Control Of Serum Phosphorus Research Articles

Safety and efficacy of nicotinamide in the management of hyperphosphatemia in patients on hemodialysis

Hyperphosphatemia is an important modifiable risk factor for death and cardiovascular events in patients on hemodialysis (HD). As nicotinamide has been shown as an inhibitor of sodium–dependent phosphate co–transport in rat renal tubule and small intestine, we examined whether nicotinamide reduces hyperphosphatemia in patients undergoing HD. The study was conducted in 30 end-stage renal disease (ESRD) patients [20 (66.7%) males and 10 (33.3%) females; mean age 54 ± 14.9 years] undergoing twice/thrice weekly HD for more than 3 months. Patients on other phosphate binders were given a 2-week wash-out period. Nicotinamide 250 mg capsules were given twice daily for 25 patients with serum phosphorus greater than 5 mg/dL and thrice daily for 5 patients with serum phosphorus greater than 8 mg/dL immediately after food for 8 weeks. Serum phosphate and calcium levels were estimated every month prior to HD session, and complete blood count, blood sugar, renal profile, liver function tests were estimated at beginning and end of the study. Patients were regularly monitored for side effects. There were significant decreases in the serum phosphate (6.85 ± 1.35 mg/dL at the baseline to 5.74 ± 1.18 mg/dL at the 4th week and to 4.54 ± 0.86 mg/dL at the 8th week), the serum calcium-phosphorus product (57.8 ± 12.21 at the baseline to 48.3 ± 10.71 on 4th week and to 38.201 ± 8.21 at the 8th week), and alkaline phosphatase levels (130.23 ± 50.13 IU/L at the baseline to 116.40 ± 48.27 IU/L after 8 weeks) on treatment with nicotinamide (P < 0.001). Other parameters remained unchanged. Watery stools reported by seven patients resolved during the course of the therapy. Nicotinamide is safe, cheap and effective in controlling serum phosphorus, Ca × P product and alkaline phosphatase levels in patients on maintenance HD.

Long-term treatment with lanthanum carbonate reduces mineral and bone abnormalities in rats with chronic renal failure

Background. Lanthanum carbonate (FOSRENOL®, Shire Pharmaceuticals) is an effective non-calcium, non-resin phosphate binder for the treatment of hyperphosphataemia in patients with chronic kidney disease (CKD). In this study, we used a rat model of chronic renal failure (CRF) to examine the long-term effects of controlling serum phosphorus with lanthanum carbonate treatment on the biochemical and bone abnormalities associated with CKD–mineral and bone disorder (CKD–MBD).Methods. Rats were fed a normal diet (normal renal function, NRF), or a diet containing 0.75% adenine for 3 weeks to induce CRF. NRF rats continued to receive normal diet plus vehicle or normal diet supplemented with 2% (w/w) lanthanum carbonate for 22 weeks. CRF rats received a diet containing 0.1% adenine, with or without 2% (w/w) lanthanum carbonate. Blood and urine biochemistry were assessed, and bone histomorphometry was performed at study completion.Results. Treatment with 0.75% adenine induced severe CRF, as demonstrated by elevated serum creatinine. Hyperphosphataemia, hypocalcaemia, elevated calcium × phosphorus product and secondary hyperparathyroidism were evident in CRF + vehicle animals. Treatment with lanthanum carbonate reduced hyperphosphataemia and secondary hyperparathyroidism in CRF animals (P < 0.05), and had little effect in NRF animals. Bone histomorphometry revealed a severe form of bone disease with fibrosis in CRF + vehicle animals; lanthanum carbonate treatment reduced the severity of the bone abnormalities observed, particularly woven bone formation and fibrosis.Conclusions. Long-term treatment with lanthanum carbonate reduced the biochemical and bone abnormalities of CKD–MBD in a rat model of CRF.

Early Intervention With Intravenous or Pulse Oral Vitamin D Therapy Is More Effective in the Treatment of Secondary Hyperparathyroidism

