Effects of phosphate on vascular function under normal conditions and influence of the uraemic state.
@article{Six2012EffectsOP, title={Effects of phosphate on vascular function under normal conditions and influence of the uraemic state.}, author={Isabelle Six and Julien Maizel and Fellype de Carvalho Barreto and Ashraf Yusuf Rangrez and S{\'e}bastien Dupont and Michel Slama and Christophe Tribouilloy and Gabriel Choukroun and Jean Claude Mazi{\`e}re and Stefanie M. Bode-Boeger and Jan T Kielstein and Tilman B. Dr{\"u}eke and Ziad A. Massy}, journal={Cardiovascular research}, year={2012}, volume={96 1}, pages={ 130-9 } }
AIMS
Increased serum phosphorus levels are associated with cardiovascular disease in patients with chronic kidney disease (CKD) and in the general population. High phosphate levels may play a direct role in vascular dysfunction. We investigated here the effects of phosphate loading and of the phosphate binder sevelamer-HCl on vascular function.
METHODS AND RESULTS
CKD and non-CKD C57/BL6 mice were used to study the effects of CKD, phosphate, and sevelamer-HCl on vascular function and…
79 Citations
Reduction of NO-mediated Relaxing Effects in the Thoracic Aorta in an Experimental Chronic Kidney Disease Mouse Model.
- Biology, MedicineJournal of atherosclerosis and thrombosis
- 2015
It is indicated that spontaneous and stimulated NO release from the endothelium is decreased in the CKD model mouse aorta, and the NO-mediated correlation between renal and elastic arterial endothelial dysfunction is suggested to be a cause of cardiovascular events in patients with CKD.
A phosphate-centric paradigm for pathophysiology and therapy of chronic kidney disease
- Biology, MedicineKidney international supplements
- 2013
Observations have raised the possibility that CPPs may contribute to the pathophysiology of CKD, and this notion, if validated, is expected to provide new diagnostic and therapeutic targets for CKD.
Strategies for Phosphate Control in Patients With CKD
- Medicine, BiologyKidney international reports
- 2019
Use of Nicotinamide to Treat Hyperphosphatemia in Dialysis Patients
- Medicine, BiologyDrugs in R&D
- 2013
In vitro and in vivo data show that nicotinamide reduces hyperphosphatemia by inhibiting sodium-dependent phosphate co-transport in the renal proximal tubule and in the intestine, and this compound may be a therapeutic option for modulating serum phosphate in CKD.
Cardiovascular problems in dialysis patients - focus on correcting hyperphosphatemia
- Medicine, BiologyMeditsinskiy sovet = Medical Council
- 2020
The review presents the main approaches for the correction of hyperphosphatemia in CKD, such as nutritional correction, modifica-tion of dialysis methods, and prescribing of phosphate binders.
Most exposed: the endothelium in chronic kidney disease
- Biology, MedicineNephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
- 2019
Abstract Accumulating evidence indicates that the pathological changes of the endothelium may contribute to the development of cardiovascular complications in chronic kidney disease (CKD).…
Roles of phosphate and fibroblast growth factor 23 in cardiovascular disease
- Biology, MedicineNature Reviews Nephrology
- 2014
It is suggested that future population-level and individual-level interventions will need to simultaneously target these molecules to reduce the risk of associated cardiovascular events.
Direct, Acute Effects of Klotho and FGF23 on Vascular Smooth Muscle and Endothelium
- BiologyPloS one
- 2014
Klotho mitigates the effects of phosphate and FGF23 on contractility via increased NO production, thereby protecting the vessel to some extent against potentially noxious effects of high phosphate or F GF23 concentrations.
Para‐cresyl sulfate acutely impairs vascular reactivity and induces vascular remodeling
- Biology, MedicineJournal of cellular physiology
- 2015
Elevated PCS concentrations such as those observed in CKD patients, by promoting both vascular dysfunction and vascular remodeling, may contribute to the development of hypertension and to cardiovascular mortality in CKd.
