***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Background : Ferric citrate ( FC ) is a new phosphorus binder shown to increase serum iron stores while reducing intravenous iron and erythropoiesis-stimulating agent usage . Such reductions could lower hospitalization rates and associated costs . Methods : Hospitalizations during a Phase III trial were compared between FC and active control ( AC ) .  Hospitalization costs were estimated using the 2013 US Renal Data System Annual Data Report . Results : 34.6 % of FC patients were hospitalized at least once versus 45.6 % of the AC group ( risk reduction 24.2 % ; p = 0.02 ) . There were 181 unique hospitalizations in the FC group versus 239 in the AC group , for a difference of 58 hospitalizations . Total potential savings was US$ 867,622 in hospitalization costs in the FC group . If the hospitalization reduction in our study was applied to the general end-stage renal disease population , this could translate into a savings of US$ 3002/patient/year . Conclusions : Patients receiving FC  experienced fewer hospitalizations with the potential for significant savings BACKGROUND AND OBJECTIVES Vascular calcification and endothelial dysfunction contribute to the development of cardiovascular disease in patients with chronic kidney disease ( CKD ) .  Sevelamer , a non-calcium-based phosphate binder , has been shown to attenuate cardiovascular calcification in CKD patients , although the exact mechanism has not been clarified . This study was design ed to investigate the effect of short-term sevelamer treatment on both serum fetuin-A concentrations and endothelial dysfunction seen in CKD patients . DESIGN , SETTING , PARTICIPANTS , & MEASUREMENTS Fifty nondiabetic stage 4 CKD patients whose phosphate levels were > or = 5.5 mg/dl were enrolled in this 8-wk r and omized prospect i ve study . Thirty-six healthy volunteers served as matched controls . Patients were treated with either sevelamer ( n = 25 , 12 males ) or calcium acetate ( n = 25 , 13 males ) . Fetuin-A , high-sensitivity C-reactive protein , Ca x PO4 product , flow-mediated dilation ( FMD ) , insulin , and homeostasis model assessment ( HOMA ) were obtained at baseline and after the treatment period . RESULTS As expected , CKD patients had significantly lower levels of fetuin-A and FMD , and significantly higher levels of intact parathyroid hormone , Ca x PO4 product , and high-sensitivity C-reactive protein than controls ( P < 0.001 for all ) . The use of sevelamer led to a significant increase in the fetuin-A concentration with improvement in FMD , whereas no significant difference was observed in the calcium acetate group . In a multiple regression analysis , FMD levels were independently related to fetuin-A both before ( beta = 0.63 , P < 0.001 ) and after ( beta = 0.38 , P = 0.004 ) treatment . CONCLUSIONS This small , r and omized , prospect i ve study shows that short-term sevelamer treatment significantly increases fetuin-A levels and improves FMD in nondiabetic stage 4 CKD patients Background Fetuin-A is known as a circulating inhibitor of vascular calcification . Factors associated with serum fetuin-A concentrations after long-term use of different phosphate binders in hemodialysis patients is still uncertain . Methods In the post-hoc study , we analyzed serum fetuin-A and biochemical factors ( Ca , P , i-PTH , hsCRP , TG , LDL-C ) in 50 hemodialysis patients , who completed a 48-week , open-Label , controlled r and omized parallel-group study . 23 patients received sevelamer  and 27 patients received calcium carbonate . Results After the 48-week treatment , the sevelamer group had less serum calcium increment , less iPTH decrement , more ALK-P increment , more hsCRP decrement and more LDL-C decrement . There was no significant difference in the serum fetuin-A decrement between two groups . Decreased serum fetuin-A levels were found after 48-week treatment in both groups : from 210.61 ( 104.73 ) to 153.85 ( 38.64 ) ug/dl , P = 0.003 in sevelamer group , from 203.95 ( 107.87 ) to 170.90 ( 58.02 ) ug/mL , P = 0.002 in calcium group . The decrement in serum fetuin-A ( Δfetuin-A ) levels was associated with ΔCa ( ρ = - 0.230 , P = 0.040 ) , ΔiPTH ( ρ = 0.306 , P = 0.031 ) and Δalbumin ( ρ = 0.408 , P = 0.003 ) , not associated with sevelamer use , ΔP and ΔhsCRP . Conclusion After long-term sevelamer or calcium carbonate treatment , both groups of maintenance HD patients had lower serum fetuin-A levels . Serum levels of increased calcium , decreased iPTH and decreased albumin were associated with the serum fetuin-A decrement The objective of the study was to evaluate the phosphate-binding efficacy , side effects , and cost of therapy of calcium ketoglutarate granulate as compared with calcium carbonate tablets in patients on chronic hemodialysis . The study design used was a r and omized , crossover open trial , and the main outcome measurements were plasma ionized calcium levels , plasma phosphate levels , plasma intact parathyroid hormone ( PTH ) levels , requirements for supplemental aluminum-aminoacetate therapy , patient tolerance , and cost of therapy .  Nineteen patients on chronic hemodialysis were treated with a dialysate calcium concentration of 1.25 mmol/L and a fixed alfacalcidol dose for at least 2 months . All had previously tolerated therapy with calcium carbonate .  