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1.
Association between calcium-phosphorus balance and adolescent idiopathic scoliosis: A meta-analysis.
Zhu, Q, Chen, J, Chen, C, Wang, H, Yang, S
Acta orthopaedica et traumatologica turcica. 2019;(6):468-473
Abstract
STUDY DESIGN A systematic review and meta-analysis. OBJECTIVE The objective of this meta-analysis was to evaluate the association between calcium-phosphorus balance and adolescent idiopathic scoliosis (AIS). METHODS Databases, including PubMed, OVID database, Web of Science, CBM database and CNKI database were searched for the relevant case control studies and cross-sectional studies. Two authors selected studies and extracted data independently. Data analysis was performed by Review Manager Software 5.0. Subgroup analysis was performed on the serum level of vitamin D according to gender and menstruation. RESULTS Five studies were included, with a total of 646 cases of AIS and 791 controls. AIS group had a lower serum level of vitamin D compared to control group [MD = -6.74, 95% CI (-9.47, -4.00)]. Gender and menstruation condition were thought to have no effect on the primary outcome of vitamin D level by subgroup analysis [MD = -5.97, 95% CI (7.61, -4.34)]. The AIS group had a lower calcium level [SMD= -0.77, 95% CI (-1.51, -0.02)] and calcitonin level compared to control group. There was no statistical difference in phosphorus level [SMD=0.5, 95% CI (-0.46, 0.57)] and parathyroid hormone level [SMD = -0.11, 95% CI (-0.54, -0.31)]. Meanwhile, the observational indexes, including serum levels of calcium, phosphorus, parathyroid hormone and calcitonin were within normal limits. CONCLUSION Vitamin D deficiency may be involved in the pathogenesis of AIS by influencing the regulation of calcium-phosphors metabolism on human bone. Therefore, we suggest to screen vitamin D level in AIS patients. LEVEL OF EVIDENCE Level III, Therapeutic Study.
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Phosphate binders for preventing and treating chronic kidney disease-mineral and bone disorder (CKD-MBD).
Ruospo, M, Palmer, SC, Natale, P, Craig, JC, Vecchio, M, Elder, GJ, Strippoli, GF
The Cochrane database of systematic reviews. 2018;(8):CD006023
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Abstract
BACKGROUND Phosphate binders are used to reduce positive phosphate balance and to lower serum phosphate levels for people with chronic kidney disease (CKD) with the aim to prevent progression of chronic kidney disease-mineral and bone disorder (CKD-MBD). This is an update of a review first published in 2011. OBJECTIVES The aim of this review was to assess the benefits and harms of phosphate binders for people with CKD with particular reference to relevant biochemical end-points, musculoskeletal and cardiovascular morbidity, hospitalisation, and death. SEARCH METHODS We searched the Cochrane Kidney and Transplant Register of Studies up to 12 July 2018 through contact with the Information Specialist using search terms relevant to this review. Studies in the Register are identified through searches of CENTRAL, MEDLINE, and EMBASE, conference proceedings, the International Clinical Trials Register (ICTRP) Search Portal and ClinicalTrials.gov. SELECTION CRITERIA We included randomised controlled trials (RCTs) or quasi-RCTs of adults with CKD of any GFR category comparing a phosphate binder to another phosphate binder, placebo or usual care to lower serum phosphate. Outcomes included all-cause and cardiovascular death, myocardial infarction, stroke, adverse events, vascular calcification and bone fracture, and surrogates for such outcomes including serum phosphate, parathyroid hormone (PTH), and FGF23. DATA COLLECTION AND ANALYSIS Two authors independently selected studies for inclusion and extracted study data. We applied the Cochrane 'Risk of Bias' tool and used the GRADE process to assess evidence certainty. We estimated treatment effects using random-effects meta-analysis. Results were expressed as risk ratios (RR) for dichotomous outcomes together with 95% confidence intervals (CI) or mean differences (MD) or standardised MD (SMD) for continuous outcomes. MAIN RESULTS We included 104 studies involving 13,744 adults. Sixty-nine new studies were added to this 2018 update.Most placebo or usual care controlled studies were among participants with CKD G2 to G5 not requiring dialysis (15/25 studies involving 1467 participants) while most head to head studies involved participants with CKD G5D treated with dialysis (74/81 studies involving 10,364 participants). Overall, seven studies compared sevelamer with placebo or usual care (667 participants), seven compared lanthanum to placebo or usual care (515 participants), three compared iron to placebo or usual care (422 participants), and four compared calcium to placebo or usual care (278 participants). Thirty studies compared sevelamer to calcium (5424 participants), and fourteen studies compared lanthanum to calcium (1690 participants). No study compared iron-based binders to calcium. The remaining studies evaluated comparisons between sevelamer (hydrochloride or carbonate), sevelamer plus