Sevelamer therapy for pediatric end-stage renal disease

Sevelamer, a non-calcium-containing, non-aluminum-containing phosphate binder, is frequently prescribed for treatment in adults with hyperphosphatemia secondary to end-stage renal disease (ESRD). However, published information regarding sevelamer use in children younger than 11 years is lacking. We report the use of sevelamer as a phosphate binder in a 19-month-old girl with ESRD who was receiving calcium carbonate 1250 mg 3 times/day for hyperphosphatemia. The patient's initial serum phosphorus concentration was 8.6 mg/dl, and the calcium-phosphorus product was 75 mg(2)/dl(2). This was well above the level that places patients at risk for complications such as joint, vessel, and soft-tissue calcification. An aluminum-containing phosphate binder was not an option given the patient's renal disease and the concern for neurotoxicity. Sevelamer was considered, but a MEDLINE search revealed no pediatric dosing information. An initial dosage of 100 mg/kg/day divided every 8 hours was administered, as extrapolated from adult data, and then titrated to 130 mg/kg/day divided every 8 hours based on the patient's response. The child's dietary phosphorus intake remained constant throughout her hospital stay. During sevelamer therapy, her serum phosphorus concentration dropped as low as 5.2 mg/dl; at discharge it was 6.5 mg/dl, with a corresponding calcium-phosphorus product in the upper 50s. No adverse effects associated with sevelamer were observed. In the dosages we used, sevelamer resulted in an acceptable calcium-phosphorus product and returned the patient's serum phosphorus concentration to near normal. Sevelamer appears to be a viable option as a phosphate binder in children with ESRD.     

Protein-Bound Uremic Toxins: New Culprits of Cardiovascular Events in Chronic Kidney Disease Patients

Chronic kidney disease (CKD) has been considered a major risk factor for cardiovascular diseases. Although great advances have recently been made in the pathophysiology and treatment of cardiovascular diseases, CKD remains a major global health problem. Moreover, the occurrence rates of cardiovascular events among CKD patients increase even in cases in which patients undergo hemodialysis, and the mechanisms underlying the so-called “cardiorenal syndrome” are not clearly understood. Recently, small-molecule uremic toxins have been associated with cardiovascular mortality in CKD and/or dialysis patients. These toxins range from small uncharged solutes to large protein-bound structures. In this review, we focused on protein-bound uremic toxins, such as indoxyl sulfate and p-cresyl sulfate, which are poorly removed by current dialysis techniques. Several studies have demonstrated that protein-bound uremic toxins, especially indoxyl sulfate, induce vascular inflammation, endothelial dysfunction, and vascular calcification, which may explain the relatively poor prognosis of CKD and dialysis patients. The aim of this review is to provide novel insights into the effects of indoxyl sulfate and p-cresyl sulfate on the pathogenesis of atherosclerosis.     

Exploring Protein Binding of Uremic Toxins in Patients with Different Stages of Chronic Kidney Disease and during Hemodialysis

As protein binding of uremic toxins is not well understood, neither in chronic kidney disease (CKD) progression, nor during a hemodialysis (HD) session, we studied protein binding in two cross-sectional studies. Ninety-five CKD 2 to 5 patients and ten stable hemodialysis patients were included. Blood samples were taken either during the routine ambulatory visit (CKD patients) or from blood inlet and outlet line during dialysis (HD patients). Total (C_T) and free concentrations were determined of p-cresylglucuronide (pCG), hippuric acid (HA), indole-3-acetic acid (IAA), indoxyl sulfate (IS) and p-cresylsulfate (pCS), and their percentage protein binding (%PB) was calculated. In CKD patients, %PB/C_T resulted in a positive correlation (all p < 0.001) with renal function for all five uremic toxins. In HD patients, %PB was increased after 120 min of dialysis for HA and at the dialysis end for the stronger (IAA) and the highly-bound (IS and pCS) solutes. During one passage through the dialyzer at 120 min, %PB was increased for HA (borderline), IAA, IS and pCS. These findings explain why protein-bound solutes are difficult to remove by dialysis: a combination of the fact that (i) only the free fraction can pass the filter and (ii) the equilibrium, as it was pre-dialysis, cannot be restored during the dialysis session, as it is continuously disturbed.     

A comparative review of the efficacy and safety of established phosphate binders: calcium,sevelamer, and lanthanum carbonate*

ABSTRACT

Background: Obstacles to successful management of hyperphosphatemia in chronic kidney disease include inadequate control of dietary phosphate and non-compliance with phosphate-binder therapy. Three major classes of phosphate binders include calcium-based binders, sevelamer HCl, and lanthanum carbonate.

