***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 
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    Input: Background Progression of coronary artery calcification ( CAC ) has been described in hemodialysis patients , and severe CAC has been associated with the occurrence of cardiovascular events in this population . Little information is available regarding  peritoneal patients . Aim To prospect ively evaluate  peritoneal dialysis patients in order to identify the variables associated with the rate of CAC progression , as well as to determine the impact that baseline CAC has on clinical outcomes over a 1-year follow-up period . Methods Using multislice coronary tomography , calcium scores were estimated at baseline and after 12 months in 49 peritoneal dialysis patients . Patients with and without CAC progression were compared with respect to clinical characteristics and biochemical variables , including lipid profile , parameters of mineral metabolism , and markers of inflammation . Cardiovascular events , hospitalizations , and all-cause mortality were recorded . Results At baseline , 29 patients ( 59 % ) presented CAC and a median calcium score of 234.7 ( range 10.3 – 2351 ) Agatston units . Progression of CAC was observed in 13 patients ( 43 % ) who , in comparison with those presenting no CAC progression , were older , presented higher baseline calcium scores , and had higher mean glucose levels , lower mean high density lipoprotein cholesterol levels , and more months using low calcium peritoneal solution . We also observed a trend toward more often presenting with a history of hypertension , exhibiting more hyperphosphatemic and hyperglycemic events , and having lower albumin levels . In multiple logistic regression , only baseline calcium score was independently associated with progression of CAC . A shorter cardiovascular event-free time and a trend toward lower survival rates were observed in the group with CAC . Hospitalization event-free time did not differ between the groups . Conclusion Determining CAC provides important prognostic data in  peritoneal dialysis patients .  Baseline calcium score and disturbances in glucose , mineral , and lipid metabolism were indicative of higher risk of CAC progression in this population BACKGROUND AND OBJECTIVES Vascular calcification is increasingly recognized as an important component of cardiovascular disease in chronic kidney disease . The objective of this study was to investigate prospect ively the determinants , cardiovascular functional consequences , and survival associated with vascular calcification over 24 mo . DESIGN , SETTING , PARTICIPANTS , & MEASUREMENTS A total of 134 patients ( 60 on hemodialysis , 28 on peritoneal dialysis , and 46 with stage 4 chronic kidney disease ) were studied . Vascular calcification of the superficial femoral artery was assessed using multislice spiral computed tomography ; pulse wave velocity ; all medications and time-averaged biochemical parameters were recorded at baseline and 12 and 24 mo . RESULTS A total of 101 patients remained at 24 mo . Progressive calcification was seen in 58 of 101 patients . Most ( 31 of 46 ) patients with an initial calcification score of zero did not develop calcification . The hemodialysis group demonstrated a greater degree of progression than patients who were on peritoneal dialysis or had stage 4 chronic kidney disease . Progressive calcification was associated with age , male gender , serum alkaline phosphatase , beta blockers , and lipid-lowering agents . Increases in vascular calcification correlated with increased arterial stiffness . Vascular calcification was present in 20 of 21 patients who died . Cox proportional hazard analysis identified change in calcification score , calcium intake from phosphate binders , and low albumin as risk factors for death . CONCLUSIONS Patients with stages 4 and 5 chronic kidney disease and preexisting vascular calcification exhibit significantly increased calcification over 24 mo . Rapid progression of calcification is associated with arterial stiffness and mortality 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 aim ed 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 r and omized controlled trials should examine whether nondietary control of phosphorus or restriction of nonprotein sources of phosphorus is safer and more effective BACKGROUND Hypocalcemia and hyperphosphatemia with secondary hyper-parathyroidism are characteristic of end-stage renal disease ( ESRD ) . Although calcium levels critically affect almost all cellular processes , the impact of chronic hypocalcemia and other abnormalities of calcium-phosphate homeostasis on the prognosis of ESRD patients is unknown . METHODS An inception cohort of 433 patients starting ESRD therapy  was followed prospect ively for an average of 41 months .  Serum calcium and other parameters were measured monthly . The mean calcium levels were 9.4 + /- 0.7 mg/dl . 