calcium, lanthanum, iron (ferric citrate, sucroferric oxyhydroxide, stabilised polynuclear iron(III)-oxyhydroxide), calcium (acetate, ketoglutarate, carbonate), bixalomer, colestilan, magnesium (carbonate), magnesium plus calcium, aluminium hydroxide, sucralfate, the inhibitor of phosphate absorption nicotinamide, placebo, or usual care without binder. In 82 studies, treatment was evaluated among adults with CKD G5D treated with haemodialysis or peritoneal dialysis, while in 22 studies, treatment was evaluated among participants with CKD G2 to G5. The duration of study follow-up ranged from 8 weeks to 36 months (median 3.7 months). The sample size ranged from 8 to 2103 participants (median 69). The mean age ranged between 42.6 and 68.9 years.Random sequence generation and allocation concealment were low risk in 25 and 15 studies, respectively. Twenty-seven studies reported low risk methods for blinding of participants, investigators, and outcome assessors. Thirty-one studies were at low risk of attrition bias and 69 studies were at low risk of selective reporting bias.In CKD G2 to G5, compared with placebo or usual care, sevelamer, lanthanum, iron and calcium-based phosphate binders had uncertain or inestimable effects on death (all causes), cardiovascular death, myocardial infarction, stroke, fracture, or coronary artery calcification. Sevelamer may lead to constipation (RR 6.92, CI 2.24 to 21.4; low certainty) and lanthanum (RR 2.98, CI 1.21 to 7.30, moderate certainty) and iron-based binders (RR 2.66, CI 1.15 to 6.12, moderate certainty) probably increased constipation compared with placebo or usual care. Lanthanum may result in vomiting (RR 3.72, CI 1.36 to 10.18, low certainty). Iron-based binders probably result in diarrhoea (RR 2.81, CI 1.18 to 6.68, high certainty), while the risks of other adverse events for all binders were uncertain.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 infarction, stroke, fracture, or coronary artery calcification. The finding of lower death with sevelamer compared with calcium was present when the analysis was restricted to studies at low risk of bias (RR 0.50, CI 0.32 to 0.77). In absolute terms, sevelamer may lower risk of death (all causes) from 210 per 1000 to 105 per 1000 over a follow-up of up to 36 months, compared to calcium-based binders. Compared with calcium-based binders, lanthanum had uncertain effects with respect to all-cause or cardiovascular death, myocardial infarction, stroke, fracture, or coronary artery calcification and probably had reduced risks of treatment-related hypercalcaemia (RR 0.16, CI 0.06 to 0.43, low certainty). There were no head-to-head studies of iron-based binders compared with calcium. The paucity of placebo-controlled studies in CKD G5D has led to uncertainty about the effects of phosphate binders on patient-important outcomes compared with placebo.It is uncertain whether the effects of binders on clinically-relevant outcomes were different for patients who were and were not treated with dialysis in subgroup analyses. AUTHORS' CONCLUSIONS 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 clinically important benefits of any phosphate binder on cardiovascular death, myocardial infarction, stroke, fracture or coronary artery calcification. The effects of binders on patient-important outcomes compared to placebo are uncertain. 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.
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Calcium and Phosphate Metabolism, Blood Lipids and Intestinal Sterols in Human Intervention Studies Using Different Sources of Phosphate as Supplements-Pooled Results and Literature Search.
Trautvetter, U, Ditscheid, B, Jahreis, G, Glei, M
Nutrients. 2018;(7)
Abstract
Phosphates are associated with negative physiological effects. The objectives of this publication were to compare differential effects of supplementation with calcium phosphate or phosphate alone in healthy humans. Four adult human studies were conducted with pentacalcium hydroxy-trisphosphate supplementation (CaP; 90 subjects) and their data were pooled for assessment. For literature search; PubMed and ISI Web of Knowledge were used and 21 items were assigned to three main topics. The pooled study results show that following CaP supplementation, faecal calcium and phosphorus and urinary calcium were increased, blood lipids were positively modulated, and faecal bile acids were increased, as compared with placebo. The literature search reveals that following calcium phosphate supplementation, urinary calcium was increased. Following solely phosphate supplementation, urinary phosphorus was increased and urinary calcium was decreased. Postprandial calcium concentrations were increased following calcium phosphate supplementation. Postprandial phosphate concentrations were increased following solely phosphate supplementation. Calcium phosphate supplementation resulted in rather positively modulated blood lipids and gut-related parameters. The presented results show the relevance to distinguish between calcium phosphate and solely phosphate supplementations, and the importance of a balanced calcium and phosphorus intake.
