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Plasma glycocalyx pattern: a mirror of endothelial damage in chronic kidney disease

Citation

Valera, G., Figuer, A., Caro, J., Yuste, C., Morales, E., Ceprián, N., Bodega, G., Ramírez, R., Alique, M., & Carracedo, J. (2023). Plasma glycocalyx pattern: a mirror of endothelial damage in chronic kidney disease. Clinical Kidney Journal, 16(8), 1278-1287. https://doi.org/10.1093/CKJ/SFAD051

Abstract

Background. Endothelial damage and cardiovascular disease complicate chronic kidney disease (CKD). The increased atherogenicity observed in patients with CKD can be linked to microinflammation and endothelial damage. Circulating endothelial glycocalyx degradation products, such as perlecan and decorin, tend to be elevated in CKD. We aimed to explore the association between the plasma perlecan and decorin levels and this pro-inflammatory and atherogenic state by studying monocyte subpopulations and intracellular adhesion molecule (ICAM)-1 expression in patients with CKD. Methods. We studied 17 healthy controls, 23 patients with advanced CKD, 25 patients on haemodialysis, 23 patients on peritoneal dialysis and 20 patients who underwent kidney transplantation. Perlecan and decorin levels were evaluated using enzyme-linked immunosorbent assays, and the monocyte phenotype was analysed using direct immunofluorescence and flow cytometry. Results. The plasma perlecan levels were higher in patients with CKD than in the healthy controls. These levels were associated with a higher prevalence of ICAM-1+ monocytes. Conversely, patients with advanced CKD (pre-dialysis) had higher plasma decorin levels, which were associated with a reduced ICAM-1 expression per monocyte. Conclusions. Elevated perlecan levels in CKD may be associated with a higher prevalence of ICAM-1+ monocytes and a pro-inflammatory phenotype. Elevated decorin levels may act as a negative regulator of ICAM-1 expression in monocytes. Therefore, perlecan and decorin may be related to inflammation and monocyte activation in CKD and may act as potential markers of endothelial damage.

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Instituto de Salud Carlos III funded this study through the projects ‘PI17/01029’, ‘PI19/00240’ and ‘PI20/01321’ (co-funded by the European Regional Development Fund ‘A way to make Europe’). Instituto de Salud Carlos III (ISCIII) FEDER funds the RICORS program to RICORS2040 (RD21/0005/0002), Ayuda Adicional-Excelencia Profesorado Programa Propio UAH, Comunidad de Madrid (CAM) CIFRA_COR-CM (P2022/BMD-7223), and Sociedad Española de Nefrología. A.F. was a fellow of the program ‘Contratos Predoctorales de Investigación en Salud, Instituto de Salud Carlos III’ (FI20/00 018). G.V. was issued a grant (number: PI20/01 321).

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