A 1-Year Randomized Trial of Calcium Acetate Versus Sevelamer on Progression of Coronary Artery Calcification in Hemodialysis Patients With Comparable Lipid Control: The Calcium Acetate Renagel Evaluation-2 (CARE-2) Study

Qunibi, Wajeh Y.; Moustafa, Moustafa; Muenz, Larry R.; He, Donghong; Kessler, Paul D.; Díaz-Buxó, José A.; Budoff, Matthew J.

doi:10.1053/j.ajkd.2008.02.298

Cited by 279 publications

(192 citation statements)

References 43 publications

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“…Eighteen trials 4,9,10,[15][16][17][18][19][20][21][22][23][24][25][26][27][28][29] met the predefined inclusion criteria and were included in our meta-analysis ( Figure 1). The 18 trails included 3676 patients (Table 1).…”

Section: Resultsmentioning

confidence: 99%

“…The 18 trails included 3676 patients (Table 1). CAC score was reported 4,9,10,[15][16][17][18][19][20][21]23,24,[27][28][29] After adjustment for the agreement between reviewers, the j coefficient on the agreement of the included studies was 0.92 (95% confidence interval 0.83 to 0.95), suggesting good agreement between reviewers in data extraction. All studies were randomized controlled trials.…”

Section: Resultsmentioning

confidence: 99%

“…Several studies demonstrated that taking the NCBPs could reduce progression of vascular calcification and improve CKD-MBD status among HD patients. 9,10 Lanthanum carbonate (LC) and sevelamer are phosphate binders that do not contain aluminium or calcium. Studies have showed that LC and sevelamer are not only as effective as calcium-based binders, but also potentially improve bone health and helps in reduction of vascular calcification by reducing exogenous calcium.…”

Section: Introductionmentioning

confidence: 99%

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The effects of non-calcium-based phosphate binders versus calcium-based phosphate binders on cardiovascular calcification and bone remodeling among dialysis patients: a meta-analysis of randomized trials

et al. 2014

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Background: Vascular calcification significantly increases the rates of cardiovascular mortality in hemodialysis (HD) patients. Abnormalities in mineral metabolism may play a role in the pathogenesis of arterial calcification. Whether patients treated with non-calcium-based phosphate binders had reduced aortic vascular calcification compared to those treated with calcium-based phosphate binders is still unclear. Methods: We searched multiple databases for studies published through August 2013 that evaluated the effects of non-calcium-based phosphate binders (NCBP) versus calcium-based phosphate binders (CBP) on cardiovascular calcification and bone remodeling among dialysis patients. We summarized test performance characteristics with the use of forest plots, fixed and random effects models, and Egger regression test. Results: Eighteen eligible randomized controlled trials totaling 3676 patients were included. Meta-analysis results showed NCBP could significantly attenuate the progression of coronary artery calcification than CBP (WMD: À144.62, 95% CI: À285.62 to À3.63). The serum calcium levels significant lower in NCPB group than in CPB groups (WMD: À0.26, 95% CI: À0.37 to À0.14), but the serum iPTH levels were significantly higher in NCPB groups (WMD: 57.1, 95% CI: 13.42 to 100.78). The osteoid volume and osteoblast numbers were significant higher in NCPB group than in CPB group (WMD: 1.75, 95% CI: 0.78 to 2.73 for osteoid volume; WMD: 4.49, 95% CI: 1.83 to 7.15 for osteoblast numbers). The Egger regression test also showed no potential publication bias (p ¼ 0.725). Conclusions: Based on available data, NCBPs have equally effective with CBPs for serum phosphate control. But there was significantly lower incidence of coronary artery calcification and a significant higher bone formatting rate in NCBP groups than in CBP groups. So we recommend NCBPs as phosphate binders for HD patients.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The effects of non-calcium-based phosphate binders versus calcium-based phosphate binders on cardiovascular calcification and bone remodeling among dialysis patients: a meta-analysis of randomized trials

et al. 2014

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“…[1][2][3][4] Because the presence of vascular calcification is strongly associated with increased cardiovascular morbidity and mortality, several studies in both animals and humans have sought ways to reduce the extent of vascular calcification. [5][6][7][8][9][10] However, satisfactory therapies have not yet been established. 11 Adenine-induced renal failure is one of the commonly used animal models for studying the development of vascular calcification, but the prevalence of vascular calcification in this model is not very high.…”