The K/DOQI clinical practice guidelines recommend vitamin D therapy should be started when the intact parathyroid hormone (iPTH) exceeds 300 pg/mL in patients with secondary hyperparathyroidism. To examine whether the effect of vitamin D therapy on mineral metabolism and parathyroid gland growth varies according to the stage of secondary hyperparathyroidism and iPTH level, 47 patients with secondary hyperparathyroidism received either intravenous or pulse oral vitamin D therapy. The patients were divided into two groups based on the iPTH level at the start of vitamin D therapy: the P(<300) group (N = 23) with iPTH <300 pg/mL; and the P(>or=300) group (N = 24) with iPTH >or=300 pg/mL. We examined serial changes in several serum mineral parameters and parathyroid gland volume and the cumulative incidence of parathyroidectomy in the first two years. Serum calcium, phosphorus, calcium-phosphorus product, and iPTH levels of the P(>or=300) group were significantly higher than those of the P(<300) group, and could not be maintained within the target ranges set by the K/DOQI guidelines. In contrast, the serum levels of phosphorus, calcium-phosphorus product, and iPTH were maintained within the target ranges and the parathyroid gland did not enlarge in the P(<300) group. The cumulative incidence of parathyroidectomy in the P(>or=300) group was significantly higher than in the P(<300) group. Early intervention with intravenous or pulse oral vitamin D therapy at serum iPTH <300 pg/mL can control serum phosphorus, calcium-phosphorus product, and PTH levels to the target ranges and slow the progression of secondary hyperparathyroidism.

Lanthanum Carbonate Provides Control of Phosphorus Levels in Patients New to Phosphate Binder Therapy and Patients Changed From Other Phosphate Binders

This retrospective study examined whether patients in an outpatient clinical setting with chronic kidney disease (CKD) stage 5, and who were either new to phosphate binder treatment or were previously treated with other phosphate binders, received benefit from treatment with lanthanum carbonate (LC). This was a retrospective analysis of patient records. Patients were treated at the Western New York Dialysis Center, LLC (Orchard Park, NY). Patients (n = 33) were identified through records as having CKD stage 5 and currently receiving or about to begin dialysis treatment. Naive patients (n = 16) had serum phosphorus levels >5.5 mg/dL and did not have previous exposure to phosphate binder treatment. "Changed" patients (n = 17) were treated with sevelamer hydrochloride or calcium-based binders before changing treatment to LC. Patients received 500 to 1,500 mg LC thrice daily as needed, to achieve serum phosphorus levels ≤5.5 mg/dL. Serum phosphorus control with LC was rapid (within 1 month) and sustained (after 6 months) in 81% of naive patients; serum albumin levels were maintained at 3.61 ± 0.28 g/dL over a period of 13.81 ± 8.4 months. Treatment with LC maintained serum phosphorus control after 10 to 12 months in 65% of patients in whom treatment was changed from other phosphate binders; serum albumin levels were maintained at 3.78 ± 0.35 g/dL after the change. In this clinical setting, outpatients treated with LC maintained serum phosphorus control and serum albumin levels, suggesting that LC may be effective as an alternative to other phosphate binders or as first-line therapy for controlling serum phosphorus for ≤6 months in patients with CKD stage 5 beginning dialysis.

Ironing out the phosphorus problem

Control of serum phosphorus remains a vexing problem in chronic kidney disease. Although novel dialysis regimens may provide excellent phosphorus control, phosphate binders remain necessary for most dialysis patients. Block et al. present a phase I clinical trial examining the safety and efficacy of SBR759, a novel non-calcium, iron-based phosphate binder. Although the risks of iron accumulation and hypocalcemia must be addressed, this phosphate binder appears to be well tolerated and effective and offers a powder-based formulation.

286: Iron Absorption With Higher Doses of Ferric Citrate in Controlling Serum Phosphorus in ESRD Patients

286: Iron Absorption With Higher Doses of Ferric Citrate in Controlling Serum Phosphorus in ESRD Patients

287: The Safety and Tolerability of Higher Doses of Ferric Citrate (FC) in Controlling Serum Phosphorus (P) In ESRD Patients

287: The Safety and Tolerability of Higher Doses of Ferric Citrate (FC) in Controlling Serum Phosphorus (P) In ESRD Patients

