Specific risk factors for cerebrovascular disorders in patients with chronic kidney disease in the pre-dialysis period

Abstract

Cerebral vascular disorders are one of the leading causes of disability and mortality in patients with chronic kidney disease (CKD). The article presents the currently available data on risk factors (RF) for the development of cerebrovascular disorders in pre-dialysis patients with CKD. Two groups of RF are identified: traditional and non-traditional (specific). Traditional RF, which include arterial hypertension, diabetes mellitus and hypercholesterolemia, independently affect the cerebral vascular bed and get worse against the background of CKD. Specific RF is associated with features of the CKD pathogenesis. It includes increased blood levels of homocysteine, β2-microglobulin, impaired calcium-phosphorus metabolism, accumulation of uremic toxins and toxins of intestinal bacteria, anemia and other factors. In the present review, special attention is paid to specific RF and pathogenetic mechanisms of the development of cerebrovascular disorders in predialysis patients with CKD. Timely detection of cerebral risk factors may lead to the improvement of early diagnosis and prevention of cerebral vascular disorders, optimization of therapy for patients with CKD.

Pathogenetic Subtypes and Ischemic Stroke Outcomes in Patients with Chronic Kidney Disease

“…The additional specific CKD pathological conditions, including increased levels of oxidative stress, chronic inflammation, endothelial dysfunction, vascular calcification, anemia, thrombogenic factors caused by the uremic environment, predispose to vascular damage and endotheliopathy [10,12]. Hypergomocysteinemia, which plays an important role in the malignant atherosclerosis and thrombosis development [9]; lowmolecular β2-M peptide accumulation leading to cerebral amyloid angiopathy development [9] predispose to the cerebrovascular disorders. Accumulation of uremic toxins with reduced kidney function can enhance oxidative stress, chronic inflammation, endothelial dysfunction and vascular calcification [9].…”

“…Hypergomocysteinemia, which plays an important role in the malignant atherosclerosis and thrombosis development [9]; lowmolecular β2-M peptide accumulation leading to cerebral amyloid angiopathy development [9] predispose to the cerebrovascular disorders. Accumulation of uremic toxins with reduced kidney function can enhance oxidative stress, chronic inflammation, endothelial dysfunction and vascular calcification [9]. This CKD-specific factors probably predispose to the formation of blood clots in the left atrium and increase the risk of TOAST2 stroke in CKD patients.…”

“…Recently many studies have been devoted to the study of CKD association with cerebrovascular diseases [1,8,9]. Chronic kidney disease, defined as reduced glomerular filtration rate or increased urinary albumin excretion, has been proven to be a risk factor for cerebrovascular diseases [8].…”

Specific Cerebrovascular Risk Factors, Colon Microbiocenosis and Its Correction in Patients Receiving Long-Term Programmed Hemodialysis

“…The spectrum of specific factors of cerebrovascular risk in patients with dialysis stage of the CKD includes specific dialysis factors that form during programmed HD, as well as impaired phosphorus-calcium metabolism, increased blood levels of β2-microglobulin, homocysteine, malondialdehyde and superoxide dismutase, a decrease in the level of nitric oxide (II) metabolites, accumulation of uremic toxins and toxins of intestinal bacteria, development of nephrogenic anemia, dietary features of patients with renal pathology, etc.) [16][17][18]. Some of them are presented in more detail below.…”

“…β2-microglobulin is normally eliminated by the kidneys. Impaired elimination of β2-microglobulin from the body by the natural nephrogenic way leads to further deposition of amyloid in the walls of the microvasculature, the formation of secondary amyloidosis and CAA with the risk of cerebral microbleeds [17]. The high incidence of cerebral microbleeds (according to our data, 47% of the examined patients, mainly in the subcortical nuclei and supratentorial localization), can be explained by the development in this category of patients of both sporadic non-amyloid CMA and CAA, including against the background of persistent β2-microglobulinemia.…”