Phosphate binders for the treatment of hyperphosphatemia in chronic kidney disease patients on dialysis: a comparison of safety profiles

Locatelli, Francesco; Vecchio, Lucia Del; Violo, Leano; Pontoriero, Giuseppe

doi:10.1517/14740338.2014.907791

Cited by 57 publications

(45 citation statements)

References 78 publications

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“…Although calcium-based phosphate binders are very useful to control hyperphosphatemia, they can lead to positive calcium balance and cardiovascular calcification. On the other hand, sevelamer prevents or muffles VC [14]. These effects were encountered when such agents were used in the recommended doses.…”

Section: Discussionmentioning

confidence: 99%

Low Dose of Sevelamer is Enough to Prevent Coronary Artery Calcification Progression in Prevalent Hemodialysis Patients

Din¹

2016

OAJUN

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Objective: Our objective is to study the possible role of low dose sevelamer hydrochloride on the rate of progression of coronary artery calcification among prevalent hemodialysis (HD) patients. Methods:Eighty HD patients were selected to this study. These patients were receiving oral calcium carbonate (CaCO3) as 200mg of elemental calcium with each meal (total of 1500 mg/day). They were randomized into two equal groups. The first group was administered sevelamer hydrochloride as 800 mg with each meal (2400 mg/day) instead of CaCO3 [Group I], while the oral CaCO3 was maintained as 200mg of elemental calcium with each meal in the 2 nd group [Group II]. Coronary artery calcification score (CCs) was assessed before stating and at the end of the trial. In addition, serum fibroblast growth factor 23 (FGF23), calcium, phosphorus, lipids and intact parathyroid hormone (PTH) were estimated in these two events. Results:The baseline CCs and serum FGF23 were comparable in the 2 groups (200 ± 98.45 vs. 198 ± 69.68 A and 4669.5 ± 3540.9 vs. 4737 ± 2578.2 pg/ml, P=0.75 and 0.34 for CCs and serum FGF23 in group I vs. group II respectively). On the other hand, CCs and serum FGF23 were significantly lower in group I compared to group II by the end of the trial (203 ± 97.95 vs. 292 ± 100.16 A and 3011.8 ± 1853.7 vs. 7071.5 ± 2650.4 pg/ml, p= 0.012 and <0.001 for CCs and serum FGF23 in group I vs. group II respectively). These significant changes were associated with a highly significant decrease of CaxP product after using sevelamer (53.7 ± 6.5 vs. 65.3 ± 5.55, in group I vs. group II respectively, p<0.001). CCS showed significant correlation with FGF 23 (r=0.634, p<0.001) but failed to show similar correlation with other studied parameters in both groups. Conclusion:Low dose Sevelamer HCL can withhold coronary artery calcification progression in prevalent HD patients, and significantly decreases FGF 23 level. These results may help to overcome the patient intolerance and economic burden of the full dose of sevelamer. Further studies comparing low dose versus full dose of sevelamer are needed in these patients

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Section: Discussionmentioning

confidence: 99%

Low Dose of Sevelamer is Enough to Prevent Coronary Artery Calcification Progression in Prevalent Hemodialysis Patients

Din¹

2016

OAJUN

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“…while lowering serum phosphorus and attenuating the progression of secondary hyperparathyroidism [117] . Calcium-based phosphate binders are still very useful to control hyperphosphatemia, but can lead to hypercalcemia and/or positive calcium balance and cardiovascular calcification [118] . The higher the dose ingested the greater the extent of V.C.…”

Section: Sharaf El Din Uaa Et Al Stop Chronic Kidney Disease Progrementioning

confidence: 99%

Stop chronic kidney disease progression: Time is approaching

Din¹,

Salem²,

Abdulazim³

2016

WJN

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Progression of chronic kidney disease (CKD) is inevitable. However, the last decade has witnessed tremendous achievements in this field. Today we are optimistic; the dream of withholding this progression is about to be realistic. The recent discoveries in the field of CKD management involved most of the individual diseases leading the patients to end-stage renal disease. Most of these advances involved patients suffering diabetic kidney disease, chronic glomerulonephritis, polycystic kidney disease, renal amyloidosis and chronic tubulointerstitial disease. The chronic systemic inflammatory status and increased oxidative stress were also investigated. This inflammatory status influences the antisenescence Klotho gene expression. The role of Klotho in CKD progression together with its therapeutic value are explored. The role of gut as a major source of inflammation, the pathogenesis of intestinal mucosal barrier damage, the role of intestinal alkaline phosphatase and the dietary and therapeutic implications add a novel therapeutic tool to delay CKD progression.

