***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 Secondary hyperparathyroidism ( SHPT ) is common in end-stage renal disease . Our primary objective was to evaluate the efficacy of oral paricalcitol versus oral calcitriol on serum intact parathyroid hormone ( iPTH ) and mineral bone parameters in continuous ambulatory peritoneal dialysis ( CAPD ) patients with SHPT . The secondary objective was to analyze highly sensitive C-reactive protein ( hsCRP ) and peritoneal membrane function in both groups . Methods This was a prospect i ve r and omized control trial . CAPD patients with SHPT were r and omized to paricalcitol or calcitriol for 15 weeks . Serum intact iPTH , calcium , phosphate and alkaline phosphatase ( ALP ) were measured at baseline and every 3 weeks . Serum hsCRP and peritoneal membrane functions were measured at baseline and at week 15 . Results A total of 26 patients were enrolled and r and omized—12 to paricalcitol and 14 to calcitriol . Serum iPTH reduced significantly in both groups and there was no difference in the incidence of ≥50 % reduction of iPTH between both groups . There was a significant increase in serum calcium in both groups but there were no differences in serum phosphorus across the visits . The incidence of hypercalcemia was the same in both groups . Serum calcium – phosphorus ( Ca × P ) product increased in the paricalcitol group but decreased in the calcitriol  group . Serum ALP decreased significantly in both groups . There were also no differences in pre- and post-treatment serum hsCRP and peritoneal function test ( PFT ) in both groups . Conclusion Both oral paricalcitol and calcitriol were equally efficacious in reducing serum iPTH but were associated with significantly higher serum calcium . Serum Ca × P product increased in the paricalcitol group and decreased in the calcitriol group . Serum hsCRP level and PFT were not affected by either treatment . A larger r and omized controlled trial is indicated to confirm these initial findings BACKGROUND The safety and efficacy of paricalcitol injection have been well established for the prevention and treatment of  secondary hyperparathyroidism ( SHPT ) in patients with chronic kidney disease ( CKD ) stage 5 . The capsule form of paricalcitol was developed to provide a convenient dosage form for patients with stages 3 and 4 CKD . METHODS Three r and omized , placebo-controlled , phase-3 trials were conducted in patients with stages 3 and 4 CKD with SHPT . Enrollment criteria included an estimated glomerular filtration rate between 15 and 60 mL/min/1.73 m2 ( 0.25 and 1.00 mL/s/1.73 m2 ) , an average of 2 consecutive intact parathyroid hormone ( iPTH ) levels greater than 150 pg/mL ( ng/L ) , 2 consecutive serum calcium levels between 8.0 and 10.0 mg/dL ( 2.00 and 2.50 mmol/L ) , and 2 consecutive serum phosphorus levels of 5.2 mg/dL or less ( < or = 1.68 mmol/L ) . Two studies used a thrice-weekly dosing regimen and 1 study used a once-daily dosing regimen for 24 weeks . Dosing was based on serum iPTH , calcium , and phosphorus levels . The primary efficacy end point is 2 consecutive decreases in iPTH levels greater than 30 % from baseline .  RESULTS Two hundred twenty patients participated ( n = 107 , paricalcitol ; n = 113 , placebo ) . At least 2 consecutive decreases in iPTH levels of 30 % or greater from baseline occurred in 91 % of paricalcitol versus 13 % of placebo patients ( P < 0.001 ) . Incidences of hypercalcemia , hyperphosphatemia , and elevated calcium-phosphorus product levels were not significantly different between groups . Similarly , no significant differences in urinary calcium and phosphorus excretion or deterioration in kidney function were detected in patients administered paricalcitol compared with placebo . CONCLUSION Paricalcitol capsule was well tolerated and effectively decreased iPTH levels with minimal or no impact on calcium levels , phosphorus balance , and kidney function in patients with stages 3 and 4 CKD Background / Aims : Increased