Uso del sevelamer en la enfermedad renal crónica. Más allá del control del fósforo

Rodríguez-Osorio, Laura; Zambrano, Diana Pazmiño; Gracia-Iguacel, Carolina; Rojas-Rivera, Jorge; Ortíz, Alberto; Egido, Jesús; Parra, Emilio González

doi:10.1016/j.nefro.2015.05.022

Cited by 14 publications

(3 citation statements)

References 82 publications

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“…In patients with ESKD, use of non-calcium-based phosphate binding agent sevelamer reduced serum cholesterol and markers of inflammation (70). Additionally, sevelamer has shown to be effective in slowing down CAC progression and EF in dialysis patients (46).…”

Section: Therapeutic Approachesmentioning

confidence: 99%

Cardiorenal Fat: A Cardiovascular Risk Factor With Implications in Chronic Kidney Disease

et al. 2021

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There is a growing interest in the potential role of adipose tissues in cardiac and renal pathophysiology, and determining the mechanisms by which fat compartments around the heart and kidneys influence cardiovascular disease is of clinical importance in both general and high-risk populations. Epicardial fat and perirenal fat have been associated with adverse outcomes in chronic kidney disease (CKD) patients. Epicardial fat is a rich source of free fatty acids and is capable of secreting inflammatory and pro-atherogenic cytokines that promote atherosclerosis through a local paracrine effect. Recent evidence has demonstrated that perirenal fat has a closer correlation with kidney diseases than other visceral fat deposits in obesity or metabolic disturbances. Moreover, perirenal fat has been reported as an independent risk factor for CKD progression and even associated with cardiorenal dysfunction. Accordingly, these forms of organ-specific fat deposits may act as a connecter between vascular and cardiorenal disease. This review explores the possible links between epicardial and perirenal fat and its significant role as a modulator of cardiorenal dysfunction in CKD patients.

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Section: Therapeutic Approachesmentioning

confidence: 99%

Cardiorenal Fat: A Cardiovascular Risk Factor With Implications in Chronic Kidney Disease

et al. 2021

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“…The effects of sevelamer also include actions on oxidative stress, inflammation, lipid profile, endothelial dysfunction, and vascular calcification have been reported. [ 16 ]…”

Section: Introductionmentioning

confidence: 99%

Linkage of Fibroblast Growth Factor 23 and Phosphate in Serum: Phosphate and Fibroblast Growth Factor 23 Reduction by Increasing Dose of Sevelamer

et al. 2018

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BackgroundHigh serum phosphate and fibroblast growth factor-23 (FGF-23) levels are well-recognized independent risk factors of mortality and morbidity in patients with chronic kidney diseases (CKDs). Sevelamer, as a phosphate chelating agent, reduces serum phosphate and FGF-23 levels produced by bone osteocytes. This study aimed to determine the best dose at which sevelamer could successfully reduce serum phosphate and FGF-23 levels in rat models of adenine-induced CKD.MethodsCKD was induced using adenine. Healthy and CKD-induced rats were divided into 6 groups as follows: healthy controls; CKD controls; rats treated with 1%, 2%, and 3% sevelamer for CKDs; and healthy rats administered 3% sevelamer. Biochemical factors and serum FGF-23 levels were measured using spectrophotometry and enzyme-linked immunosorbent assay methods.ResultsSerum phosphate levels were best decreased in rats receiving 3% sevelamer in their diet (5.91±1.48 mg/dL vs. 8.09±1.70 mg/dL, P<0.05) compared with the CKD control rats. A dose-dependent decrease in serum FGF-23 levels was observed, and the most significant results were obtained in rats receiving 3% sevelamer compared with the CKD control rats (142.60±83.95 pg/mL vs. 297.15±131.10 pg/mL, P<0.01).ConclusionsHigher sevelamer doses significantly reduced serum phosphate and FGF-23 levels in adenine-induced CKD rats.

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“…We have previously demonstrated that sevelamer reduces systemic inflammatory response both in an animal model of CKD and in hemodialysis (HD) patients [18, 19]. Other studies have also demonstrated that sevelamer may decrease systemic inflammation in patients with CKD, as it reduces circulating levels of uremic toxins such as AGEs [20] as well as indoxyl sulfate, and p -cresol [17, 21]. Moreover, sevelamer can reduce the expression of adhesion molecules intercellular adhesion molecule-1 (ICAM-1) and VCAM-1 (markers of vascular injury) consequently it reduces circulating and cellular levels of AGEs, increases antioxidant defense, and decreases circulating levels of pro-oxidants molecules [22–24].…”

Section: Introductionmentioning

confidence: 99%

Sevelamer reduces endothelial inflammatory response to advanced glycation end products

Gregório

Favretto

Sassaki

et al. 2017

Clinical Kidney Journal

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BackgroundAdvanced glycation end products (AGEs) have been related to the pathogenesis of cardiovascular diseases (CVD), chronic kidney disease (CKD) and diabetes mellitus. We sought to investigate the binding capacity of sevelamer to both AGEs and uremic serum in vitro and then test this pharmaceutical effect as a potential vascular anti-inflammatory strategy.MethodsAGEs were prepared by albumin glycation and characterized by absorbance and electrophoresis. Human endothelial cells were incubated in culture media containing AGEs and uremic serum with or without sevelamer. Receptor for advanced glycation end product (RAGE) expression was evaluated through immunocytochemistry and western blot to explore the interactions between AGEs and the endothelium. Inflammatory and endothelial dysfunction biomarkers, such as interleukin 6 (IL-6) and IL-8, monocyte chemoattractant protein-1 (MCP-1), plasminogen activator inhibitor-1 (PAI-1) and serum amyloid A (SAA) were also measured in cell supernatant. The chemotactic property of the supernatant was evaluated. ResultsAGEs significantly induced the expression of RAGE, inflammatory and endothelial activation biomarkers [IL-6, (P < 0.005); IL-8, MCP-1, PAI-1 and SAA (P < 0.001)] and monocyte chemotaxis as compared with controls. In addition, AGEs increased the levels of inflammatory biomarkers, which were observed after 6 h of endothelial cell incubation with uremic serum [IL-6 (P < 0.001) IL-8, MCP-1 and PAI-1 (P < 0.05)]. On the other hand, after 6 h of endothelial cell treatment with sevelamer, RAGE expression (P < 0.05) and levels of inflammatory biomarkers [IL-6 and IL-8 (P < 0.001), MCP-1 (P < 0.01), PAI-1 and SAA (P < 0.005)] significantly decreased compared with the AGEs/uremic serum treatment alone.ConclusionsSevelamer decreased both endothelial expression of RAGE and endothelial dysfunction biomarkers, induced by AGEs, and uremic serum. Further studies are necessary for a better understanding of the potential protective role of sevelamer on uremic serum and AGEs-mediated endothelial dysfunction.

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Uso del sevelamer en la enfermedad renal crónica. Más allá del control del fósforo

Cited by 14 publications

References 82 publications

Cardiorenal Fat: A Cardiovascular Risk Factor With Implications in Chronic Kidney Disease

Cardiorenal Fat: A Cardiovascular Risk Factor With Implications in Chronic Kidney Disease

Linkage of Fibroblast Growth Factor 23 and Phosphate in Serum: Phosphate and Fibroblast Growth Factor 23 Reduction by Increasing Dose of Sevelamer

Sevelamer reduces endothelial inflammatory response to advanced glycation end products

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