289: Lanthanum Carbonate Offers Sustained Control of Serum Phosphorus

289: Lanthanum Carbonate Offers Sustained Control of Serum Phosphorus

Mineral and bone disease pattern in elderly haemodialysis patients

Although many studies have recently addressed the mineral and bone disorder of chronic kidney disease (CKD-MBD), only limited information is available for elderly dialysis patients. We prospectively collected serum phosphorus, calcium, parathyroid hormone (PTH), 25(OH) vitamin D, albumin, C-reactive protein, protein intake and CKD-MBD treatments in 9169 maintenance haemodialysis patients in France in June 2008. We then compared biological and treatment patterns in 3403 patients aged 75 or over to their younger counterparts. Elderly patients exhibited lower serum phosphorus and parathyroid hormone concentrations (-8 and -18%, respectively) but slightly higher corrected serum calcium levels (+2%) compared to patients aged below 75 years. Elderly patients had higher mean C-reactive protein, lower serum albumin levels and reduced protein intake. Calcium and non-calcium phosphate binders as well as cinacalcet usage and dosage were significantly reduced in elderly patients, with a trend towards lower active vitamin D derivatives usage. Elderly patients were better controlled according to the Kidney Disease Outcome Quality Initiative (K/DOQI) targets compared to patients aged below 75. In this large 2008 cohort of elderly haemodialysis patients, it appears easier to control serum parameters of CKD-MBD as compared to younger dialysis patients. A better control of serum phosphorus was observed, with less phosphate binder and reduced cinacalcet dosage.

Clinical use of non-calcium phosphate binder:an advance

Controlling serum phosphorus levels is critical in patients with renal failure. Currently phosphate-binding agents are widely used to reduce phosphate absorption in patients with endstage renal disease. If possible,serum phosphorus level should be reduced without disturbing calcium homeostasis or increasing accumulation of potentially toxic elements. Aluminum hydroxide and traditional calcium -based phosphate binders are commonly used to control serum phosphorus level. Aluminum hydroxide can effectively lower serum phosphorus level,but aluminum can accumulates in the body and results in toxic effect. Traditional calcium-based phosphate binders tend to promote hypercalcemia and calcium overloading,and accelerate cardiovascular calcification. Therefore aluminum -free and calcium-free phosphate-binding agents have become the focus of study; however,agents like sevelamer hydrochloride and lanthanum carbonate are not widely used due to high price,although they are effective in controlling serum phosphorus level. New generation of phosphate binders,such as colestilan,nicotinic acid and magnesium salt,are cheaper than their previous counterparts,but their long -term effect still needs to be observed. This article summarizes the progress of non-calcium phosphate binders in treatment of end-stage renal diseases,hoping to help clinical drug usage.

Sevelamer Carbonate

To review the pharmacology, pharmacokinetics, clinical efficacy, safety data, and place in therapy of sevelamer carbonate for the treatment of hyperphosphatemia in patients with chronic kidney disease (CKD). A literature search of MEDLINE and MEDLINE In-Process & Other Non-Indexed Citations Databases (1966-August 2009) was conducted using the key words chronic kidney disease, hyperphosphatemia, and sevelamer carbonate. All published articles regarding sevelamer carbonate were included. References of selected articles, data from multiple presentations, and abstract publications were reviewed. Available English-language data from reviews, abstracts, presentations, and clinical trials of sevelamer carbonate in humans were reviewed; relevant clinical data were selected and included. Sevelamer carbonate is approved to control serum phosphorus levels and treat hyperphosphatemia in patients with CKD who are on dialysis. In clinical trials, sevelamer carbonate has been shown to lower serum phosphorus levels and calcium-phosphorus product to a similar extent as sevelamer hydrochloride. Significantly fewer patients receiving treatment with sevelamer carbonate were likely to report any gastrointestinal adverse event compared with those on sevelamer hydrochloride treatment. Further, sevelamer carbonate is associated with significant effects on decreasing low-density lipoprotein cholesterol levels and may cause less metabolic acidosis than sevelamer hydrochloride. Additionally, sevelamer hydrochloride was removed from the market in October 2009; sevelamer carbonate is now the only available formulation. Sevelamer carbonate is a treatment option for hyperphosphatemia in patients with CKD who are on dialysis. Clinical data indicate that sevelamer carbonate effectively lowers serum phosphorus levels while having minimal effect on serum calcium or serum chloride levels. The role of sevelamer carbonate in the treatment of hyperphosphatemia relative to other phosphate-binding drugs, including calcium salts and lanthanum, has not yet been established.