Scope: A literature search was performed using MEDLINE and EMBASE databases to identify clinical trials from January 1966 to May 2007 comparing classes of phosphate binders with regard to efficacy, safety, compliance, or pharmacoeconomics. Search terms included lanthanum AND sevelamer, lanthanum AND calcium, and sevelamer AND calcium. A total of 1372 articles were identified in the search, with 125 review articles and clinical trials of interest identified.

Findings: Calcium-based binders are effective, but their potential to contribute to total body calcium overload and vascular calcification is an important long-term clinical concern. Sevelamer HCl is effective in reducing serum phosphate, has no systemic absorption, and does not increase total body calcium load. However, sevelamer HCl binds bile acids, is not an efficient phosphate binder in an acidic environment, and contributes to metabolic acidosis. Lanthanum carbonate is a potent and selective phosphate binder that retains high affinity for phosphate over a wide pH range, does not bind bile acids or contribute to metabolic acidosis, and has the potential to reduce pill burden and increase patient compliance compared with other phosphate binders.

Conclusions: All three classes of phosphate binders are effective at reducing serum phosphate levels. Lanthanum carbonate may result in increased adherence by decreasing the pill burden.     

Serum P-Cresyl Sulfate Level Is an Independent Marker of Peripheral Arterial Stiffness as Assessed Using Brachial-Ankle Pulse Wave Velocity in Patients with Non-Dialysis Chronic Kidney Disease Stage 3 to 5

p-Cresyl sulfate (PCS) is a uremic toxin that causes cardiovascular injury and progression in patients with chronic kidney disease (CKD). Peripheral arterial stiffness (PAS) as measured using the brachial-ankle pulse wave velocity (baPWV) is considered a valuable predictor of cardiovascular event risk in the general population. The study investigated the correlation between serum PCS levels and PAS (baPWV > 18.0 m/s) in 160 patients with stage 3–5 CKD. Liquid chromatography–mass spectrometry was used to assay serum PCS levels. PAS was detected in 54 patients (33.8%), and it was linked to older age, a higher prevalence of hypertension, higher systolic and diastolic blood pressure, higher serum calcium–phosphorus product and PCS levels, and lower height and body weight. Multivariable logistic regression analysis for independent factors associated with PAS illustrated that, in addition to age and diastolic blood pressure, serum PCS levels exhibited an odds ratio (OR) of 1.098 (95% confidence interval = 1.029–1.171, p = 0.005). These findings demonstrated that serum PCS levels were associated with PAS among patients with stage 3–5 CKD.     

Targeting protein-bound uremic toxins in chronic kidney disease

Introduction: Protein-bound uremic toxins such as indoxyl sulfate cannot be removed efficiently by hemodialysis. These protein-bound uremic toxins have emerged as important risk factors for the progression of chronic kidney disease (CKD) as well as cardiovascular disease (CVD).

Areas covered: Indoxyl sulfate shows toxic effects on a variety of cells such as renal proximal tubular cells, glomerular mesangial cells, vascular smooth muscle cells, vascular endothelial cells, cardiomyocytes, cardiac fibroblasts, monocytes, osteoblasts and osteoclasts. This review overviews the cellular toxicity of indoxyl sulfate, its molecular mechanism and its role in the progression of CKD and CVD. Further, this review summarizes the clinical effects of AST-120 and the other strategies to reduce serum levels of indoxyl sulfate.

Expert opinion: Protein-bound uremic toxins such as indoxyl sulfate have emerged as target molecules for therapeutic intervention of not only CKD but also CVD. An oral sorbent AST-120 reduces serum level of indoxyl sulfate by adsorbing indole in the intestine. The modulation of intestinal bacteria by prebiotics/probiotics might be effective in reducing the production of indole in the intestine followed by reduced serum levels of indoxyl sulfate. An alternative approach might be antagonist which can counteract indoxyl sulfate-induced cellular effects and signaling pathways.     

