Are Calcium-Based Phosphate Binders Ever Preferable in Dialysis Patients?

2014 ◽  
Vol 27 (3) ◽  
pp. 269-272
Author(s):  
Nishank Jain ◽  
Robert F. Reilly
Renal Failure ◽  
2014 ◽  
Vol 37 (1) ◽  
pp. 7-15 ◽  
Author(s):  
Chun-Juan Zhai ◽  
Xin-Shuang Yu ◽  
Xiao-Wei Yang ◽  
Jing Sun ◽  
Rong Wang

2008 ◽  
Vol 28 (2_suppl) ◽  
pp. 42-46 ◽  
Author(s):  
Jean Francis ◽  
David B. Simon ◽  
Peter Jeurgensen ◽  
Fredric O. Finkelstein

Secondary hyperparathyroidism is a common complication in patients with end-stage renal disease. It has been associated with increased cardiovascular events and mortality. Traditional therapy has been based on vitamin D analogs and phosphate binders; but these therapies often do not control secondary hyperparathyroidism, particularly in peritoneal dialysis patients for whom phosphate clearances are limited and intravenous vitamin D is impractical. Cinacalcet, a calcimimetic, suppresses parathormone secretion by interacting with the calcium-sensing receptor on the surface of parathyroid gland cells. The resulting suppression of parathyroid hormone secretion produces a reduction in serum phosphate level and CaxPO4 product. The present paper reviews the efficacy of cinacalcet in the management of secondary hyperparathyroidism in peritoneal dialysis patients.


2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Ramya Bhargava ◽  
Philip A. Kalra ◽  
Paul Brenchley ◽  
Helen Hurst ◽  
Alastair Hutchison

Background. Retrospective, observational studies link high phosphate with mortality in dialysis patients. This generates research hypotheses but does not establish “cause-and-effect.” A large randomised controlled trial (RCT) of about 3000 patients randomised 50 : 50 to lower or higher phosphate ranges is required to answer the key question: does reducing phosphate levels improve clinical outcomes? Whether such a trial is technically possible is unknown; therefore, a study is necessary to inform the design and conduct of a future, definitive trial.Methodology. Dual centre prospective parallel group study: 100 dialysis patients randomized to lower (phosphate target 0.8 to 1.4 mmol/L) or higher range group (1.8 to 2.4 mmol/L). Non-calcium-containing phosphate binders and questionnaires will be used to achieve target phosphate. Primary endpoint: percentage successfully titrated to required range and percentage maintained in these groups over the maintenance period. Secondary endpoints: consent rate, drop-out rates, and cardiovascular events.Discussion. This study will inform design of a large definitive trial of the effect of phosphate on mortality and cardiovascular events in dialysis patients. If phosphate lowering improves outcomes, we would be reassured of the validity of this clinical practice. If, on the other hand, there is no improvement, a reassessment of resource allocation to therapies proven to improve outcomes will result.Trial Registration Number. This trial is registered with ISRCTN registration numberISRCTN24741445.


Nephron ◽  
1995 ◽  
Vol 71 (3) ◽  
pp. 350-353 ◽  
Author(s):  
M. Gonella ◽  
G. Calabrese ◽  
A.G. Aleo ◽  
G. Vagelli ◽  
P. Deambrogio

2014 ◽  
Vol 34 (4) ◽  
pp. 345-352 ◽  
Author(s):  
Angela Yee-Moon Wang

Like hemodialysis patients, peritoneal dialysis (PD) patients are facing an excessively increased burden of vascular and valvular calcification. According to some surveys, more than 80% of prevalent PD patients are complicated with vascular calcification, and more than one third have heart valve calcification.Dysregulated phosphate metabolism is well recognized to play an important role in inducing vascular calcification, but increasing evidence is suggesting that dysregulated calcium metabolism also promotes vascular calcification and might in fact be more potent than phosphate in inducing that calcification. Growing evidence from randomized controlled trials shows more progression of vascular calcification and higher mortality among chronic kidney disease (CKD) patients receiving calcium-based phosphate binders than among those receiving non-calcium-containing phosphate binders. Those results raise important safety concern about the use of high-dose calcium-based phosphate binders in the CKD population, including both non-dialysis and dialysis patients (especially anuric dialysis patients), who have markedly reduced urinary calcium excretion. To prevent calcium overload, this review recommends restricting the dose of calcium-based phosphate binders in CKD patients, especially those who are elderly, who have increased cardiovascular risk, who already have baseline vascular or valvular calcification, or who have low intact parathyroid hormone and adynamic bone disease.


2014 ◽  
Vol 82 (2014) (12) ◽  
pp. 372-378 ◽  
Author(s):  
Chun-Juan Zhai ◽  
Xin-Shuang Yu ◽  
Qiao-Ling Sun ◽  
Lin Li ◽  
Li-Ting Zhang ◽  
...  

2016 ◽  
Vol 44 (2) ◽  
pp. 104-112 ◽  
Author(s):  
Stuart M. Sprague ◽  
Adrian C. Covic ◽  
Jürgen Floege ◽  
Markus Ketteler ◽  
Jaco Botha ◽  
...  

Background: Many patients with chronic kidney disease are prescribed vitamin D receptor agonists (VDRAs) for the management of secondary hyperparathyroidism. Oral phosphate binders may interact with, and potentially reduce the therapeutic activity of, oral VDRAs. This post hoc analysis of a Phase 3 study evaluated the pharmacodynamic effects of the iron-based phosphate binder sucroferric oxyhydroxide (SFOH) and sevelamer (SEV) carbonate on VDRA activity in dialysis patients. Methods: One thousand and fifty nine patients were randomized to SFOH 1.0-3.0 g/day (n = 710) or SEV 2.4-14.4 g/day (n = 349) for up to 52 weeks. Potential interactions of SFOH and SEV with VDRAs were assessed using serum intact parathyroid hormone (iPTH) concentrations as a pharmacodynamic biomarker. Three populations of SFOH- and SEV-treated patients were analyzed: Population 1 (n = 187), patients taking concomitant stable doses of oral VDRAs only; Population 2 (n = 250), patients taking no concomitant VDRAs; Population 3 (n = 68), patients taking concomitant stable doses of intravenous paricalcitol only. Populations were compared using a mixed-effects model to obtain the least squares mean change in iPTH from baseline to Week 52. Differences between treatment groups were also compared. Results: In Population 1, iPTH decreased from baseline to Week 52 in the SFOH group (-25.3 pg/ml) but increased in the SEV group (89.8 pg/ml) (p = 0.02). In Population 2, iPTH increased to a similar extent in both treatment groups. In Population 3, iPTH concentrations in both treatment groups decreased to a similar degree (-29.6 and -11.4 pg/ml for SFOH and SEV, respectively; p = 0.87). Conclusions: In contrast with SEV, SFOH did not appear to impact the iPTH-lowering effect of oral VDRAs.


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