Phosphate binders for preventing and treating chronic kidney disease-mineral and bone disorder (CKD-MBD)

Ruospo, Marinella; Palmer, Suetonia C.; Natale, Patrizia; Craig, Jonathan C.; Vecchio, Mariacristina; Elder, Grahame J.; Strippoli, Giovanni F.M.

doi:10.1002/14651858.cd006023.pub3

Cited by 95 publications

(108 citation statements)

References 282 publications

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“…Hyperphosphatemia frequently occurs as a consequence of impaired renal function [ 2 ] and is associated with vascular calcification [ 2 , 6 ] as well as increased risk for cardiovascular events and death [ 18 ]. However, the effects of phosphate binders on vascular calcification are still uncertain [ 19 ], which may be also attributed to the complex interplay of systemic phosphate handling and the availability of bone as a large source of phosphate [ 20 ]. Phosphate handling and development of hyperphosphatemia in CKD have been reviewed in detail elsewhere [ 20 – 24 ].…”

Section: Phosphate and Vascular Calcification In Ckdmentioning

confidence: 99%

Signaling pathways involved in vascular smooth muscle cell calcification during hyperphosphatemia

Voelkl

Läng

Eckardt

et al. 2019

Cell. Mol. Life Sci.

125

184

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Medial vascular calcification has emerged as a putative key factor contributing to the excessive cardiovascular mortality of patients with chronic kidney disease (CKD). Hyperphosphatemia is considered a decisive determinant of vascular calcification in CKD. A critical role in initiation and progression of vascular calcification during elevated phosphate conditions is attributed to vascular smooth muscle cells (VSMCs), which are able to change their phenotype into osteo-/chondroblasts-like cells. These transdifferentiated VSMCs actively promote calcification in the medial layer of the arteries by producing a local pro-calcifying environment as well as nidus sites for precipitation of calcium and phosphate and growth of calcium phosphate crystals. Elevated extracellular phosphate induces osteo-/chondrogenic transdifferentiation of VSMCs through complex intracellular signaling pathways, which are still incompletely understood. The present review addresses critical intracellular pathways controlling osteo-/chondrogenic transdifferentiation of VSMCs and, thus, vascular calcification during hyperphosphatemia. Elucidating these pathways holds a significant promise to open novel therapeutic opportunities counteracting the progression of vascular calcification in CKD.

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Section: Phosphate and Vascular Calcification In Ckdmentioning

confidence: 99%

Signaling pathways involved in vascular smooth muscle cell calcification during hyperphosphatemia

Voelkl

Läng

Eckardt

et al. 2019

Cell. Mol. Life Sci.

125

184

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“…Notably, whether sevelamer prevented deaths, calcium binders caused deaths, or a combination of both could not be determined. 7 In 2017, KDIGO updated its chronic kidney disease-mineral bone disorder clinical practice guideline to suggest restricting the dose of calcium-containing phosphate binders regardless of serum calcium levels. 8 This change was based on moderate-quality evidence (graded 2B) from 3 open-label RCTs showing improved survival among dialysis patients treated with sevelamer versus calcium-containing binders.…”

mentioning

confidence: 99%

Time to Reconsider Calcium-Based Phosphate Binders in Dialysis? A Call for a Well-Designed Randomized Controlled Trial

Jovanovich

2020

American Journal of Kidney Diseases

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“…Another systematic review and meta-analysis revealed decreased all-cause mortality by non-calcium-based PB, compared to CBB in CKD patients [35]. A Cochrane systematic review and meta-analysis of randomized clinical trials (RCT) showed that sevelamer compared to CBB decreased all-cause mortality in ESRD patients [36], while sevelamer had no effect on CV mortality [37]. Based on these findings, the Kidney Disease: Improving Global Outcomes (KDIGO) 2017 guideline recommends PB treatment for progressively elevated phosphate and a restriction of CBB treatment [11], with a limited dietary phosphate intake [11].…”

Section: Phosphate Bindermentioning

confidence: 99%

Cardiovascular Calcification in Chronic Kidney Disease—Therapeutic Opportunities

Himmelsbach

Ciliox

Goettsch

2020

Toxins

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Patients with chronic kidney disease (CKD) are highly susceptible to cardiovascular (CV) complications, thus suffering from clinical manifestations such as heart failure and stroke. CV calcification greatly contributes to the increased CV risk in CKD patients. However, no clinically viable therapies towards treatment and prevention of CV calcification or early biomarkers have been approved to date, which is largely attributed to the asymptomatic progression of calcification and the dearth of high-resolution imaging techniques to detect early calcification prior to the ‘point of no return’. Clearly, new intervention and management strategies are essential to reduce CV risk factors in CKD patients. In experimental rodent models, novel promising therapeutic interventions demonstrate decreased CKD-induced calcification and prevent CV complications. Potential diagnostic markers such as the serum T50 assay, which demonstrates an association of serum calcification propensity with all-cause mortality and CV death in CKD patients, have been developed. This review provides an overview of the latest observations and evaluates the potential of these new interventions in relation to CV calcification in CKD patients. To this end, potential therapeutics have been analyzed, and their properties compared via experimental rodent models, human clinical trials, and meta-analyses.

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Phosphate binders for preventing and treating chronic kidney disease-mineral and bone disorder (CKD-MBD)

Cited by 95 publications

References 282 publications

Signaling pathways involved in vascular smooth muscle cell calcification during hyperphosphatemia

Signaling pathways involved in vascular smooth muscle cell calcification during hyperphosphatemia

Time to Reconsider Calcium-Based Phosphate Binders in Dialysis? A Call for a Well-Designed Randomized Controlled Trial

Cardiovascular Calcification in Chronic Kidney Disease—Therapeutic Opportunities

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