Sevelamer hydrochloride: a review of its use for hyperphosphataemia in patients with end-stage renal disease on haemodialysis

Sevelamer (Renagel), an orally administered metal-free cationic hydrogel polymer/resin that binds dietary phosphate in the gastrointestinal (GI) tract, is approved for use in the US, Europe and several other countries for the treatment of hyperphosphataemia in adult patients with end-stage renal disease (ESRD) on haemodialysis or peritoneal dialysis.Clinical evidence shows that sevelamer was at least as effective as calcium acetate and calcium carbonate at controlling serum phosphorus, calcium-phosphorus product (Ca x P) and intact parathyroid hormone (iPTH) levels, but generally reduced serum calcium levels to a greater extent and was associated with a lower risk of hypercalcaemic episodes than calcium-based phosphate binders. Sevelamer appeared to slow the progression of cardiovascular calcification in patients with ESRD and also had a beneficial effect on serum low-density lipoprotein-cholesterol (LDL-C) levels. In patients receiving chronic haemodialysis, there was no between-group difference in all-cause mortality between sevelamer and calcium-based phosphate binder therapy in the primary efficacy analysis in the large (n >2100), 3-year DCOR trial; in the smaller (n = 109) nonblind RIND trial in patients new to dialysis, data suggest there is an overall survival benefit with sevelamer versus calcium-based phosphate binder treatment. The relative survival benefits and cost effectiveness of these phosphate binder therapies remains to be fully determined. Sevelamer treatment was generally as well tolerated as calcium acetate or calcium carbonate treatment. Overall, sevelamer is a valuable option for the management of hyperphosphataemia in patients with ESRD on haemodialysis.     

The role of sevelamer in achieving the kidney disease outcomes quality initiative (K/DOQI) guidelines for hyperphosphatemia

SUMMARY

Background: End-stage renal disease (ESRD) is a chronic health care problem associated with multiple co-morbidities and escalating costs. Disregulation of mineral metabolism (principally hyperphosphatemia and hypercalcemia) contributes to substantial morbidity and mortality. Accordingly, new and more-aggressive Kidney Disease Outcomes Quality Initiative (K/DOQI) Guidelines from the National Kidney Foundation promote lower serum phosphorus (3.5–5.5?mg/dL), lower calcium (8.4–9.5?mg/dL), and lower calcium-phosphorus product (< 55?mg²/dL²) targets.

Review findings: Traditional calcium-based and metal-based phosphate binders are effective but are associated with side effects and toxicity that limit their use. Achieving rigorous K/DOQI goals demands higher therapeutic doses of phosphate binders and may require more-aggressive use of calcium-free and metal-free phosphate binders. Sevelamer hydrochloride is a calcium- and metal-free polymer that binds phosphate effectively without contributing to calcium load or metal accumulation. In the Treat-to-Goal trial, sevelamer-treated dialysis patients had less progression of coronary and aortic calcification than patients treated with calcium-based binders. This offers the potential promise of reducing cardiovascular morbidity and mortality. The 800-mg tablet (Renagel*) increases the daily sevelamer dose while reducing the number of tablets required per meal. Nine of the 800-mg tablets per day (3 × 800-mg tablets tid with meals) of sevelamer monotherapy have been shown to achieve K/DOQI serum phosphorus and calcium-phosphorus product targets.

Conclusion: In summary, this review of the current evidence-base concludes that the new, more-aggressive, K/DOQI goals limit the use of metal-based and calcium-based phosphate binders. Sevelamer offers the advantages of lowering serum phosphorus without the risks of calcium or metal accumulation – and offers the promise of slowing the progression of vascular calcification and potentially reducing the morbidity and mortality of hemodialysis patients.     

Vascular calcification and secondary hyperparathyroidism of severe chronic kidney disease and its relation to serum phosphate and calcium levels

Background and purpose:

Various complications consequent on disordered calcium and phosphate homeostasis occur frequently in chronic kidney disease (CKD) patients. Particularly, vascular calcification has high morbidity and mortality rates. There is a clear need for a better CKD model to examine various aspects of this disordered homeostasis.

Experimental approach:

Oral dosing with adenine induced CKD in rats in only 10 days. Serum calcium, phosphate and parathyroid hormone were measured and calcification in aorta was assessed histologically. The effects of varying phosphorus content of diet or treatment with phosphate binders or active vitamin D₃ on these parameters were examined.

Key results:

After adenine dosing, significant hyperphosphatemia, hypocalcemia and secondary hyperparathyroidism (2HPT) were observed during the experimental period of 15 weeks. Aortic calcification was detected in only some of the animals even at 15 weeks (∼40%). Treatment with vitamin D₃ for 18 days, even at a low dose (100 ng·kg⁻¹, 3–4 times week⁻¹, p.o), caused aortic calcification in all animals and increases in serum calcium levels up to the normal range. The vitamin D₃-induced calcification was significantly inhibited by phosphate binders which lowered serum phosphate levels and the calcium × phosphate product, although serum calcium levels were elevated.