Emerging Roles of Cinacalcet Hydrochloride in the Management of CKD‐MBD

Derangement of mineral metabolism is one of the most popular complications in patients with chronic kidney disease (CKD), especially those on maintenance dialysis therapy. These abnormalities used to be collectively called as renal osteodystrophy (ROD), and the management was aimed at controlling parathyroid hormone (PTH) levels to maintain normal bone turnover. It has recently been widely recognized that abnormal mineral metabolism in CKD patients not only results in bone abnormalities, but also results in vascular calcification, which increases risk for cardiovascular events and death. In order to represent its nature as a systemic disease, a new term, “Chronic Kidney Disease-Mineral and Bone Disorder” (CKDMBD) has been proposed in 2006 (1). Reflecting such a paradigm shift, recently released clinical practice guidelines (2,3) clearly aimed at better survival of patients, for which appropriate control of serum phosphorus and calcium level is one of the most important therapeutic targets (4). Cinacalcet hydrochloride, a calcimimetic agent, suppresses PTH secretion through activating calcium-sensing receptor on the cell membrane of parathyroid cells. In sharp contrast to vitamin D analogues, cinacalcet suppresses PTH level without increasing serum level of phosphorus and calcium (5,6), thus might be beneficial for preventing vascular calcification and cardiac death. In this supplement issue of Therapeutic Aphresis and Dialysis, several emerging roles and critical issues of cinacalcet hydrochloride in the management of CKD-MBD are discussed based on their one-year clinical experiences of cinacalcet use in Japan. We hope that this information would be helpful for the better management of CKD-MBD in dialysis patients. Acknowledgements: This supplemental issue was based on the symposium at the 20th Annual Meeting of the Japanese Society for Kidney Bone Disease on 28 February 2009 in Tokyo.We greatfully acknowledge the educational grants provided by Kyowa-Hakko Kirin, Co. Ltd, Japan, which have made this supplement possible.

Benefits and Harms of Phosphate Binders in CKD: A Systematic Review of Randomized Controlled Trials

Phosphate binders are widely used to control serum phosphorus levels in patients with chronic kidney disease (CKD). We analyzed the effects of phosphate binders on biochemical and patient-level end points in patients with CKD. Systematic review and meta-analysis by searching MEDLINE (1966 to April 2009), EMBASE (1980 to April 2009), and the Cochrane Renal Group Specialised Register and the Cochrane Central Register of Controlled Trials (CENTRAL). Patients with CKD. Randomized controlled trials. Phosphate binders. Serum phosphorus, calcium, and parathyroid hormone levels; incidence of hypercalcemia; all-cause mortality; adverse effects. 40 trials (6,406 patients) were included. There was no significant decrease in all-cause mortality (10 randomized controlled trials; 3,079 patients; relative risk [RR], 0.73; 95% confidence interval [CI], 0.46 to 1.16), hospitalization, or end-of-treatment serum calcium-phosphorus product levels with sevelamer compared with calcium-based agents. There was a significant decrease in end-of-treatment phosphorus and parathyroid hormone levels with calcium salts compared with sevelamer and a significant decrease in risk of hypercalcemia (RR, 0.47; 95% CI, 0.36 to 0.62) with sevelamer compared with calcium-based agents. There was a significant increase in risk of gastrointestinal adverse events with sevelamer in comparison to calcium salts (RR, 1.39; 95% CI, 1.04 to 1.87). Compared with calcium-based agents, lanthanum significantly decreased end-of-treatment serum calcium and calcium-phosphorus product levels, but with similar end-of-treatment phosphorus levels. Effects of calcium acetate on biochemical end points were similar to those of calcium carbonate. Existing data are insufficient to conclude for a differential impact of any phosphate binder on cardiovascular mortality or other patient-level outcome. Few long-term studies of the efficacy of phosphate binders on mortality and musculoskeletal morbidity, significant heterogeneity for many surrogate outcomes, and suboptimal reporting of study methods to determine trial quality. Currently, there are insufficient data to establish the comparative superiority of non-calcium-binding agents over calcium-containing phosphate binders for such important patient-level outcomes as all-cause mortality and cardiovascular end points. Additional trials are still required to examine the differential effects of phosphate-binding agents on these end points and the mineral homeostasis pathway.

A randomized, crossover design study of sevelamer carbonate powder and sevelamer hydrochloride tablets in chronic kidney disease patients on haemodialysis

