, (ii) soluble VCAM-1, (iii) transforming growth factor beta (TGFB), and (iv) intrarenal hemodynamics. Increased number of circulating endothelial cells was significantly observed. A significant depletion of vascular endothelial growth factor (VEGF) or a depleted VEGF/TGFB ratio was also documented. Results showed that sVCAM was not significantly different from normal control. Intrarenal hemodynamic alteration demonstrated a characteristic of hemodynamic maladjustment. Since increased number of circulating endothelial cells is a sensitive biomarker for endothelial cell injury in chronic kidney diseases, such injury is supported by the depletion of VEGF. The endothelial cell loss correlates with the glomerular endothelial dysfunction characterized by hemodynamic maladjustment at the efferent arteriole and reduction in peritubular capillary flow. In conclusion, correction of such hemodynamic maladjustment with multidrug vasodilators can effectively restore renal function in chronic kidney diseases.
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