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“…Sevelamer compounds are resin-based binders that can prevent or muffle VC [103]. In a recent meta-analysis, the use of sevelamer in CKDG 3-5 patients is associated with significant decrease in all-cause mortality inspite of the insignificant difference in serum phosphorus and the significant increase in serum PTH compared to ISSN: 2380-0585 calcium-based phosphate binders [104].…”

Section: Management Of Non-traditional Risk Factorsmentioning

confidence: 99%

Arterial Calcification in Chronic Kidney Disease: Whom? When? and How to Handle?

2016

J Urol Nephrol

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Chronic kidney disease (CKD) patients have the highest mortality rate compared to other chronic diseases. Cardiovascular events account for up to 60% of the mortalities, with cardiovascular calcifications affecting the majority of those CKD patients. Most of this calcification is related to disturbed renal phosphate handling. Fibroblast growth factor 23 (FGF23) and Klotho were incriminated in the pathogenesis of vascular calcification (VC) through different mechanisms including their effect on endothelium and arterial wall smooth muscle cells. In addition, deficient Klotho gene expression is a constant feature in CKD patients. This deficiency, not only promotes vascular pathology, but also has a role in the progression of the CKD. This review will cover the medical history, prevalence, pathogenesis, clinical relevance, diagnostic tools, the ideal timing to prevent or to withhold the progression of VC and the different medications and medical procedures that can help to prolong the survival of CKD patients. IntroductionThe problematic increase of cardiovascular morbidity and mortality is behind the increased interest in VC among CKD patients. VC is a strong predictor of increased cardiovascular mortality among CKD patients. However, almost all of the clinical studies that have tried to manipulate the various risk factors for VC in dialysis patients have failed to show a significant impact on patient survival. On the other hand, when pre-dialysis patients underwent similar studies, there was a significant decrease in cardiovascular and overall mortality rates, as well as a comparable effect on VC progress rate. These results point toward the importance of early intervention. The ideal timing and dynamics of this intervention will be thoroughly discussed. VC In CKD PatientsThe prevalence of VC among pre-dialysis CKD G3-5 patients is 79% as reported in a recent study [1]. It might approach 100% in patients starting dialysis [2]. Upto 3-4 fold increase in VC has been reported in the earliest phases of CKD [3].VC in CKD can affect the tunica intima and/or the tunica media layers. Intimal calcification is mainly a feature of atherosclerosis [4]. Medial calcification is restricted to CKD and is encountered even at young ages [5,6]. Hemodialysis (HD) patients have higher calcification scores than both peritoneal dialysis (PD) and CKD G4 patients. More heavily calcified patients were significantly older and mostly male [7]. In HD patients, coronary calcification progresses steadily [8]. High serum phosphate concentration was a strong independent risk factor only in non-diabetic patients. Diabetic patients lack similar associations [9]. Patients starting dialysis at the age of 25-29 years have an expected survival 33 years less than the general populous. Arterial calcification is one of the predictors of this increased cardiovascular mortality [10].The prevalence of coronary artery calcification (CAC) in kidney transplant recipients (KTRs) is higher (61-75%) than that assessed in CKD G3, [11,12] and lower than tha...

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Phosphate binders for the treatment of hyperphosphatemia in chronic kidney disease patients on dialysis: a comparison of safety profiles

Cited by 57 publications

References 78 publications

Low Dose of Sevelamer is Enough to Prevent Coronary Artery Calcification Progression in Prevalent Hemodialysis Patients

Low Dose of Sevelamer is Enough to Prevent Coronary Artery Calcification Progression in Prevalent Hemodialysis Patients

Stop chronic kidney disease progression: Time is approaching

Arterial Calcification in Chronic Kidney Disease: Whom? When? and How to Handle?

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