Abstract:Objective To evaluate the efficacy and safety of sevelamer carbonate in the treatment of maintenance hemodialysis (MHD) patients with hyperphosphatemia. Methods Eigyty-one MHD patients treated in the Army General Hospital between May 2017 and January 2018 were enrolled in this study. They were divided into two groups.The treatment group (n=39) received sevelamer carbonate for 6 months while the control group (n=42) received calcium acetate. The therapeutic effect was evaluated according to the changes of serum phosphorus, calcium, calcium-phosphate products, iPTH and LDL-C. The adverse effect was recorded simultaneously. Results (1) After treatment, levels of serum phosphorus decreased significantly at 2, 4 and 6 months (P<0.05) in the treatment group, but at 4 and 6 months in the control group(P<0.05). Two months after treatment, these levels in the treatment group were lower than those of the control group (P<0.05). (2) There was no significant change in serum calcium levels at 2, 4, and 6 months after treatment in the treatment group, but they were increased in the control group at 4 and 6 months after treatment (P<0.05). Compared with the control group, the serum calcium level in the treatment group was lower at 6 months after treatment (P<0.05). (3) Calcium and phosphorus levels were significantly decreased (P<0.05) after 2, 4 and 6 months of treatment in the treatment group, but after 6 months of treatment in the control group (P<0.05). They were lower in the treatment group than in the control group after 6 months of treatment (P<0.05).(4) iPTH levels decreased significantly after treatment in both groups (P<0.05). (5)Low density lipoprotein in the experimental group decreased significantly after 6 months of treatment (P<0.05), but there was no significant change after 6 months of treatment in the control group. (6)There was no significant difference in the incidence of adverse reactions between the two groups. Conclusions Sevelamer carbonate is safe and effective in treating hyperphosphatemia in patients with maintenance dialysis, and has the advantage of reducing the level of calcium-phosphorus products and low density lipoprotein compared with calcium acetate.
Goldsmith D, Ritz E, Covic A. Vascular calcification: a stiff challenge for the nephrologist. Does preventing bone disease cause arterial disease[J]. Kid Int, 2004, 66(4):1315-1333.
[2]
Palmer S C, Hayen A, Macaskill P, et al. Serum levels of phosphorus, parathyroid hormone, and calcium and risks of death and cardiovascular disease in individuals with chronic kidney disease: a systematic review and Meta-analysis[J]. JAMA, 2011, 305(11):1119-1127.
[3]
Barreto F C, Barreto D V, Moysés R M A, et al. K/DOQI-recommended intact PTH levels do not prevent low-turnover bone disease in hemodialysis patients[J]. Kid Int, 2008, 73(6):771-777.
[4]
Shinaberger C S, Kopple J D, Kovesdy C P, et al. Ratio of paricalcitol dosage to serum parathyroid hormone level and survival in maintenance hemodialysis patients[J]. Clin J Am Soc Nephrol Cjasn, 2008, 3(6):1769.
[5]
Kalantarzadeh K, Gutekunst L, Mehrotra R, et al. Understanding sources of dietary phosphorus in the treatment of patients with chronic kidney disease[J]. Clin J Am Soc Nephrol, 2010, 5(3):519-530..
[6]
Levey A S, Coresh J, Levin A, et al. Clinical practice guidelines for chronic kidney disease in adults: Part I. Definition, disease stages, evaluation, treatment, and risk factors[J]. Am Fam Physician, 2004, 70(5): 869-876.
[7]
Lopes A A, Tong L, Thumma J, et al. Phosphate binder use and mortality among hemodialysis patients in the Dialysis Outcomes and Practice Patterns Study (DOPPS): evaluation of possible confounding by nutritional status.[J]. Am J Kid Dis, 2012, 60(1):90-101.
[8]
Isakova T; Gutiérrez O M; Chang Y; et al. Phosphorus binders and survival on hemodialysis.[J]. J Am Soc Nephrol , 2009, 20(2):388-396..
[9]
Adrian C, Jutta P D, Miroslaw K, et al. A comparison of calcium acetate/magnesium carbonate and sevelamer-hydrochloride effects on fibroblast growth factor-23 and bone markers:post hocevaluation from a controlled, randomized study[J]. Nephrol Dial Transpl, 2013, 28(9):2383-2392.
[10]
Jamal S A, Fitchett D, Lok C E, et al. The effects of calcium-based versus non-calcium-based phosphate binders on mortality among patients with chronic kidney disease: a meta-analysis[J]. Nephrol, Dialysis, Transpl, 2009, 24(10):3168.
[11]
Delmez J, Block G, Robertson J, et al. A randomized, double-blind, crossover design study of sevelamer hydrochloride and sevelamer carbonate in patients on hemodialysis[J]. Clin Nephrol, 2007, 68(6):386-391.
[12]
Kakuta T, Tanaka R, Hyodo T, et al. Effect of sevelamer and calcium-based phosphate binders on coronary artery calcification and accumulation of circulating advanced glycation end products in hemodialysis patients[J]. Am J Kid Dis, 2011, 57(3):422-431.
[13]
Vlassara H, Uribarri J, Cai W, et al. Effects of sevelamer on HbA1c, inflammation, and advanced glycation end products in diabetic kidney disease[J]. Clin J Am Soc Nephrol, 2012, 7(6):934-942.
[14]
Rosenbaum D P, Holmesfarley S R, Mandeville W H, et al. Effect of RenaGel, a non-absorbable, cross-linked, polymeric phosphate binder, on urinary phosphorus excretion in rats[J]. Nephrol Dial Transpl, 1997, 12(5):961-964.
[15]
St Peter W L, Fan Q, Weinhandl E, et al. Economic evaluation of sevelamer versus calcium-based phosphate binders in hemodialysis patients: a secondary analysis using Centers for Medicare & Medicaid Services Data[J]. Clin J Am Soc Nephrol Cjasn, 2009, 4(12):1954.
[16]
Bernard L, Mendelssohn D, Dunn E, et al. A modeled economic evaluation of sevelamer for treatment of hyperphosphatemia associated with chronic kidney disease among patients on dialysis in the United Kingdom.[J]. J Med Econom, 2013, 16(1):1-9.