Vascular toxicity of phosphate in chronic kidney disease: beyond vascular calcification .
- Medicine, BiologyCirculation journal : official journal of the Japanese Circulation Society
- 2014
The present article reviews the direct and indirect mechanisms by which hyperphosphatemia influence the onset of VC and ED in CKD and concludes that phosphate is involved in ED.
References
SHOWING 1-10 OF 33 REFERENCES
Short-term treatment with sevelamer increases serum fetuin-a concentration and improves endothelial dysfunction in chronic kidney disease stage 4 patients.
- MedicineClinical journal of the American Society of Nephrology : CJASN
- 2008
This small, randomized, prospective study shows that short-term sevelamer treatment significantly increases fetuin-A levels and improves FMD in nondiabetic stage 4 CKD patients.
Adverse effects of hyperphosphatemia on myocardial hypertrophy, renal function, and bone in rats with renal failure.
- Medicine, BiologyKidney international
- 2004
Myocardial hypertrophy, impaired renal function, and adverse effects on bone remodeling were associated with hyperphosphatemia and were not corrected by PTH replacement, highlighting the importance of phosphorus control in reducing morbidity and mortality in CRF patients.
Phosphate regulation of vascular smooth muscle cell calcification.
- Medicine, BiologyCirculation research
- 2000
It is suggested that elevated phosphate may directly stimulate HSMCs to undergo phenotypic changes that predispose to calcification and offer a novel explanation of the phenomenon of vascular calcification under hyperphosphatemic conditions.
Role of increased oxygen free radical activity in the pathogenesis of uremic hypertension.
- Biology, MedicineKidney international
- 1998
The results suggest that increased OFR activity is, in part, responsible for CRF-associated HTN and points to hydroxyl radicals as the major source of OFR in CRF animals.
Increased inorganic phosphate induces human endothelial cell apoptosis in vitro.
- Biology, MedicineAmerican journal of physiology. Renal physiology
- 2008
Findings show that hyperphosphatemia causes endothelial cell apoptosis, a process that impairs endothelial integrity, and may be an initial event leading to vascular complications in patients with chronic kidney disease.
Mechanisms of Aortic and Cardiac Dysfunction in Uremic Mice With Aortic Calcification
- Medicine, BiologyCirculation
- 2009
In a mouse model of CRF, left ventricular hypertrophy, cardiac diastolic dysfunction, and increased aortic stiffness were not related to structural changes in the aorta or high serum cholesterol levels, and alterations in vascular reactivity, the upregulation of adhesion molecule expression, and CRF status were significant.
Pleiotropic effects of the non-calcium phosphate binder sevelamer.
- BiologyKidney international. Supplement
- 2006
Sevelamer hydrochloride is a phosphate binder that offers an effective control of hyperphosphatemia as calcium-rich binders but without increase of calcium load.
Reversal of the adynamic bone disorder and decreased vascular calcification in chronic kidney disease by sevelamer carbonate therapy.
- Medicine, BiologyJournal of the American Society of Nephrology : JASN
- 2007
Results suggest that sevelamer may have important actions in decreasing diabetic and uremic vasculopathy and that seVELamer carbonate may be capable of increasing bone formation rates that are suppressed by diabetic nephropathy.
Vascular calcification: in vitro evidence for the role of inorganic phosphate.
- Biology, MedicineJournal of the American Society of Nephrology : JASN
- 2003
Calcification of vascular cells can occur early in a phosphate-rich environment similar to that seen in patients with renal failure and in a platelet-derived growth factor-rich atherosclerotic region under normal phosphorus conditions, which seems to reduce coronary calcification and its associated morbidity and mortality for patients on dialysis.
FGF23 induces left ventricular hypertrophy.
- Biology, MedicineThe Journal of clinical investigation
- 2011
It is reported that elevated FGF23 levels are independently associated with LVH in a large, racially diverse CKD cohort and suggested that chronically elevated F GF23 levels contribute directly to high rates of LVH and mortality in individuals with CKD.