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Overview of chronic kidney disease-mineral and bone disorder (CKD-MBD)

Wajeh Y Qunibi, MD
William L Henrich, MD, MACP
Section Editor
Jeffrey S Berns, MD
Deputy Editor
Alice M Sheridan, MD


Chronic kidney disease (CKD) is commonly associated with disorders of mineral and bone metabolism, manifested by either one or a combination of the following three components:

Abnormalities of calcium, phosphorus, parathyroid hormone (PTH), fibroblast growth factor 23 (FGF23), and vitamin D metabolism

Abnormalities in bone turnover, mineralization, volume linear growth, or strength

Extraskeletal calcification

The work group of the Kidney Disease: Improving Global Outcomes (KDIGO) recommended in 2006 the use of the term chronic kidney disease-mineral and bone disorder (CKD-MBD) to describe a systemic disorder that incorporates these abnormalities [1]. The work group recommended that the traditional term "renal osteodystrophy" be exclusively used to define alterations in bone morphology associated with CKD and stated that definitive diagnosis of renal osteodystrophy can only be made by bone biopsy [1,2]. Following the introduction of the term CKD-MBD, various clinical practice guidelines have recommended laboratory targets and therapeutic approaches aimed at ameliorating the consequences of this systemic disorder.

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Literature review current through: Nov 2017. | This topic last updated: Jan 19, 2017.
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  1. Moe S, Drüeke T, Cunningham J, et al. Definition, evaluation, and classification of renal osteodystrophy: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO). Kidney Int 2006; 69:1945.
  2. Chapter 1: Introduction and definition of CKD-MBD and the development of the guideline statements. Kidney Int 2009; 76113:S3.
  3. Fang Y, Ginsberg C, Sugatani T, et al. Early chronic kidney disease-mineral bone disorder stimulates vascular calcification. Kidney Int 2014; 85:142.
  4. Pereira RC, Juppner H, Azucena-Serrano CE, et al. Patterns of FGF-23, DMP1, and MEPE expression in patients with chronic kidney disease. Bone 2009; 45:1161.
  5. Sabbagh Y, Graciolli FG, O'Brien S, et al. Repression of osteocyte Wnt/β-catenin signaling is an early event in the progression of renal osteodystrophy. J Bone Miner Res 2012; 27:1757.
  6. Oliveira RB, Cancela AL, Graciolli FG, et al. Early control of PTH and FGF23 in normophosphatemic CKD patients: a new target in CKD-MBD therapy? Clin J Am Soc Nephrol 2010; 5:286.
  7. Isakova T, Wahl P, Vargas GS, et al. Fibroblast growth factor 23 is elevated before parathyroid hormone and phosphate in chronic kidney disease. Kidney Int 2011; 79:1370.
  8. Hamdy NA, Kanis JA, Beneton MN, et al. Effect of alfacalcidol on natural course of renal bone disease in mild to moderate renal failure. BMJ 1995; 310:358.
  9. Coen G, Ballanti P, Bonucci E, et al. Renal osteodystrophy in predialysis and hemodialysis patients: comparison of histologic patterns and diagnostic predictivity of intact PTH. Nephron 2002; 91:103.
  10. Qunibi WY, Abouzahr F, Mizani MR, et al. Cardiovascular calcification in Hispanic Americans (HA) with chronic kidney disease (CKD) due to type 2 diabetes. Kidney Int 2005; 68:271.
  11. Budoff MJ, Rader DJ, Reilly MP, et al. Relationship of estimated GFR and coronary artery calcification in the CRIC (Chronic Renal Insufficiency Cohort) Study. Am J Kidney Dis 2011; 58:519.
  12. Cunningham J, Locatelli F, Rodriguez M. Secondary hyperparathyroidism: pathogenesis, disease progression, and therapeutic options. Clin J Am Soc Nephrol 2011; 6:913.
  13. Levin A, Bakris GL, Molitch M, et al. Prevalence of abnormal serum vitamin D, PTH, calcium, and phosphorus in patients with chronic kidney disease: results of the study to evaluate early kidney disease. Kidney Int 2007; 71:31.
