Chronic kidney disease is a public health problem. The purpose of this study was to compare the effects of sevelamer and calcium- based binders on mortality of hemodialysis patients. PubMed, EMBASE and Web of Science were searched for related articles published before May 14, 2020. We included six studies with 43330 participants, of which 21147 and 22183 received calcium- based phosphate binders and sevelamer, respectively. In the analysis of unadjusted data, sevelamer could lower cardiovascular mortality. When adjusted HRs was pooled, the cardiovascular mortality did not differ significantly in the sevelamer and calcium-based phosphate binders groups. Additionally, the all-cause mortality rate in sevelamer group was different from that in calcium-based phosphate binders group. However, sevelamer could not lower all-cause mortality in terms of the adjusted data. No significant difference was found in calcium and phosphorus between calcium-based phosphate binders and sevalmer. Sensitivity analysis showed that partial results of the study were inconsistent. There was no difference in the effect of sevelamer and calcium- based phosphate binders on the risk of all-cause mortality in patients with hemodialysis, after adjusting confounders. However, given the instability of the results, the results need to be further confirmed by a large sample and high quality RCTs.

Introduction. Nontraditional risk factors for cardiovascular disease (CVD), including mineral disorder, high fibroblast growth factor 23 (FGF23), low klotho, and low soluble TWEAK could predict the incipient risk of CVD in chronic kidney disease (CKD). The present study evaluates the effect of sevelamer on soluble tumor necrosis factor-like weak inducer of apoptosis (TWEAK), and klotho levels in adenine-induced CKD rats. Methods and Materials. Normal control rats without sevelamer were compared with 3 groups of adenine-induced CKD rats, including CKD rats without sevelamer, CKD rats treated with 3% sevelamer, and rats receiving adenine and 3% sevelamer concurrently. After 4 weeks of sevelamer treatment, serum levels of klotho and soluble TWEAK were measured, along with biochemical parameters related to kidney function. Results . Sevelamer significantly reduced serum levels of phosphate and increased serum levels of klotho and soluble TWEAK. Decreased levels of phosphate were negatively correlated with elevated levels of klotho and soluble TWEAK (r = -0.70, P = .003; r = -0.58, P = .02; respectively) in serum.
Conclusions. Sevelamer successfully reduced serum levels of phosphate, and meanwhile, it led to an elevation in serum levels of klotho and soluble TWEAK in rat models of CKD.

Control of the phosphorus in dialysis’ patients is very important and can be done in many ways. The purpose of the study is to determine the effect of Nicotinic acid (Niacin) and Sevelamer on the serum phosphorus of hemodialysis patients. This double-blind randomized clinical trial study includes two groups: 60 patients (taking Niacin) and 60 patients control groups (taking Sevelamer).Niacin dose was increasing monthly in three steps from 200 to 600 mg and Sevelamer from 400 to 1200 mg. Serum phosphorus was measured in the both groups and the results were compared. In this study P<0.05 was significant. A total of 120 patients attending in this study, mean age of case group were 51.5± 21.3 years and control group was 50.7± 22.5 years that no have difference. Phosphor level in starter study in case group was 6.67±1.37 mg/dl and control group was 6.77±0.95 mg/dl that no has difference. Niacin significantly decreased the blood phosphorus levels (P<0.001) that with increasing the dose of niacin, this decreasing was more than Sevelamer. Nicotinic acid can decrease serum phosphorous; however, it is need a longer trial study for determining the most effective doses of the Nicotinic acid.

 Chronic kidney disease (CKD) is a life-threatening disease with numerous complications. Hemodialysis (HD) patients are prone to magnesium deficiency due to malnutrition, which can cause cardiovascular complications and increase mortality. The present study aimed to investigate the effects of sevelamer and calcium carbonate, as phosphate binders, on serum levels of magnesium, calcium, and phosphorus in HD patients. 

 A parallel clinical trial was conducted on 54 patients undergoing HD at Kosar Hospital of Semnan. The inclusion criteria were end-stage renal disease (ESRD), alternative HD treatment for at least 3 months 3 times a week, and serum phosphate levels greater than 4.5 mg/dL. The participants were randomly assigned to two groups of sevelamer (n = 27) and calcium carbonate (n = 27). If the participants were taking a phosphate binder, they were asked to stop it for 3 weeks. Participants in the sevelamer group received 800 mg of sevelamer at most three times a day and those in the calcium carbonate group were treated with 500 mg of calcium carbonate at most 3 times a day. Before and 3 months after the intervention, the serum levels of calcium, magnesium, and phosphorus were measured through the Arsenazo method using the Pars Azmun kit in the Selectra auto-analyzer. Twenty-one patients in the sevelamer group and 22 patients in the calcium carbonate group finished the study. 