Background. Sevelamer carbonate is an improved, buffered form of sevelamer hydrochloride developed for the treatment of hyperphosphataemia in CKD patients. Sevelamer carbonate formulated as a powder for oral suspension presents a novel, patient-friendly alternative to tablet phosphate binders. This study compared the safety and efficacy of sevelamer carbonate powder with sevelamer hydrochloride tablets in CKD patients on haemodialysis.Methods. This was a multi-centre, open-label, randomized, crossover design study. Thirty-one haemodialysis patients were randomly assigned to either sevelamer carbonate powder or sevelamer hydrochloride tablets for 4 weeks followed by a crossover to the other regimen for an additional 4 weeks.Results. The mean serum phosphorus was 1.6 ± 0.5 mmol/L (5.0 ± 1.5 mg/dL) during sevelamer carbonate powder treatment and 1.7 ± 0.4 mmol/L (5.2 ± 1.1 mg/dL) during sevelamer hydrochloride tablet treatment. Sevelamer carbonate powder and sevelamer hydrochloride tablets are equivalent in controlling serum phosphorus; the geometric least square mean ratio was 0.95 (90% CI 0.87–1.03). No statistically significant or clinically meaningful differences were observed in calcium × phosphorus product and lipid levels between sevelamer carbonate powder and sevelamer hydrochloride tablets. Serum bicarbonate levels increased 2.7 ± 3.7 mmol/L (2.7 ± 3.7 mEq/L) during sevelamer carbonate treatment. No statistically significant change in bicarbonate was observed during sevelamer hydrochloride treatment. Sevelamer carbonate powder and sevelamer hydrochloride were well tolerated during this study.Conclusions. Sevelamer carbonate powder and sevelamer hydrochloride tablets are equivalent in controlling serum phosphorus and well tolerated in CKD patients on haemodialysis. Bicarbonate levels improved only during sevelamer carbonate treatment. Sevelamer carbonate powder should provide a welcomed new option for the treatment of hyperphosphataemia for CKD patients on dialysis.

Novel phosphate binders under development

Controlling serum phosphorus levels in patients with chronic kidney disease is crucial. Since hyperphosphatemia is an established risk factor for not only secondary hyperparathyroidism, but also cardiovascular mortality in these patients, the adequate control of serum phosphorus is necessary. The target levels of serum phosphorus, however, are not consistently being met. To achieve better control of serum phosphorus levels, some novel phosphate binders, which do not contain calcium or metal, have been developed. In this manuscript we discuss some novel phosphate binders, which are now in clinical trials.

Management of hyperphosphatemia ; phosphate-binder

Numerous experimental and clinical studies have recently addressed the underlying mechanisms in particular the marked increase in cardiovascular mortality in patients with CKD. Hyperphosphatemia is a major problem in these patients with advanced stage of CKD. Calcium carbonate became the most widely used phosphate binders ; however, increasing evidence now suggests that prolonged use of these agents increases the total body calcium load, induces adynamic bone, and potentially increases the risk of cardiovascular and soft tissue calcification. Sevelamer is the first phosphate-binding agent that is non-absorbed, calcium-free, and metal-free. To date, this agent has been shown to effectively control serum phosphorus levels in patients with CKD. It may also attenuate coronary and aortic calcification and has a number of other beneficial effects on lipid metabolism and inflammation among others.

Therapeutic use of the phosphate binder lanthanum carbonate

Hyperphosphatemia is recognized as a principal mineral disorder in chronic kidney disease (CKD) that leads to the development of secondary hyperparathyroidism. Recent data indicate that hyperphosphatemia is associated with accelerated cardiac calcification and increased mortality in patients with CKD. Control of serum phosphorus is accomplished with phosphate binder therapies that include calcium and aluminum salts. Recently, calcium-based binders have undergone reevaluation because of their association with cardiac calcification. The non-calcium, non-aluminum binder sevelamer hydrochloride has been associated with slower progression of cardiac calcification in clinical trials. Lanthanum carbonate is a newer phosphate binder with phosphate binding activity similar to aluminum salts making this agent a compelling alternative; however, more data are needed to evaluate long-term safety and effects on cardiovascular end points.

Is controlling phosphorus by decreasing dietary protein intake beneficial or harmful in persons with chronic kidney disease?

Background:Dietary restrictions to control serum phosphorus, which are routinely recommended to persons with chronic kidney disease, are usually associated with a reduction in protein intake. This may lead to protein-energy wasting and poor survival. Objective:We aimed to ascertain whether a decline in serum phosphorus and a concomitant decline in protein intake are associated with an increase in the risk of death. Design:In a 3-y study (7/2001–6/2004) of 30 075 prevalent maintenance hemodialysis (MHD) patients, we examined changes in serum phosphorus and in normalized protein nitrogen appearance (nPNA), a surrogate of dietary protein intake, during the first 6 mo and the subsequent mortality. Four groups of MHD patients were defined on the basis of the direction of the changes in serum phosphorus and nPNA. Results:Baseline phosphorus had a J-shaped association with mortality, whereas higher baseline nPNA was linearly associated with greater survival. Compared with MHD patients whose serum phosphorus and nPNA both rose over 6 mo, those whose serum phosphorus decreased but whose nPNA increased had greater survival, with a case mix–adjusted death risk ratio of 0.90 (95% confidence limits: 0.86, 0.95;P < 0.001), whereas those whose phosphorus increased but whose nPNA decreased or those whose phosphorus and nPNA both decreased had worse mortality with a risk ratio of 1.11 (1.05,1.17;P < 0.001) and 1.06 (1.01,1.12;P = 0.02), respectively. Conclusions:The risk of controlling serum phosphorus by restricting dietary protein intake may outweigh the benefit of controlled phosphorus and may lead to greater mortality. Additional studies including randomized controlled trials should examine whether nondietary control of phosphorus or restriction of nonprotein sources of phosphorus is safer and more effective.