Conclusions:

These data suggest that rats dosed orally with adenine provide a more useful model for analysing calcium/phosphate homeostasis in severe CKD. Controlling serum calcium/phosphate levels with phosphate binders may be better than vitamin D₃ treatment in hyperphosphatemia and 2HPT, to avoid vascular calcification.     

新型磷结合剂的研究进展

慢性肾脏病（CKD）患者肾功能减退,引发钙磷的代谢紊乱,进一步导致各种疾病的发生。高磷血症可能会升高CKD患者的发病率和死亡率。因而,有效控制血清磷的水平将是CKD患者预后的关键。传统磷结合剂常含钙、铝成分,虽能有效降低血清磷,但不良反应较多。综述上市的和临床研究中的新型磷结合剂如司维拉姆、碳酸镧、考来替兰和柠檬酸铁等,其不含钙、铝,能有效控制血清磷水平,却不升高血钙,为控制高磷血症和减少血管钙化风险提供了治疗前景。     

新型磷结合剂的研究进展

慢性肾脏病(CKD)患者肾功能减退,引发钙磷的代谢紊乱,进一步导致各种疾病的发生。高磷血症可能会升高CKD患者的发病率和死亡率。因而,有效控制血清磷的水平将是CKD患者预后的关键。传统磷结合剂常含钙、铝成分,虽能有效降低血清磷,但不良反应较多。综述上市的和临床研究中的新型磷结合剂如司维拉姆、碳酸镧、考来替兰和柠檬酸铁等,其不含钙、铝,能有效控制血清磷水平,却不升高血钙,为控制高磷血症和减少血管钙化风险提供了治疗前景。     

The role of sevelamer in achieving the kidney disease outcomes quality initiative (K/DOQI) guidelines for hyperphosphatemia

BACKGROUND: End-stage renal disease (ESRD) is a chronic health care problem associated with multiple co-morbidities and escalating costs. Disregulation of mineral metabolism (principally hyperphosphatemia and hypercalcemia) contributes to substantial morbidity and mortality. Accordingly, new and more-aggressive Kidney Disease Outcomes Quality Initiative (K/DOQI) Guidelines from the National Kidney Foundation promote lower serum phosphorus (3.5-5.5 mg/dL), lower calcium (8.4-9.5 mg/dL), and lower calcium-phosphorus product (< 55 mg(2)/dL(2)) targets. REVIEW FINDINGS: Traditional calcium-based and metal-based phosphate binders are effective but are associated with side effects and toxicity that limit their use. Achieving rigorous K/DOQI goals demands higher therapeutic doses of phosphate binders and may require more-aggressive use of calcium-free and metal-free phosphate binders. Sevelamer hydrochloride is a calcium- and metal-free polymer that binds phosphate effectively without contributing to calcium load or metal accumulation. In the Treat-to-Goal trial, sevelamer-treated dialysis patients had less progression of coronary and aortic calcification than patients treated with calcium-based binders. This offers the potential promise of reducing cardiovascular morbidity and mortality. The 800-mg tablet (Renagel) increases the daily sevelamer dose while reducing the number of tablets required per meal. Nine of the 800-mg tablets per day (3 x 800-mg tablets tid with meals) of sevelamer monotherapy have been shown to achieve K/DOQI serum phosphorus and calcium-phosphorus product targets. CONCLUSION: In summary, this review of the current evidence-base concludes that the new, more-aggressive, K/DOQI goals limit the use of metal-based and calcium-based phosphate binders. Sevelamer offers the advantages of lowering serum phosphorus without the risks of calcium or metal accumulation - and offers the promise of slowing the progression of vascular calcification and potentially reducing the morbidity and mortality of hemodialysis patients.     