Of the 19 patients included , 10 completed both treatment arms . After 12 weeks of therapy , the mean ( + /-SEM ) plasma ionized calcium level was significantly lower in the ketoglutarate arm compared with the calcium carbonate arm ( 4.8+/-0.1 mg/dL v 5.2+/-0.1 mg/dL ; P = 0.004 ) , whereas the mean plasma phosphate ( 4.5+/-0.3 mg/dL v 5.1+/-0.1 mg/dL ) and PTH levels ( 266+/-125 pg/mL v 301+/-148 pg/mL ) did not differ significantly between the two treatment arms . Supplemental aluminum-aminoacetate was not required during calcium ketoglutarate treatment , while two patients needed this supplement when treated with calcium carbonate . Five of 17 ( 29 % ) patients were withdrawn from calcium ketoglutarate therapy within 1 to 2 weeks due to intolerance ( anorexia , vomiting , diarrhea , general uneasiness ) , whereas the remaining 12 patients did not experience any side effects at all . The five patients with calcium ketoglutarate intolerance all had pre-existing gastrointestinal symptoms ;  four of them had received treatment with cimetidine or omeprazol before inclusion into the study . Calculations based on median doses after 12 weeks showed that the cost of the therapy in Denmark was 10 times higher for calcium ketoglutarate compared with calcium carbonate ( US$ 6.00/d v US$ 0.65/d ) . Calcium ketoglutarate may be an effective and safe alternative to treatment with aluminum-containing phosphate binders in patients on hemodialysis who are intolerant of calcium carbonate or acetate because of hypercalcemia . However , care must be exercised when dealing with patients with pre-existing gastrointestinal discomfort . Due to the high cost of the therapy , calcium ketoglutarate should be used only for selected patients 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 , r and omized , crossover design study . Thirty-one haemodialysis patients were r and omly 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 clinical ly 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 Background / Aims : Colestilan is a new non-calcium-based phosphate binder licensed in Europe for the treatment of hyperphosphatemia in chronic kidney disease patients on dialysis ( CKD 5D ) . This study was conducted to evaluate efficacy in a North American patient population and also to examine secondary actions of colestilan on lipid profile and glycated hemoglobin ( HbA1c ) . Methods : This was a multicenter , r and omized , double-blind , placebo-controlled withdrawal study , after an initial open-label titration period . Patients ( n = 245 ) with stable phosphate control received 6 - 15 g/day  colestilan during a 12-week , flexible titration period after which 169 were r and omized to continue the same dose ( n = 85 ) or switch to placebo ( n = 84 ) for 4 weeks . The primary endpoint was the change in serum phosphorus level during the placebo-controlled withdrawal period . Results : A significant difference of -1.01 mg/dl ( -0.33 mmol/l ) in mean change in serum phosphorus , favoring colestilan , was seen during the placebo-controlled withdrawal period ( p < 0.001 ) . Colestilan  reduced serum phosphorus significantly from baseline to week 12 ( -1.54 mg/dl ( -0.50 mmol/l ) ; p < 0.001 ) . Serum calcium levels were not affected . Colestilan significantly reduced and maintained reductions in calcium × phosphorus ion product ( Ca × P ) , parathyroid hormone , total cholesterol , low-density lipoprotein cholesterol , uric acid and also HbA1c in patients with elevated baseline HbA1c . Colestilan was generally well tolerated ; most adverse events were gastrointestinal . Conclusion : In this first clinical trial with colestilan in a North American patient population  , colestilan demonstrated significant efficacy in controlling serum phosphorus levels in CKD 5D patients with hyperphosphatemia , without increasing calcium levels BACKGROUND Colestilan is a non-absorbed , non-calcium-based , phosphate binder . It also binds bile acids and reduces serum levels of low-density lipoprotein cholesterol ( LDL-C ) . This study evaluated the efficacy of a range of fixed doses of colestilan compared with placebo for the control of serum phosphorus and LDL-C levels in patients with CKD stage 5 on dialysis . METHODS This was a multicentre , r and omized , double-blind , placebo-controlled , multiple fixed-dose trial in which 642 patients with CKD stage 5 on dialysis who had both hyperphosphataemia and dyslipidaemia , were r and omized to treatment with colestilan 3 , 6 , 9 , 12 or 15 g/day or placebo for 12 weeks . The co- primary endpoints were the mean changes in serum phosphorus and the mean per cent change in LDL-C from baseline to Week 12 . RESULTS A significantly greater mean reduction in serum phosphorus level from baseline to Week 12 than seen with placebo was seen with 
    Output:
    
In CKD G5D sevelamer may lead to lower death ( all causes ) ( RR 0.53 , CI 0.30 to 0.91 , low certainty ) and induce less hypercalcaemia ( RR 0.30 , CI 0.20 to 0.43 , low certainty ) when compared with calcium-based binders , and has uncertain or inestimable effects on cardiovascular death , myocardial infa rct ion , stroke , fracture , or coronary artery calcification .
It is uncertain whether the effects of binders on clinical ly-relevant outcomes were different for patients who were and were not treated with dialysis in subgroup analyses .
In studies of adults with CKD G5D treated with dialysis , sevelamer may lower death ( all causes ) compared to calcium-based binders and incur less treatment-related hypercalcaemia , while we found no clinical ly important benefits of any phosphate binder on cardiovascular death , myocardial infa rct ion , stroke , fracture or coronary artery calcification .
In patients with CKD G2 to G5 , the effects of sevelamer , lanthanum , and iron-based phosphate binders on cardiovascular , vascular calcification , and bone outcomes compared to placebo or usual care , are also uncertain and they may incur constipation , while iron-based binders may lead to diarrhoea