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Nutrient-limited conditions determine the responses of foliar nitrogen and phosphorus stoichiometry to nitrogen addition: A global meta-analysis.
You, C, Wu, F, Yang, W, Xu, Z, Tan, B, Yue, K, Ni, X
Environmental pollution (Barking, Essex : 1987). 2018;:740-749
Abstract
To test the hypothesis that nutrient-limited conditions can determine the responses of nitrogen (N) and phosphorus (P) stoichiometry to N addition, a meta-analysis was conducted to identify the different responses of foliar N and P concentrations and N-to-P ratios to N addition under N limitation, N and P co-limitation and P limitation. N addition increased the foliar N-to-P ratios and N concentrations by 46.2% and 30.2%, respectively, under N limitation, by 18.7% and 19.7% under N and P co-limitation, and by 4.7% and 12.9% under P limitation. However, different responses of foliar P concentrations to N addition were observed under different nutrient limitations, and negative, positive, and neutral effects on P concentrations were observed under N limitation, P limitation and N and P co-limitation, respectively. Generally, the effects of N addition on N-to-P ratios and N concentrations in herbaceous plants were dramatically larger than those in woody plants (with the exception of the N-to-P ratio under N limitation), but the opposite situation was true for P concentrations. The changes in N-to-P ratios were closely correlated with the changes in N and P concentrations, indicating that the changes in both N and P concentrations due to N addition can drive N and P stoichiometry, but the relative sizes of the contributions of N and P varied greatly with different nutrient limitations. Specifically, the changes in N-to-P ratios may indicate a minimum threshold, which is consistent with the homeostatic mechanism. In brief, increasing N deposition may aggravate P limitation under N-limited conditions but improve P limitation under P-limited conditions. The findings highlight the importance of nutrient-limited conditions in the stoichiometric response to N addition, thereby advancing our ability to predict global plant growth with increasing N deposition in the future.
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Phosphorus and mortality risk in end-stage renal disease: A meta-analysis.
Hou, Y, Li, X, Sun, L, Qu, Z, Jiang, L, Du, Y
Clinica chimica acta; international journal of clinical chemistry. 2017;:108-113
Abstract
BACKGROUND Studies on the association of abnormal serum phosphorus level with all-cause mortality in patients with end-stage renal disease (ESRD) have yielded inconsistent results. OBJECTIVE To evaluate the association of abnormal serum phosphorus level with all-cause mortality in patients with ESRD requiring dialysis by conducting a meta-analysis. METHODS Pubmed and Embase databases were searched through March 2017 to identify all observational studies that assessed the association between abnormal serum phosphorus level and all-cause mortality risk in patients with ESRD requiring dialysis. Pooled hazard risk (HR) with 95% confidence interval (CI) was calculated for the highest versus referent phosphorus category and lower versus referent phosphorus category, separately. RESULTS Nine cohort studies were eligible for analysis. During 12 to 97.6months follow-up duration, 24,463 death events occurred among 1,992,869 ESRD patients. Meta-analysis showed that the pooled HR of all-cause mortality was 1.16 (95% CI 1.06-1.28) for the lower versus referent serum phosphorus category. Similarly, patients with highest serum phosphorus levels were associated with an increased risk of all-cause mortality (HR 1.39; 95% CI 1.31-1.47) compared with those in the referent phosphorus category. Subgroup analyses revealed that the effect of phosphorus on the all-cause mortality risk appeared to be stronger within 2years follow-up. CONCLUSIONS Both very high and very low values of phosphorus are independently associated with an increased risk for all-cause mortality in ESRD patients requiring dialysis. This meta-analysis highlighted a non-linear association of serum phosphorus with all-cause mortality among dialysis-dependent ESRD patients.
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QTL meta-analysis of root traits in Brassica napus under contrasting phosphorus supply in two growth systems.
