The Role of Endothelial Glycocalyx in the Pathophysiology of Chronic Kidney Disease and Hypertension: From Molecular Mechanisms to Clinical Biomarkers

Hypertension and chronic kidney disease (CKD) are closely linked conditions and represent common global health problems. Hypertension is a leading risk factor for cardiovascular disease, which is the main cause of mortality in CKD. Endothelial injury underlies the etiopathogenesis of both hypertension and CKD. The endothelial glycocalyx (eGC) is a dynamic, negatively charged, carbohydrate-rich layer that covers the luminal surface of endothelial cells. Its primary physiological function is to protect the endothelium, including the regulation of vascular permeability and homeostasis. Damage to the eGC, known as "shedding", is an early predictor of endothelial dysfunction and is driven by oxidative stress and low-grade inflammation. In hypertension, loss of eGC integrity-often impaired by a high-salt diet-can reduce the bioavailability of nitric oxide (NO) and increase arterial stiffness. Similarly, in CKD, uremic toxicity, hypertension, and inflammation damage the eGC, resulting in increased permeability, albuminuria, and higher cardiovascular risk. This review summarizes current evidence and underscores the potential of eGC shedding markers, especially syndecan 1 (SDC-1) and hyaluronic acid (HA), as early predictors of vascular risk and disease progression in hypertension and CKD.