 The results showed that calcium carbonate and sevelamer increased serum magnesium level by 0.20 (P = 0.028) and 0.26 (P = 0.002), on average, which were statistically significant. The administration of calcium carbonate did not significantly change serum calcium levels (P = 0.53), whereas sevelamer reduced serum calcium levels by 0.23 (P = 0.017), on average. This reduction was statistically significant. The results also indicated that none of the calcium carbonate (P = 0.099) and sevelamer (P = 0.543) caused significant changes in serum phosphorus levels. The study findings showed no significant difference between the two groups in terms of changes in the serum levels of magnesium (0.590), calcium (0.116), and phosphorus (0.113). 

 Both drugs (Sevelamer and calcium carbonate) prevented hypomagnesemia and increased serum magnesium levels, but no significant differences were found in blood levels of calcium, phosphorus, and magnesium compared to the two drugs. Considering the effect of magnesium on cardiovascular diseases, increasing the serum magnesium levels through the administration of calcium carbonate and sevelamer can prevent the likelihood of cardiovascular diseases. However, none of the studied drugs was superior to the other in this regard.

Calcium-based and non-calcium-based phosphate binders are frequently used to treat hyperphosphatemia in patients with chronic kidney disease (CKD).

This study aimed to compare the effects of calcium acetate and sevelamer carbonate on the progression of aortic vascular calcification in patients with CKD stages 4 and 5.

This was an open-label randomized prospective comparative study, in which the participants encompassed both male and female patients with ambulatory hyperphosphatemic CKD stages 4 and 5 aged above 18 years. One hundred fifty patients with CKD stages 4 and 5 were screened for Aortic vascular calcification using digital X-ray lumbar spine and multi-slice CT scan, of whom fifty patients with vascular calcification were selected and randomly assigned into two groups. The participants were then serially studied for the effects of phosphate binders on the progression of vascular calcification over one year. One group was prescribed calcium acetate, and the other group was prescribed sevelamer carbonate.

Fifty hyperphosphatemic CKD patients with a mean age of 57 years were randomly assigned into two groups. There was no statistically significant difference between the two groups; however, the patients assigned to the sevelamer group were older and higher aortic calcification index (ACI) (P = 0.035) and Kauppila scores (P = 0.04), and elevated serum calcium (P = 0.04), Ca X PO4 (P = 0.006), and vitamin D. In calcium acetate-treated patients, the mean ACI increased significantly during six months and one year; however, the increase was not significant in the sevelamer group. Serum cholesterol, serum triglycerides, serum iPTH level, and the inflammatory markers of atherosclerosis-high sensitivity of C-reactive protein (hs-CRP), interleukin-6 (IL-6), decreased significantly in the sevelamer group.

The prevalence of vascular (abdominal aortic) calcification in pre-ESRD (CKD stage 4 and 5) patients was 75%. Abdominal aortic calcification increased significantly in calcium acetate-treated patients during six months and one year; however, the progression was not significant regarding sevelamer. Because of its pleiotropic properties, sevelamer is more effective and consistent in retarding the progression of vascular calcification than calcium acetate in patients with CKD stages 4 and 5.

Vascular calcification is a well-known complication of chronic kidney disease and one of the main predictors for increased cardiovascular morbidity and mortality in these patients. It may happen in 2 main types of intimal calcification, as a part of diffuse atherosclerosis, and medial calcification, which is generally focal in distribution, unrelated to atherosclerotic risk factors, and seen in younger hemodialysis patients. Pathogenesis may be genetic, mineral metabolism related, or nonmineral metabolism related. Increased calcium, phosphorus, and calcium- phosphorus product; decreased parathyroid hormone level; and overzealous use of active vitamin D supplements are the main mineral metabolism-related mechanisms of vascular calcification. Other mechanisms are formation of matrix vesicles and cellular apoptosis, with generation of hydroxyapatite crystals within vesicles and apoptotic bodies. The interplay of various activator proteins of vascular calcification such as bone morphogenetic proteins and receptor activator of nuclear factor-kappa B ligand, or inhibitor proteins like matrix Gla protein, bone morphogenetic protein-7, osteopontin, osteoprotegerin, fetuin-A, Smad6, and pyrophosphate are important in establishment of vascular calcification. Vascular calcification is related to all-cause and cardiovascular mortality both in general population and dialysis patients. Minimizing traditional risk factors of vascular calcification, prevention of hypercalcemia, and avoidance of high doses of calcium-based phosphate binders and vitamin D analogues are important measures for prevention or attenuation of progression of vascular calcification. Sevelamer and cinacalcet may prevent progression of vascular calcification. With the evolving knowledge of the pathogenesis of vascular calcification, we can look forward to emergence of novel therapies for this complication in the future.

