Uraemic toxins and cardiovascular disease across the chronic kidney disease spectrum: An observational study

The aim of the present study is to investigate the prevalance of chronic kidney disease (CKD), of cardiovascular disease (CVD) and dyslipidemia in patients with diabetes mellitus (DM). We conducted a prospective, controlled study involving 420 diabetic patients (120 T1DM, 300 T2DM) and investigate the following aspects: the presence of vascular complications (stroke, coronary artery disease, peripheral artery disease), lipid profile (total cholesterol, LDL-cholesterol, HDL-cholesterol, triglycerides), kidney function (glomerular filtration rate, albuminuria), blood pressure, HbA1C. The results that in diabetic patients with CKD there is an increased prevalence of CVD and of dislipidemia. Also we noticed a negative correlation between total cholesterol level and decease in eGFR in all patients, with or without CKD.

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Hyperuricemia and Cardiovascular Disease

Current Pharmaceutical Design ◽

10.2174/1381612825666190408122557 ◽

2019 ◽

Vol 25 (6) ◽

pp. 700-709 ◽

Cited By ~ 4

Author(s):

Shuangshuang Zhang ◽

Yong Wang ◽

Jinsong Cheng ◽

Ning Huangfu ◽

Ruochi Zhao ◽

...

Keyword(s):

Cardiovascular Disease ◽

Metabolic Syndrome ◽

Chronic Kidney Disease ◽

Uric Acid ◽

Kidney Disease ◽

Kidney Stones ◽

Treatment Plan ◽

Circulatory System ◽

Special Focus ◽

Positive Effects

Purine metabolism in the circulatory system yields uric acid as its final oxidation product, which is believed to be linked to the development of gout and kidney stones. Hyperuricemia is closely correlated with cardiovascular disease, metabolic syndrome, and chronic kidney disease, as attested by the epidemiological and empirical research. In this review, we summarize the recent knowledge about hyperuricemia, with a special focus on its physiology, epidemiology, and correlation with cardiovascular disease. This review also discusses the possible positive effects of treatment to reduce urate levels in patients with cardiovascular disease and hyperuricemia, which may lead to an improved clinical treatment plan.

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Uremic toxin indoxyl sulfate promotes proinflammatory macrophage activation by regulation of β-catenin and YAP pathways

Journal of Molecular Histology ◽

10.1007/s10735-020-09936-y ◽

2021 ◽

Author(s):

Ying Li ◽

Jing Yan ◽

Minjia Wang ◽

Jing Lv ◽

Fei Yan ◽

...

Keyword(s):

Cardiovascular Disease ◽

Chronic Kidney Disease ◽

Kidney Disease ◽

Inflammatory Response ◽

Macrophage Polarization ◽

Indoxyl Sulfate ◽

Uremic Toxin ◽

Lps Challenge ◽

Hla Dr ◽

M1 Macrophage

AbstractEvidence has been shown that indoxyl sulfate (IS) could impair kidney and cardiac functions. Moreover, macrophage polarization played important roles in chronic kidney disease and cardiovascular disease. IS acts as a nephron-vascular toxin, whereas its effect on macrophage polarization during inflammation is still not fully elucidated. In this study, we aimed to investigate the effect of IS on macrophage polarization during lipopolysaccharide (LPS) challenge. THP-1 monocytes were incubated with phorbol 12-myristate-13-acetate (PMA) to differentiate into macrophages, and then incubated with LPS and IS for 24 h. ELISA was used to detect the levels of TNFα, IL-6, IL-1β in THP-1-derived macrophages. Western blot assay was used to detect the levels of arginase1 and iNOS in THP-1-derived macrophages. Percentages of HLA-DR-positive cells (M1 macrophages) and CD206-positive cells (M2 macrophages) were detected by flow cytometry. IS markedly increased the production of the pro-inflammatory factors TNFα, IL-6, IL-1β in LPS-stimulated THP-1-derived macrophages. In addition, IS induced M1 macrophage polarization in response to LPS, as evidenced by the increased expression of iNOS and the increased proportion of HLA-DR+ macrophages. Moreover, IS downregulated the level of β-catenin, and upregulated the level of YAP in LPS-stimulated macrophages. Activating β-catenin signaling or inhibiting YAP signaling suppressed the IS-induced inflammatory response in LPS-stimulated macrophages by inhibiting M1 polarization. IS induced M1 macrophage polarization in LPS-stimulated macrophages via inhibiting β-catenin and activating YAP signaling. In addition, this study provided evidences that activation of β-catenin or inhibition of YAP could alleviate IS-induced inflammatory response in LPS-stimulated macrophages. This finding may contribute to the understanding of immune dysfunction observed in chronic kidney disease and cardiovascular disease.

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