Higher Strength Lanthanum Carbonate Provides Serum Phosphorus Control With a Low Tablet Burden and Is Preferred by Patients and Physicians

Management of hyperphosphatemia, a predictor of mortality in chronic kidney disease, is challenging. Nonadherence to dietary phosphate binders, in part, contributes to uncontrolled serum phosphorus levels. This phase IIIb trial assessed the efficacy of increased dosages (3000 to 4500 mg/d) of reformulated lanthanum carbonate (500-, 750-, and 1000-mg tablets) in nonresponders to dosages of up to 3000 mg/d. This 8-wk study with a 4-mo open-label extension enrolled 513 patients who were undergoing maintenance hemodialysis. Patients who achieved serum phosphorus control at week 4 with <or=3000 mg/d lanthanum carbonate entered cohort A; nonresponders were randomly assigned to receive 3000, 3750, or 4500 mg/d (cohort B). The primary outcome measure was the control rate for predialysis serum phosphorus levels at the end of week 8, among patients in cohort B. At the end of week 4, 54% of patients achieved serum phosphorus control at dosages <or=3000 mg/d administered as one tablet per meal. Among patients who entered cohort B, control rates of 25, 38, and 32% for patients who were randomly assigned to 3000, 3750, or 4500 mg/d lanthanum carbonate, respectively, were achieved, with no increase in adverse events. Patients and physicians reported significantly higher levels of satisfaction with reformulated lanthanum carbonate compared with previous phosphate binders, partly because of reduced tablet burden with higher dosage strengths. Physicians and patients also expressed a preference for lanthanum carbonate over previous medication. Reformulated lanthanum carbonate is an effective phosphate binder that may reduce daily tablet burden.

Effects of Sevelamer on the Progression of Vascular Calcification in Patients on Chronic Haemodialysis

Background/Aim: Vascular calcification is thought to be associated with a high cardiovascular mortality rate in patients with end-stage renal disease. Control of hyperphosphataemia is important for the treatment of the vascular calcification. The aim of the present study was to evaluate the effects of sevelamer hydrochloride on the progression of aortic calcification in haemodialysis (HD) patients. Methods: 42 HD patients were studied in this study and divided into two groups (sevelamer vs. calcium). Sevelamer was added and titrated up to achieve serum P control for 6 months. The estimations of aortic calcification index (ACI) by abdominal computed tomography scans were performed twice in each patient. We compared the changes in serum calcium, phosphorus, intact parathyroid hormone, and lipids in two groups. Results: Serum phosphorus levels decreased significantly from 6.7 ± 0.7 to 6.2 ± 0.5 mg/dl with no changes in serum intact parathyroid hormone levels in the sevelamer group (p < 0.01), and increased from 6.5 ± 1.0 to 6.7 ± 1.1 mg/dl in the calcium group (p < 0.05). Serum calcium levels did not change in the sevelamer group and calcium group. The serum levels of total cholesterol decreased significantly from 158.5 ± 20.7 to 146.2 ± 24.1 mg/dl (p = 0.024) and the low-density lipoprotein cholesterol level from 65.3 ± 14.4 to 54.7 ± 11.6 mg/dl (p = 0.014) in the sevelamer group. Serum C-reactive protein decreased significantly from 0.14 ± 0.13 to 0.08 ± 0.11 mg/dl in the sevelamer group (p = 0.038) and significantly increased (0.18 ± 0.09 vs. 0.22 ± 0.12 mg/dl) in the calcium group (p = 0.042). The mean changes in ACI (ΔACI) were 3.6 ± 1.5% in the sevelamer group and 8.2 ± 3.1% in the calcium group. Conclusions: Sevelamer allows a better serum phosphorus control compared with calcium-based phosphate binder and suppresses the progression of aortic calcification in HD patients.