Chronic kidney disease related mineral and bone disease (CKD-MBD) is a worldwide challenge in hemodialysis patients. In Senegal, number of dialysis patients is growing but few data are available about their bone disorders.. To describe patterns of CKD-MBD in Senegalese dialysis patients..Patients and We performed a cross-sectional study including patients from three dialysis centres in Senegal. Diagnosis of different types of CKD-MBD relied on clinical, biological and radiological data collected from medical records in dialysis.. We included 118 patients and 79 of them presented CKD-BMD (prevalence of was 66.9 %). Mean age of CKD-MBD patients was 47.8 ± 15.7 years (16-81 years) and sex-ratio (Male/Female) was 1.15. Secondary hyperparathyroidism was the most frequent disorder (57 patients) followed by adynamic bone disease (21 patients) and osteomalacia (1 patients). The main clinical manifestations were bone pain (17.5% of cases), pruritus (36.8% of cases) and pathological fractures (2.5% of cases). Bone biopsy was not available. Valvular and peripheral vascular calcification were present in 24.5% and 21.2% of patients respectively. Management of CKD-MBD included optimization of dialysis, calcium bicarbonate, sevelamer, vitamin D analogues and calcimimetics. The NKF/DOQI recommended levels of serum calcium, phosphate and parathormone PTH were not achieved in one third of patients. Six patients presented major cardiovascular events during their dialysis period.. CKD-MBD are frequent in Senegalese hemodialysis patients and they are dominated by high turn-over disease. Clinical and biological manifestations are unspecific and accurate diagnoses are often difficult in absence of histomorphometry. Treatment is suboptimal for many patients in a context of limited resources.

This study was designed to evaluate the adherence of maintenance hemodialysis patients to medications and its correlation with quality of life and depressive symptoms. A total of 150 maintenance hemodialysis patients with a mean age of 56.4 ± 16.4 years (52.7% women) were included. Medication adherence was evaluated via the Simplified Medication Adherence Questionnaire, based on which nonadherent patients were identified. Specifically, the Drug-Intake Percentage Questionnaire was used for evaluation of adherence to phosphate binders, quality of life was assessed with short Form-36 and depression by the Beck Depression Inventory (BDI). A BDI score of 15 and greater was documented in 40.7%, and nonadherence in 24.7% of the patients. Adherent patients were significantly older than nonadherent ones, had a lower mean parathyroid hormone level, and had lower BDI scores. The quality of life scores were not significantly different between adherent and nonadherent patients. Multivariable analysis demonstrated that BDI score was a significant predictor of nonadherence (odds ratio for each unit increase, 1.11; 95% confidence interval, 1.04 to 1.18; P =. 001). Overall, 55.5% of patients were taking more than 66% of their prescribed dose of calcium carbonate, while 10.3% and 53.8% of patients were taking more than 66% of their prescribed dose of aluminum hydroxide and sevelamer, respectively. Adherence to medication was mainly associated with hemodialysis patients'' depressive symptom scores. Control of depression may significantly improve adherence to medications and patient management.

Hyperphosphatemia alone or in combination with hypercalcemia has been associated with increased mortality and morbidity among patients with chronic kidney disease (CKD). The present study aimed to review some of published articles about treatment of hyperphosphatemia among patients with CKD. To collect the current data, many articles were reviewed in a variety of sources such as PubMed, Scopus, Current Content, Embase, and IranMedex with keywords of "hyperphosphatemia" and "chronic kidney disease". Only articles published in English language, as full-text manuscripts, were included in this article. Common treatment of hyperphosphatemia among patients with CKD is dietary phosphate restriction and administration of phosphate binders to block absorption of ingested phosphate from the intestine. Phosphate restriction should primarily include unnecessary dietary phosphate (as many processed foods, colas, dairy products and certain vegetables). Phosphate-binding agents are categorized as calcium-containing phosphate binders (calcium carbonate and calcium acetate) and noncalcium-containing phosphate binders (sevelamer and lanthanum). All of phosphate-binding agents are effective in lowering serum phosphate however, noncalcium-containing phosphate binders are preferred among hypercalcemic patients, normocalcemic patients who also received vitamin D analogs, patients with vascular calcification and patients with adynamic bone disease. There is a concern about safety of calcium-containing binders for long-term use and these agents may be associated with hypercalcemia, vascular calcification and adynamic bone disease.