parathyroid activity associated with chronic kidney disease is often managed with calcitriol , which can elevate serum calcium ( Ca ) by increasing bone resorption and intestinal absorption , whereas paricalcitol promotes less bone resorption . This study compared intestinal Ca absorption in hemodialysis patients treated with calcitriol versus paricalcitol  ( dose ratio 1:3 ) . Methods : Patients ( n = 22 ) aged ≧20 years , on maintenance hemodialysis for ≧2 months with intact parathyroid hormone ( iPTH ) levels of > 200 pg/ml were enrolled in a single-center , double-blind , active-controlled , r and omized , crossover trial . Mean fractional intestinal Ca absorption ( ±SE ) was measured by the single-tracer method ( 42Ca ) and evaluated with an analysis of variance crossover model . Results : Mean fractional intestinal Ca absorption was significantly lower after paricalcitol ( 0.135 ± 0.006 ) versus calcitriol treatment ( 0.158 ± 0.006 , p = 0.022 ) , a 0.023 difference in absolute Ca absorption fraction . Overall Ca absorption was low in the study population , indicating that regulation of Ca absorption may be dysfunctional . There were no significant differences in serum PTH , Ca , phosphorus ( P ) , or Ca × P. Conclusion : Overall , paricalcitol-treated patients absorbed ∼14 % less Ca compared with calcitriol-treated patients with similar effects on PTH . In hemodialysis patients , paricalcitol may provide a benefit by lowering the Ca available for removal by dialysis and /or for deposit in bone or soft tissues CONTEXT A high level of the phosphate-regulating hormone fibroblast growth factor 23 ( FGF-23 ) is associated with mortality in patients with end-stage renal disease , but little is known about its relationship with adverse outcomes in the much larger population of patients with earlier stages of chronic kidney disease . OBJECTIVE To evaluate FGF-23 as a risk factor for adverse outcomes in patients with chronic kidney disease . DESIGN , SETTING , AND PARTICIPANTS A prospect i ve study of 3879 participants with chronic kidney disease stages 2 through 4 who enrolled in the Chronic Renal Insufficiency Cohort between June 2003 and September 2008 . MAIN OUTCOME MEASURES All-cause mortality and end-stage renal disease . RESULTS At study enrollment , the mean ( SD ) estimated glomerular filtration rate ( GFR ) was 42.8 ( 13.5 ) mL/min/1.73 m(2 ) , and the median FGF-23 level was 145.5 RU/mL ( interquartile range [ IQR ] , 96 - 239 reference unit [RU]/mL ) . During a median follow-up of 3.5 years ( IQR , 2.5 - 4.4 years ) , 266 participants died ( 20.3/1000 person-years ) and 410 reached end-stage renal disease ( 33.0/1000 person-years ) . In adjusted analyses , higher levels of FGF-23 were independently associated with a greater risk of death ( hazard ratio [ HR ] , per SD of natural log-transformed FGF-23 , 1.5 ; 95 % confidence interval [ CI ] , 1.3 - 1.7 ) . Mortality risk increased by quartile of FGF-23 : the HR was 1.3 ( 95 % CI , 0.8 - 2.2 ) for the second quartile , 2.0 ( 95 % CI , 1.2 - 3.3 ) for the third quartile , and 3.0 ( 95 % CI , 1.8 - 5.1 ) for the fourth quartile . Elevated fibroblast growth factor 23 was independently associated with significantly higher risk of end-stage renal disease among participants with an estimated GFR between 30 and 44 mL/min/1.73 m(2 ) ( HR , 1.3 per SD of FGF-23 natural log-transformed FGF-23 ; 95 % CI , 1.04 - 1.6 ) and 45 mL/min/1.73 m(2 ) or higher ( HR , 1.7 ; 95 % CI , 1.1 - 2.4 ) , but not less than 30 mL/min/1.73 m(2 ) . CONCLUSION Elevated FGF-23 is an independent risk factor for end-stage  renal disease in patients with relatively preserved kidney function and for mortality across the spectrum of chronic kidney disease Postkidney transplant hyperparathyroidism is a significant problem . Vitamin D receptor agonists are known to suppress parathyroid hormone ( PTH ) secretion . We examined the effect of oral paricalcitol on  posttransplant secondary hyperparathyroidism by conducting an open label r and