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Assessment of Kidney Function in Mouse Models of Glomerular Disease
Published on: June 30, 2018
Glycocalyx injury in adults with nephrotic syndrome: Association with endothelial function
Francisco Thiago Santos Salmito1, Fernanda Macedo de Oliveira Neves2, Gdayllon Cavalcante Meneses1
1Department of Clinical and Toxicological Analysis, Faculty of Pharmacy, Federal University of Ceara, Fortaleza, Ceara, Brazil.
Insights
Endothelial glycocalyx damage, indicated by increased syndecan-1, is present in nephrotic syndrome patients. This damage is linked to disease features and contributes to endothelial dysfunction.
Area of Science:
- Nephrology
- Cardiovascular Research
- Vascular Biology
Background:
- Glomerulopathy affects young adults, potentially leading to endothelial dysfunction, atherosclerosis, and cardiac issues.
- The role of endothelial glycocalyx in nephrotic syndrome remains unevaluated.
Purpose of the Study:
- To investigate endothelial glycocalyx integrity and endothelial function in patients with untreated primary nephrotic syndrome.
- To assess the association between endothelial markers and nephrotic syndrome characteristics.
Main Methods:
- Cross-sectional study of 49 patients with untreated primary nephrotic syndrome.
- Measured syndecan-1, intercellular adhesion molecule-1 (ICAM-1), and e-selectin.
- Assessed endothelial function using flow-mediated dilation (FMD).
Main Results:
- Nephrotic patients exhibited reduced FMD compared to controls (3.7±1.7% vs. 6.6±1.1%, p<0.001).
- Elevated levels of ICAM-1 (616.6±219.7 ng/ml) and syndecan-1 (180.3±64.1 ng/ml) were observed in nephrotic patients.
- Syndecan-1 was independently associated with FMD after adjusting for clinical factors.
Conclusions:
- Syndecan-1, a marker of endothelial glycocalyx damage, is elevated in nephrotic syndrome patients with preserved renal function.
- Increased syndecan-1 correlates with nephrotic syndrome features, suggesting a role in endothelial dysfunction.
Background:
Glomerulopathy is a group of diseases that affect mainly young adults. Endothelial dysfunction, atherosclerosis, and increased cardiac mortality can complicate the evolution of such patients. However, there is no study evaluating endothelial glycocalyx in this pathology.
Methods:
This cross-sectional study included 49 patients with untreated primary nephrotic syndrome that were otherwise healthy. In addition to routine laboratory measurements, syndecan-1, intercellular adhesion molecule-1 (ICAM-1), and e-selectin were measured. Moreover, flow-mediated dilation (FMD) was used as the main endothelial function surrogate.
Results:
Of the 49 patients with nephrotic syndrome, 25 (51.0%) were females. The mean age of patients was 39.0±12.1y. FMD was reduced in nephrotic patients in comparison with controls (3.7±1.7 vs. 6.6±1.1%, p<0.001). Nephrotic patients had higher levels of ICAM-1 (616.6±219.7 vs. 356.9±102.0ng/ml, p<0.001) and syndecan-1 (180.3±64.1 vs. 28.2±9.8ng/ml, p<0.001). No significant difference was observed regarding e-selectin (129.9±54.2 vs. 120.2±61.5ng/ml, p=0.489). After adjusting for age and glomerular filtration rate, syndecan-1 was significantly associated with 24-h urinary protein excretion, LDL-cholesterol, HDL-cholesterol, and triglycerides. While age, LDL-cholesterol, and 24-h urinary protein excretion were associated with FMD in the multivariate analysis, when syndecan-1, ICAM-1, and e-selectin were added to the model, only syndecan-1 was independently associated with FMD.
Conclusions:
We demonstrated that syndecan-1, a marker of endothelial glycocalyx damage, is increased in patients with nephrotic syndrome and near-normal renal function. Moreover, we determined its association with nephrotic syndrome features and suggest it can have a role in the endothelial dysfunction of these patients.
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