肾衰宁胶囊联合司维拉姆治疗血液透析患者高磷血症的疗效观察

目的 观察肾衰宁胶囊联合司维拉姆治疗血液透析患者高磷血症的临床疗效。方法 选择2022年11月—2023年03月在山东大学齐鲁医院（青岛）治疗的80例高磷血症的血液透析患者,按照随机数字表法将患者分为对照组和治疗组,每组各40例。对照组患者口服碳酸司维拉姆片,3次/d,起始剂量每次1片或2片。治疗组在对照组的治疗基础上口服肾衰宁胶囊,3粒/次,3次/d。两组均连续治疗16周。观察两组患者临床疗效,比较治疗前后两组患者血磷、血钙、钙磷乘积和甲状旁腺激素（iPTH）水平。结果 治疗后,治疗组总有效率为72.50%,明显高于对照组47.50%(P<0.05)。治疗后,治疗组患者血磷水平持续下降,从第4周开始显著低于治疗前（P<0.05）,从第12周开始血磷水平明显低于对照组（P<0.05）。治疗后,两组患者的血钙水平均显著低于治疗前（P<0.05）。治疗后,治疗组患者的钙磷乘积水平较治疗前持续下降（P<0.05）,治疗组内比较和两组间比较与血磷变化趋势一致。结论 肾衰宁胶囊联合司维拉姆能有效治疗血液透析患者的高磷血症,并有效降低钙磷乘积,且无明显不良反应。     

Albumin is the main plasma binding protein for indoxyl sulfate and p‐cresyl sulfate

Indoxyl sulfate and p‐cresyl sulfate are two uremic retention solutes implicated in the uremic syndrome. Removal during dialysis is limited, mainly due to protein binding. Binding characteristics to healthy albumin have recently been characterized. Whether uremia alters the binding characteristics of albumin is currently unknown. Moreover, protein binding values previously determined with ultrafiltration are in sharp contrast to recently reported values based on microcalorimetry. In the present study, indoxyl sulfate and p‐cresyl sulfate binding were therefore quantified using both equilibrium dialysis and ultrafiltration. Deming regression demonstrated good agreement between equilibrium dialysis and ultrafiltration. Free serum concentrations of indoxyl sulfate (+26.6%) and p‐cresyl sulfate (+19.7%) were slightly higher at body temperature compared with at room temperature. To investigate binding kinetics, the plasma of healthy individuals or hemodialysis patients was titrated with albumin solutions. Theoretical models of protein binding were fitted to observed titration curves. Binding coefficients of both toxins were highest in purified albumin, and were reduced from healthy to uremic plasma. In conclusion, the ultrafiltration–HPLC technique reliably measures free serum concentrations of indoxyl sulfate and p‐cresyl sulfate. Albumin is the main binding protein, both in health and in advanced stages of chronic kidney disease. Modeling suggests that albumin contains two binding sites for both toxins, a single high affinity binding site and a second low affinity binding site. The high affinity binding site accounts for at least 90% of overall binding. Competition for this binding site could be used to augment free solute concentrations during dialysis, thus improving epuration. Copyright © 2013 John Wiley & Sons, Ltd.     

Sevelamer carbonate for the treatment of hyperphosphatemia in patients with kidney failure (CKD III – V)

Importance of the field: Altered mineral metabolism in chronic kidney disease (CKD) is associated with increased morbidity, mortality, hospitalization, cost of care and reduced quality of life. Phosphorus control, one component of CKD metabolic derangements, is potentially related to impaired outcomes and has significant room for improvement.

Areas covered in this review: Historical, present and future aspects of treatment of hyperphosphatemia focusing on sevelamer hydrochloride and sevelamer carbonate.

What the reader will gain: Comprehensive insight into the background and controversies regarding phosphate binders.

Take home message: While calcium-free phosphate binders with a sevelamer backbone may offer therapeutic advantages for CKD patients at risk, more studies comprising significant patient numbers are warranted to answer compelling clinical questions.     

Clinical consequences and novel therapy of hyperphosphatemia: Lanthanum carbonate for dialysis patients

Vascular calcification is a very common event in patients affected by diabetes and chronic kidney disease (CKD). Recently, it has been well documented that abnormalities in mineral and bone metabolism in CKD patients associate with increased morbidity and mortality. Elevated serum phosphate and calcium-phosphate product levels play an important role in the pathogenesis of vascular mineralization in uremic patients and also appear to be associated with increased cardiovascular mortality. Together with classical passive precipitation of calcium-phosphate in soft tissues, during the last decade it has been demonstrated that inorganic phosphate may cause extraskeletal calcification directly through a real "ossification" of the tunica media in the vasculature of CKD patients. Therefore, control of phosphate retention is now an even more crucial target of treatment in patients affected by chronic kidney disease. The "classical" treatment of secondary hyperparathyroidism and hyperphosphatemia in CKD patients consists of either calcium or aluminium based phosphate-binders and calcitriol administration. Unfortunately, this "old generation" therapy is not free of complications. Patents are also reported discussing the role of derivatives of Lanthanum carbonate hydrates are also used for the treatment of hyperphosphataemia in patients with renal failure. New calcium- and aluminium-free phosphate binders, such as sevelamer hydrochloride and lanthanum carbonate, can be used to treat hyperphosphatemia and secondary hyperparathyroidism, reduce atherosclerotic process, and prevent vascular calcification in CKD patients.     