Zhang, Y, Thomas, CL, Xiang, J, Long, Y, Wang, X, Zou, J, Luo, Z, Ding, G, Cai, H, Graham, NS, et al
Scientific reports. 2016;:33113
Abstract
A high-density SNP-based genetic linkage map was constructed and integrated with a previous map in the Tapidor x Ningyou7 (TNDH) Brassica napus population, giving a new map with a total of 2041 molecular markers and an average marker density which increased from 0.39 to 0.97 (0.82 SNP bin) per cM. Root and shoot traits were screened under low and 'normal' phosphate (Pi) supply using a 'pouch and wick' system, and had been screened previously in an agar based system. The P-efficient parent Ningyou7 had a shorter primary root length (PRL), greater lateral root density (LRD) and a greater shoot biomass than the P-inefficient parent Tapidor under both treatments and growth systems. Quantitative trait loci (QTL) analysis identified a total of 131 QTL, and QTL meta-analysis found four integrated QTL across the growth systems. Integration reduced the confidence interval by ~41%. QTL for root and shoot biomass were co-located on chromosome A3 and for lateral root emergence were co-located on chromosomes A4/C4 and C8/C9. There was a major QTL for LRD on chromosome C9 explaining ~18% of the phenotypic variation. QTL underlying an increased LRD may be a useful breeding target for P uptake efficiency in Brassica.
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Serum phosphorus, cardiovascular and all-cause mortality in the general population: A meta-analysis.
Bai, W, Li, J, Liu, J
Clinica chimica acta; international journal of clinical chemistry. 2016;:76-82
Abstract
BACKGROUND The association between elevated serum phosphorus concentration and cardiovascular or all-cause mortality yielded conflicting results. OBJECTIVE To assess the association between elevated serum phosphorus concentration and cardiovascular or all-cause mortality in the general population by conducting a meta-analysis. METHODS We systematically searched the Pubmed and Embase databases until March 2016 for the prospective studies investigating serum phosphorus concentration and cardiovascular or all-cause mortality in the general population. We pooled risk ratio (RR) and corresponding 95% confidence intervals (CI) for the highest versus the reference category of serum concentration of phosphorus. RESULTS Six prospective cohort studies involving 120,269 subjects were identified. When compared the highest with the reference concentration of serum phosphorus, the pooled RR of cardiovascular mortality and all-cause mortality were 1.36 (95% CI 1.07-1.72) and 1.35 for all-cause mortality (95% CI 1.15-1.58), respectively. Stratified analyses revealed that elevated serum phosphorus significantly increased all-cause mortality risk among men (RR 1.33; 95% CI 1.11-1.60), but not in women (RR 1.09; 95% CI 0.89-1.33). CONCLUSIONS Elevated serum phosphorus concentration is independently associated with excessive risk of cardiovascular and all-cause mortality in the general population without chronic kidney disease. Serum phosphorus on all-cause mortality risk appears to be pronounced in men but exhibits no clear effect on women. However, gender difference of elevated serum phosphorus on mortality risk should be verified by more prospective studies.
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Effect of colestilan on serum phosphorus in dialysis patients: A meta-analysis of the literature.
Zhang, Q, Li, M, Chen, J
Nephrology (Carlton, Vic.). 2016;(3):229-35
Abstract
AIM: To evaluate the efficacy and safety of colestilan as a phosphorus binder in dialysis patients, we performed a meta-analysis of randomized controlled trials. METHODS We retrieved studies that compared colestilan with placebo in the treatment of dialysis patients from Medline, EMBASE, the Cochrane Library and conference proceedings. RESULTS Four studies were included. The treatment durations ranged from 2 to 12 weeks, median 7.5 weeks. Compared with placebo group, colestilan significantly decreased serum phosphorus (WMD, -0.22 mmol/L; 95% CI, -0.33 to -0.12, P < 0.0001), calcium phosphorus product (WMD, -0.70 mmol(2) /L(2) ; 95% CI, -1.06 to -0.35, P = 0.0001), intact PTH (WMD, -5.37 pmol/L; 95% CI, -8.38 to -2.36, P = 0.0005) and LDL cholesterol (WMD, -0.78 mmol/L; 95% CI, -0.85 to -0.71, P < 0.00001). There was no significant difference in serum calcium between the two groups. Colestilan therapy increased gastrointestinal complaints significantly (OR = 4.07, 95% CI: 3.06-6.53, P < 0.00001). Sensitivity analysis was performed by excluding studies with Jadad score of three or 3 g/day colestilan, the results did not change. CONCLUSIONS Short-term administration of colestilan is effective for the treatment of hyperphosphataemia in dialysis patients. Long-term effectiveness and safety needs to be evaluated.