23 % of the patients had mean calcium levels < 8.8 mg/dl . After adjusting for baseline age , diabetes mellitus , ischemic heart disease , smoking and cholesterol levels , as well as serial albumin , hemoglobin , mean arterial blood pressure , phosphate and alkaline phosphatase levels , chronic hypocalcemia was strongly associated with mortality ( RR 2.10 , p = 0.006 for a mean calcium level < 8.8 mg/dl ) . The association with mortality was similar in hemodialysis ( RR 2.10 , p = 0.006 ) and peritoneal dialysis patients ( 2.67 , p = 0.034 ) . Using similar covariate adjustment , chronic hypocalcemia was associated with de novo ischemic heart disease ( RR 5.23 , p < 0.001 ) , recurrent ischemic heart disease ( RR 2.46 , p = 0.006 ) , de novo cardiac failure ( RR 2.64 , p < 0.001 ) , and recurrent cardiac failure ( RR 3.30 , p < 0.001 ) . Hypocalcemia retained its independent impact on morbidity and mortality when analyzed as a time-dependent covariate . CONCLUSIONS Chronic hypocalcemia , a very common , reversible feature of chronic uremia , is independently associated with morbidity and mortality in ESRD patients BACKGROUND Obesity is associated with secondary hyperparathyroidism in the general population . It is unknown whether body mass index ( BMI ) affects parathyroid hormone ( PTH ) level and its association with mortality in dialysis patients . METHODS From a prospect i ve cohort study of incident dialysis patients in the Netherl and s ( NECOSAD ) , we selected all patients with recorded BMI and PTH at 3 months ( baseline ) after the start of dialysis [ n = 1628 , age 59 ± 15 years , BMI 24.7 ± 4.1 kg/m(2 ) , median PTH 13.0 ( interquartile range 5.3 - 29.0 ) pmol/L ] . We assessed associations between BMI and PTH at baseline and between their changes over 3 months by correlation and linear regression analyses . The effect of the changes in PTH on all-cause mortality during a subsequent mean follow-up of 3.2 ± 2 years was assessed by Cox regression analyses . RESULTS Median PTH levels at baseline were lowest in underweight patients ( 10.2 pmol/L ) , followed by normal weight ( 12.1 pmol/L ) , overweight ( 14.0 pmol/L ) and obese patients ( 17.5 pmol/L ) . The associations were similar in diabetic and non-diabetic patients . A ≥ 5 % decrease in BMI ( n = 101 ) over 3 months was accompanied by a 26 % decrease in PTH ( PTH(ratio ) 0.74 ; P = 0.039 ) , whereas a ≥ 5 % increase in BMI ( n = 143 ) was associated with an 11 % increase in PTH ( PTH(ratio ) 1.11 ; P = 0.026 ) . Compared to patients with stable PTH levels , patients with decreasing PTH in the presence of weight loss showed a 2-fold higher mortality ( hazard ratio 2.02 , 95 % confidence interval 1.45 - 2.83 ; P < 0.001 ) , in contrast to those with decreasing PTH in the absence of weight loss . Additional analyses showed that the weight loss was responsible for increased deaths . CONCLUSIONS PTH is associated with BMI and its longitudinal changes in dialysis patients , both in patients with and without diabetes mellitus . An increased mortality seen for patients with concurrent decreases in PTH and BMI was explained by the weight loss , representing an important confounder for outcome analyses according to levels of PTH . Low and decreasing PTH levels may be symptoms of wasting , which should be taken into account in the care of dialysis patients BACKGROUND Abnormalities in bone mineral metabolism parameters are common in patients with end-stage kidney disease on dialysis therapy .  The National Kidney Foundation 's Kidney Disease Outcomes Quality Initiative ( KDOQI ) guidelines propose targets for calcium , phosphate , and intact parathyroid hormone ( iPTH ) levels in patients undergoing dialysis .  However , whether achievement of these targets improves survival is unknown . STUDY DESIGN Retrospective cohort study . SETTING & PARTICIPANTS Incident patients on hemodialysis or peritoneal dialysis therapy in the United Kingdom from 2000 - 2004 who survived at least 12 months . PREDICTOR Achievement of KDOQI calcium , phosphate , and iPTH guideline targets during the first year of dialysis therapy . OUTCOMES All-cause mortality in the subsequent 2 years . MEASUREMENTS Calcium , phosphate , and iPTH at quarterly intervals , demographic and comorbid condition data at baseline . RESULTS We included 7,076 incident patients ( 4,947 hemodialysis , 2,129 peritoneal dialysis ) in our analysis . Approximately two thirds of patients were men and 21 % had diabetes as the cause of kidney failure . Guideline target achievement for each quarter varied from 23%-26 % for iPTH level , 43%-47 % for calcium level , and 54%-62 % for phosphate level targets . In adjusted Cox proportional hazards models , patients who achieved guideline targets in all 4 quarters did not have a survival advantage over patients who never achieved target ( P > 0.1 for calcium , phosphate , and iPTH ) . LIMITATIONS Missing information about medication use , vitamin D and alkaline phosphatase levels , and dialysate calcium content . CONCLUSIONS Our findings do not support the use of KDOQI bone mineral guideline achievement as a quality measure for dialysis care . Prospect i ve studies with longer term follow-up are needed to define the optimal cutoff values for calcium , phosphate , and iPTH and assess the effect of guideline implementation on patient survival Hyperphosphatemia is highly prevalent among patients with end-stage renal disease ( ESRD ) and is associated with increased mortality risk in hemodialysis ( HD ) patients . The mechanism through which this mortality risk is mediated is unclear . Data from two national r and om sample s of HD patients ( n = 12,833 ) was used to test the hypothesis that elevated serum PO(4 ) contributes mainly to cardiac causes of death . During a 2-yr follow-up , the cause-specific relative risk ( RR ) of death for patients was analyzed separately for several categories of cause of death , including coronary artery disease ( CAD ) , sudden death , and other cardiac causes , cerebrovascular and infection . Cox regression models were fit for each of the eight cause of death categories , adjusting for patient demographics and non-cardiovascular comorbid conditions . Time at risk for each cause-specific model was censored at death that result ed from any 
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Findings were less consistent for lower-than-referent values .