omized trial in which 100 incident kidney transplant recipients were r and omized 1:1 to receive oral paricalcitol , 2 μg per day , for the first year posttransplant or no additional therapy . Serial measurements of serum PTH , calcium and bone alkaline phosphatase , 24‐h urine calcium and bone density were performed . The primary endpoint was the frequency of hyperparathyroidism 1‐year posttransplant . Eighty‐seven patients completed the trial . One‐year posttransplant , 29 % of paricalcitol‐treated subjects had hyperparathyroidism compared with 63 % of untreated patients ( p = 0.0005 ) . Calcium supplementation was discontinued in two control and 15 treatment patients due to mild hypercalcemia or hypercalcuria . Paricalcitol was discontinued in four patients due to hypercalcuria/hypercalcemia and in one for preference . Two subjects required decreasing the dose of paricalcitol to 1 μg daily . Hypercalcemia was asymptomatic and reversible . Incidence of acute rejection , BK nephropathy and renal function at 1 year were similar between groups . Moderate renal allograft fibrosis was reduced in treated patients . Oral paricalcitol is effective in decreasing posttransplant hyperparathyroidism and may have beneficial effects on renal allograft histology Background Recent studies suggest that vitamin D deficiency represents an additional cofactor of renal anemia , with several mechanisms accounting for this relationship . In line with it , the administration of vitamin D or its analogues has been associated with an improvement of anemia . There are no data , however , about a direct effect of paricalcitol on hemoglobin ( Hb ) levels . Therefore , we conducted a study to determine whether paricalcitol , compared to calcitriol , improves anemia in patients with chronic kidney disease ( CKD ) . Methods In this r and omized trial 60 CKD patients stage 3b-5 and anemia ( Hb levels : 10 - 12.5 g/dL ) were assigned ( 1:1 ) to receive low doses of calcitriol ( Group Calcitriol ) or paricalcitol ( Group Paricalcitol ) for 6 months . All the patients had normal values of plasma calcium , phosphorus and PTH , a stable iron balance , and normal values of C-Reactive Protein . The primary endpoint was to evaluate the effects of the two treatments on Hb levels ; the modifications in 24hr-proteinuria ( UProt ) were also evaluated . Results A significant Group x Time interaction effect was observed in the longitudinal analysis of Hb levels ( F(1,172)=31.4 , p<0.001 ) . Subjects in Paricalcitol experienced a significant monthly increase of Hb levels equal to + 0.16 g/dL [ 95 % C.I. 0.10 to + 0.22 , p<0.001 ) while in Group Calcitriol , Hb decrease throughout the follow-up with an average monthly rate of -0.10 g/dL ( 95 % C.I. : -0.17 to -0.04 , p<0.001 ) . In Group Paricalcitol , UProt was significantly reduced after 6 months [ 0.35 ( 0.1 - 1.2 ) vs 0.59 ( 0.2 - 1.6 ) , p<0.01 ] , whereas no significant difference emerged in Group Calcitriol . Plasma levels of calcium , phosphate , PTH and of inflammation markers remained in the normal range in both groups throughout the study . Conclusions Short-term exposure to paricalcitol results in an independent increase in Hb levels , which occurred with no modification of iron balance , inflammatory markers , and PTH plasma concentrations , and was associated with a decrease in UProt . Trial Registration Clinical Trials.gov Vitamin D seems to protect against cardiovascular disease , but the reported effects of vitamin D on patient outcomes in CKD are controversial . We conducted a prospect i ve , double blind , r and omized , placebo-controlled trial to determine whether oral activated vitamin D reduces left ventricular ( LV ) mass in patients with stages 3 - 5 CKD with LV hypertrophy . Subjects with echocardiographic criteria of LV hypertrophy were r and om 
    Output:
    
Conclusions Current evidence is insufficient , showing paricalcitol is superior to active non-selective VDRAs in lowering PTH or reducing the burden of mineral loading .