司维拉姆治疗透析患者高磷血症的快速评估

摘 要 目的：快速评估司维拉姆治疗透析患者高磷血症的有效性、安全性和经济性。方法：通过计算机检索PubMed、Embase、the Cochrane Library和专业卫生技术评估数据库收集司维拉姆治疗透析患者高磷血症的卫生技术评估报告、系统评价/Meta分析和经济学评价。按照纳入排除标准筛选文献、提取资料和评价质量,对研究结果进行全面分析后得出结论。结果：共纳入22项研究,其中5项卫生技术评估报告、7项系统评价/Meta分析和10项经济学评价。结果显示司维拉姆可有效控制血磷水平,同时不增加血钙水平和高钙血症的风险。此外,和含钙磷结合剂相比,司维拉姆组患者总胆固醇、低密度脂蛋白胆固醇及C反应蛋白水平较低,且司维拉姆治疗并没有过度抑制血清全段甲状旁腺激素水平。国内外的经济学研究显示,与含钙磷结合剂相比,司维拉姆用于透析患者具有成本效果优势。国内的经济学研究显示,与碳酸镧相比,司维拉姆可能更具有成本效果优势,但仍需进一步研究。结论：基于目前可获得的证据支持司维拉姆用于透析患者高磷血症的治疗。     

Increased Proinflammatory Cytokine Production and Decreased Cholesterol Efflux Due to Downregulation of ABCG1 in Macrophages Exposed to Indoxyl Sulfate

One of the possible causes of enhanced atherosclerosis in patients with chronic kidney disease (CKD) is the accumulation of uremic toxins. Since macrophage foam cell formation is a hallmark of atherosclerosis, we examined the direct effect of indoxyl sulfate (IS), a representative uremic toxin, on macrophage function. Macrophages differentiated from THP-1 cells were exposed to IS in vitro. IS decreased the cell viability of THP-1 derived macrophages but promoted the production of inflammatory cytokines (IL-1β, IS 1.0 mM: 101.8 ± 21.8 pg/mL vs. 0 mM: 7.0 ± 0.3 pg/mL, TNF-α, IS 1.0 mM: 96.6 ± 11.0 pg/mL vs. 0 mM: 15.1 ± 3.1 pg/mL) and reactive oxygen species. IS reduced macrophage cholesterol efflux (IS 0.5 mM: 30.3% ± 7.3% vs. 0 mM: 43.5% ± 1.6%) and decreased ATP-binding cassette transporter G1 expression. However, lipid uptake into cells was not enhanced. A liver X receptor (LXR) agonist, T0901317, improved IS-induced production of inflammatory cytokines as well as reduced cholesterol efflux. In conclusion, IS induced inflammatory reactions and reduced cholesterol efflux in macrophages. Both effects of IS were improved with activation of LXR. Direct interactions of uremic toxins with macrophages may be a major cause of atherosclerosis acceleration in patients with CKD.     

Hyperphosphatemia and phosphate binders: effectiveness and safety

In patients with kidney dysfunction hyperphosphatemia is more evident as renal failure progresses. It is related to increased FGF-23 levels, secondary hyperparathyroidism, and accelerated progressive vascular calcification. In CKD patients advanced coronary artery calcification is strongly associated with future cardiovascular events, cardiovascular death, and all-cause mortality. Apart from the above, phosphate per se is suspected as a causal risk factor for CKD progression. Keeping serum phosphorus within the target values are linked to improvement in life expectancy. A low phosphate diet, an efficient dialysis removal of phosphate load, and the administration of phosphate binders are the main recommended steps to control hyperphosphatemia. Calcium-based phosphate binders can lead to a positive calcium balance, hypercalcaemia, parathyroid gland suppression, adynamic bone disease, and coronary artery and aortic calcification. On the other hand Sevelamer hydrochloride and Lanthanum carbonate has been shown to be effective, safe and useful therapeutic tools for hyperphosphatemia. When prescribe pharmacological agents, one must take into account the large increase in health-care expenditure and the choice of phosphate binder should be individualized.