mentioning

confidence: 99%

Dietary L-Lysine Prevents Arterial Calcification in Adenine-Induced Uremic Rats

Shimomura¹,

Matsui²,

Hamano

et al. 2014

Journal of the American Society of Nephrology

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Vascular calcification (VC) is a life-threatening complication of CKD. Severe protein restriction causes a shortage of essential amino acids, and exacerbates VC in rats. Therefore, we investigated the effects of dietary L-lysine, the first-limiting amino acid of cereal grains, on VC. Male Sprague-Dawley rats at age 13 weeks were divided randomly into four groups: low-protein (LP) diet (group LP), LP diet+adenine (group Ade), LP diet+adenine+glycine (group Gly) as a control amino acid group, and LP diet+adenine+L-lysinezHCl (group Lys). At age 18 weeks, group LP had no VC, whereas groups Ade and Gly had comparable levels of severe VC. L-Lysine supplementation almost completely ameliorated VC. Physical parameters and serum creatinine, urea nitrogen, and phosphate did not differ among groups Ade, Gly, and Lys. Notably, serum calcium in group Lys was slightly but significantly higher than in groups Ade and Gly. Dietary L-lysine strongly suppressed plasma intact parathyroid hormone in adenine rats and supported a proper bone-vascular axis. The conserved orientation of the femoral apatite in group Lys also evidenced the bone-protective effects of L-lysine. Dietary L-lysine elevated plasma alanine, proline, arginine, and homoarginine but not lysine. Analyses in vitro demonstrated that alanine and proline inhibit apoptosis of cultured vascular smooth muscle cells, and that arginine and homoarginine attenuate mineral precipitations in a supersaturated calcium/ phosphate solution. In conclusion, dietary supplementation of L-lysine ameliorated VC by modifying key pathways that exacerbate VC.

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“…This led to the development of non-calcium based binders, namely sevelamer (hydrochloride and carbonate) and lanthanum (carbonate). These non-calcium-based phosphate binders have not shown superior phosphate or PTH reduction compared to calcium-based phosphate binders in head-to-head studies (51, 58, 59) but the studies have also focussed on 3 other outcomes; incidence of hypercalcaemia, mortality (60) and progression of vascular calcification (52,53,56,(61)(62)(63). Three systematic reviews have been published by Navaneethan et al (51) and Jamal et al (64,65) with different conclusions on whether there is a survival benefit when using non-calcium-based compared to calcium-based phosphate binders.…”

Section: Phosphate Bindersmentioning

confidence: 99%

Pharmacological Management of Secondary Hyperparathyroidism in Patients with Chronic Kidney Disease

Salam

Khwaja

Wilkie

2016

Drugs

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or Article Brief (if supplied by editors): As a 'Therapy in Practice' article, we would like this to provide a succinct, up-to-date clinically orientated guide to the optimum management of secondary hyperparathyroidism in patients with chronic kidney disease. The review should include an appropriate background to the development of SHPT. It should focus primarily on pharmacological treatments but as appropriate, non-pharmacological approaches (dietary, surgical) may be discussed to fully place pharmacological therapy in context. Submission date: 31 st March 2016Word count: 4156 Compliance with Ethical StandardsFunding and conflict of interest statement from each author: Takeaway messages from the article SHPT is associated with adverse outcomes in CKD and dialysis patients  Optimum PTH level is unclear in pre-dialysis CKD and the recommended range is wide for dialysis patients.  Management of SHPT is largely pharmacological focussing on lowering PTH  PTH lowering treatment has not shown improved cardiovascular risk, fractures and mortality. AbstractSecondary hyperparathyroidism (SHPT) is a common complication of CKD and is part of the chronic kidney disease-mineral bone disorder (CKD-MBD). SHPT is associated with increased risk of fracture and mortality, thus SHPT control is recommended as kidney function declines. Effective SHPT management becomes more difficult once skeletal and cardiovascular adverse effects associated with severe SHPT have become established. However, interventional studies to lower parathyroid hormone (PTH) have so far shown inconsistent results in improving patient-centred outcomes such as mortality, cardiovascular events and fracture. Pharmacological treatment effect on PTH level is also inconsistent between predialysis CKD and dialysis patients which adds to the complexity of SHPT management. This review aims to give an overview on the pathophysiology, pharmacological and non-pharmacological treatment for SHPT in CKD including some of the limitations of current therapeutic options.

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A 1-Year Randomized Trial of Calcium Acetate Versus Sevelamer on Progression of Coronary Artery Calcification in Hemodialysis Patients With Comparable Lipid Control: The Calcium Acetate Renagel Evaluation-2 (CARE-2) Study

Cited by 279 publications

References 43 publications

The effects of non-calcium-based phosphate binders versus calcium-based phosphate binders on cardiovascular calcification and bone remodeling among dialysis patients: a meta-analysis of randomized trials

The effects of non-calcium-based phosphate binders versus calcium-based phosphate binders on cardiovascular calcification and bone remodeling among dialysis patients: a meta-analysis of randomized trials

Dietary L-Lysine Prevents Arterial Calcification in Adenine-Induced Uremic Rats

Pharmacological Management of Secondary Hyperparathyroidism in Patients with Chronic Kidney Disease

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