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Updated: Mar 17, 2026

Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Microvascular endothelial dysfunction is associated with albuminuria and CKD in older adults
Stephen L Seliger1,2, Shabnam Salimi3, Valerie Pierre4
1Department of Medicine, University of Maryland School of Medicine, 22 S. Greene Street, Room N3W143, Baltimore, MD, 21201, USA. sseliger@medicine.umaryland.edu.
Insights
Microvascular endothelial dysfunction is linked to albuminuria and chronic kidney disease (CKD). This impairment may explain increased cardiovascular risk in patients with these conditions.
Area of Science:
- Nephrology
- Cardiovascular Medicine
- Vascular Biology
Background:
- Glomerular endothelial dysfunction is implicated in albuminuria and chronic kidney disease (CKD) progression.
- This dysfunction may contribute to the heightened cardiovascular risk observed in patients with albuminuria.
- Previous research on vascular function in CKD has primarily focused on large arteries or end-stage renal disease, neglecting microvascular aspects in the presence of albuminuria.
Purpose of the Study:
- To investigate the association between microvascular endothelial function and albuminuria in older hypertensive men with CKD.
- To compare microvascular endothelial function in individuals with and without CKD.
- To determine if microvascular dysfunction explains the increased cardiovascular risk in albuminuria and CKD.
Main Methods:
- A cross-sectional study was conducted involving older hypertensive male veterans with stage 1-4 CKD and hypertensive controls without CKD.
- Microvascular function was assessed using Laser-Doppler flowmetry (LDF) measuring peak responses to post-occlusive reactive hyperemia (PORH) and thermal hyperemia (TH) on forearm skin.
- Statistical analyses included correlation coefficients and multiple linear regression to examine associations between LDF measures, albuminuria, estimated glomerular filtration rate (eGFR), and CKD status, controlling for confounders.
Main Results:
- Among 66 participants, those with macroalbuminuria exhibited significantly lower LDF responses to both PORH (43% lower) and TH (39% lower) compared to those with normoalbuminuria.
- Participants with CKD showed a 23.9% lower response to PORH compared to controls, even after adjustment for covariates.
- Thermal hyperemia (TH) responses did not significantly differ between individuals with and without CKD.
Conclusions:
- Microvascular endothelial function is significantly impaired in individuals with greater albuminuria and CKD.
- These findings suggest that impaired microvascular endothelial function is an independent risk factor associated with albuminuria and CKD.
- The observed microvascular dysfunction may partially account for the elevated systemic cardiovascular risk in patients with albuminuria and CKD.
Background:
Impairment in glomerular endothelial function likely plays a major role in the development of albuminuria and CKD progression. Glomerular endothelial dysfunction may reflect systemic microvascular dysfunction, accounting in part for the greater cardiovascular risk in patients with albuminuria. Prior studies of vascular function in CKD have focused on conduit artery function or those with ESRD, and have not examined microvascular endothelial function with albuminuria.
Methods:
We conducted a cross-sectional study among older hypertensive male veterans with stage 1-4 CKD, and hypertensive controls without CKD. Microvascular function was quantified by two distinct Laser-Doppler flowmetry (LDF) measures: peak responses to 1) post-occlusive reactive hyperemia (PORH) and 2) thermal hyperemia (TH), measured on forearm skin. Associations of each LDF measure with albuminuria, eGFR, and CKD status were estimated using correlation coefficients and multiple linear regression, accounting for potential confounders.
Results:
Among 66 participants (mean age 69.2 years), 36 had CKD (mean eGFR 46.1 cc/min/1.73 m(2); 30.6 % with overt albuminuria). LDF responses to PORH and TH were 43 and 39 % significantly lower in multivariate analyses among those with macroalbuminuria compared to normoalbuminuria, (β= - 0.42, p = 0.009 and β= -0.37, p = 0.01, respectively). Those with CKD had a 23.9 % lower response to PORH compared to controls (p = 0.02 after adjustment). In contrast, TH responses did not differ between those with and without CKD.
Conclusions:
Microvascular endothelial function was strongly associated with greater albuminuria and CKD, independent of diabetes and blood pressure. These findings may explain in part the excess systemic cardiovascular risk associated with albuminuria and CKD.
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