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Association of Drug Effects on Serum Parathyroid Hormone, Phosphorus, and Calcium Levels With Mortality in CKD: A Meta-analysis.
Palmer, SC, Teixeira-Pinto, A, Saglimbene, V, Craig, JC, Macaskill, P, Tonelli, M, de Berardis, G, Ruospo, M, Strippoli, GF
American journal of kidney diseases : the official journal of the National Kidney Foundation. 2015;(6):962-71
Abstract
BACKGROUND Serum parathyroid hormone (PTH), phosphorus, and calcium levels are surrogate outcomes that are central to the evaluation of drug treatments in chronic kidney disease (CKD). This systematic review evaluates the evidence for the correlation between drug effects on biochemical (PTH, phosphorus, and calcium) and all-cause and cardiovascular mortality end points in adults with CKD. STUDY DESIGN Systematic review and meta-analysis. SETTING & POPULATION Adults with CKD. SELECTION CRITERIA FOR STUDIES Randomized trials reporting drug effects on biochemical and mortality end points. INTERVENTION Drug interventions with effects on serum PTH, phosphorus, and calcium levels, including vitamin D compounds, phosphate binders, cinacalcet, bisphosphonates, and calcitonin. OUTCOMES Correlation between drug effects on biochemical and all-cause and cardiovascular mortality. RESULTS 28 studies (6,999 participants) reported both biochemical and mortality outcomes and were eligible for analysis. Associations between drug effects on surrogate biochemical end points and corresponding effects on mortality were weak and imprecise. All correlation coefficients were less than 0.70, and 95% credible intervals were generally wide and overlapped with zero, consistent with the possibility of no association. The exception was an inverse correlation between drug effects on serum PTH levels and all-cause mortality, which was nominally significant (-0.64; 95% credible interval, -0.85 to -0.15), but the strength of this association was very imprecise. Risk of bias within available trials was generally high, further reducing confidence in the summary correlations. Findings were robust to adjustment for age, baseline serum PTH level, allocation concealment, CKD stage, and drug class. LIMITATIONS Low power in analyses and combining evidence from many different drug comparisons with incomplete data across studies. CONCLUSIONS Drug effects on serum PTH, phosphorus, and calcium levels are weakly and imprecisely correlated with all-cause and cardiovascular death in the setting of CKD. Risks of mortality (patient-level outcome) cannot be inferred from treatment-induced changes in biochemical outcomes in people with CKD. Similarly, existing data do not exclude a mortality benefit with treatment. Trials need to address patient-centered outcomes to evaluate drug effectiveness in this setting.
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Serum Phosphorus and Progression of CKD and Mortality: A Meta-analysis of Cohort Studies.
Da, J, Xie, X, Wolf, M, Disthabanchong, S, Wang, J, Zha, Y, Lv, J, Zhang, L, Wang, H
American journal of kidney diseases : the official journal of the National Kidney Foundation. 2015;(2):258-65
Abstract
BACKGROUND Recent studies have indicated that phosphorus may play an independent pathogenic role in chronic kidney disease (CKD) progression, but some of those studies were underpowered and yielded inconsistent results. STUDY DESIGN Systematic review and meta-analysis. SETTING & POPULATION Non-dialysis-dependent patients with CKD (transplant recipients were excluded). SELECTION CRITERIA FOR STUDIES Studies assessing the risk ratio of serum phosphorus level on kidney failure and mortality for non-dialysis-dependent patients with CKD published from January 1950 to June 2014 were included following systematic searching of MEDLINE, EMBASE, and the Cochrane Library. PREDICTOR Serum phosphorus level. OUTCOME Kidney failure, defined as doubled serum creatinine level, 50% decline in estimated glomerular filtration rate, or end-stage kidney disease. RESULTS In 12 cohort studies with 25,546 patients, 1,442 (8.8%) developed kidney failure and 3,089 (13.6%) died. Overall, every 1-mg/dL increase in serum phosphorus level was associated independently with increased risk of kidney failure (hazard ratio, 1.36; 95% CI, 1.20-1.55) and mortality (hazard ratio, 1.20; 95% CI, 1.05-1.37). LIMITATIONS Existence of potential residual confounding could not be excluded. CONCLUSIONS This meta-analysis suggests an independent association between serum phosphorus level and kidney failure and mortality among non-dialysis-dependent patients with CKD and suggests that large-scale randomized controlled trials should target disordered phosphorus homeostasis in CKD.