Vascular dysfunction and atherosclerosis in chronic kidney disease; A distinct entity

Abstract

Cardiovascular disease (CVD) is prevalent among patients with chronic kidney disease (CKD) and its occurrence and severity cannot be fully defined by the conventional cardiovascular risk factors namely age, hypertension, dyslipidaemia, diabetes mellitus and obesity. Contemporary studies have examined the role of non-conventional risk factors such as anemia, hyperhomocysteinemia, calcium and phosphate metabolism, vascular stiffness due to endothelial dysfunction ( ED), oxidative injury, and inflammation in the causation of CVD in CKD. Therapeutic interventions used in non-CKD patients are found to be less effective on patients with CKD. The purpose of this review was to gather available evidence on the CVD risk among CKD patients. Numerous mechanisms have been postulated to describe the increased atherogenicity in CKD patients. We discuss these mechanisms especially arterial stiffness, ED and inflammation in detail. In conclusion, CVD in CKD is still an unexplored area which needs further studies to uncover the possible mechanisms. Identifying newer therapies to improve health among this group of patients is of paramount importance.

The effects of oral magnesium supplementation on glycaemic control in patients with type 2 diabetes: a systematic review and dose–response meta-analysis of controlled clinical trials

“…Diabetes is associated with an elevated risk for CVD (37,38) . Multiple laboratory tests are recommended to diagnose, manage, monitor and follow-up during the treatment of diabetic patients.…”

Exploring the role of the combination of propolis and vitamin D3 on VCAM-1 and Caspase-3 expression in preventing atherosclerosis in chronic kidney disease rats

“…The diameter of the two groups was almost the same at the beginning, while at the end of the study the control group had a diameter of even premature mortality. [19][20][21][22] CKD is also characterized by decreased antiatherogenic properties and has a role in the process of atherosclerosis in increased cardiovascular morbidity. 19,22-24 CKD can cause calcium deposition leading to vascular calcification.…”

“…13,21,25, 27 In fact, the occurrence of endothelial dysfunction begins early in renal impairment, where the filtration rate decreases and blood pressure rises. 21 This is due to the accumulation of fatty plaques on inner walls of blood vessels that contain low-density lipoprotein (LDL) and cellular waste. 13 Oxidation of LDL in the vasculature can activate endothelial cells to produce adhesion molecules that will eventually lead to proliferation of smooth muscle and connective tissue, and bulging into arterial lumen, which cause decreased tissue perfusion.…”

Decreased expression of the GLP-1 receptor after segmental artery injury in mice

“…Perivascular accumulation of inflammatory cells in the kidney was present in both models suggesting that inflammation plays a role in the vascular changes reported. Inflammation and renal vascular remodelling are well documented in rodent models of chronic kidney disease (Yuan et al 2003, Horbelt et al 2007, Basile et al 2011, Briet & Burns 2012, Silva et al 2019, whereas the Ldlr-/mouse is not commonly known for its renal pathology. Ldlr-/-mice on WD are known to exhibit chronic lowgrade inflammation, which is thought to contribute to the atherosclerotic changes seen in the model (Inoguchi et al 1992, Foote et al 2016.…”