  14. Pitts TO, Piraino BH, Mitro R, et al. Hyperparathyroidism and 1,25-dihydroxyvitamin D deficiency in mild, moderate, and severe renal failure. J Clin Endocrinol Metab 1988; 67:876.
  15. Gutierrez O, Isakova T, Rhee E, et al. Fibroblast growth factor-23 mitigates hyperphosphatemia but accentuates calcitriol deficiency in chronic kidney disease. J Am Soc Nephrol 2005; 16:2205.
  16. Martin KJ, González EA. Metabolic bone disease in chronic kidney disease. J Am Soc Nephrol 2007; 18:875.
  17. National Kidney Foundation. K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification. Am J Kidney Dis 2002; 39:S1.
  18. Kates DM, Sherrard DJ, Andress DL. Evidence that serum phosphate is independently associated with serum PTH in patients with chronic renal failure. Am J Kidney Dis 1997; 30:809.
  19. Hruska KA, Teitelbaum SL. Renal osteodystrophy. N Engl J Med 1995; 333:166.
  20. Fournier A, Morinière P, Ben Hamida F, et al. Use of alkaline calcium salts as phosphate binder in uremic patients. Kidney Int Suppl 1992; 38:S50.
  21. Llach F. Secondary hyperparathyroidism in renal failure: the trade-off hypothesis revisited. Am J Kidney Dis 1995; 25:663.
  22. Slatopolsky E, Bricker NS. The role of phosphorus restriction in the prevention of secondary hyperparathyroidism in chronic renal disease. Kidney Int 1973; 4:141.
  23. Slatopolsky E, Caglar S, Pennell JP, et al. On the pathogenesis of hyperparathyroidism in chronic experimental renal insufficiency in the dog. J Clin Invest 1971; 50:492.
  24. Llach F, Massry SG. On the mechanism of secondary hyperparathyroidism in moderate renal insufficiency. J Clin Endocrinol Metab 1985; 61:601.
  25. Portale AA, Booth BE, Halloran BP, Morris RC Jr. Effect of dietary phosphorus on circulating concentrations of 1,25-dihydroxyvitamin D and immunoreactive parathyroid hormone in children with moderate renal insufficiency. J Clin Invest 1984; 73:1580.
  26. Slatopolsky E, Robson AM, Elkan I, Bricker NS. Control of phosphate excretion in uremic man. J Clin Invest 1968; 47:1865.
  27. Silver J, Rodriguez M, Slatopolsky E. FGF23 and PTH--double agents at the heart of CKD. Nephrol Dial Transplant 2012; 27:1715.
  28. Silver J, Levi R. Cellular and molecular mechanisms of secondary hyperparathyroidism. Clin Nephrol 2005; 63:119.
  29. Slatopolsky E, Finch J, Denda M, et al. Phosphorus restriction prevents parathyroid gland growth. High phosphorus directly stimulates PTH secretion in vitro. J Clin Invest 1996; 97:2534.
  30. Fine A, Cox D, Fontaine B. Elevation of serum phosphate affects parathyroid hormone levels in only 50% of hemodialysis patients, which is unrelated to changes in serum calcium. J Am Soc Nephrol 1993; 3:1947.
  31. Naveh-Many T, Rahamimov R, Livni N, Silver J. Parathyroid cell proliferation in normal and chronic renal failure rats. The effects of calcium, phosphate, and vitamin D. J Clin Invest 1995; 96:1786.
  32. Almaden Y, Hernandez A, Torregrosa V, et al. High phosphate level directly stimulates parathyroid hormone secretion and synthesis by human parathyroid tissue in vitro. J Am Soc Nephrol 1998; 9:1845.
  33. Wetmore JB, Liu S, Krebill R, et al. Effects of cinacalcet and concurrent low-dose vitamin D on FGF23 levels in ESRD. Clin J Am Soc Nephrol 2010; 5:110.
  34. Saito H, Maeda A, Ohtomo S, et al. Circulating FGF-23 is regulated by 1alpha,25-dihydroxyvitamin D3 and phosphorus in vivo. J Biol Chem 2005; 280:2543.
  35. Paloian NJ, Giachelli CM. A current understanding of vascular calcification in CKD. Am J Physiol Renal Physiol 2014; 307:F891.
  36. Kendrick J, Ix JH, Targher G, et al. Relation of serum phosphorus levels to ankle brachial pressure index (from the Third National Health and Nutrition Examination Survey). Am J Cardiol 2010; 106:564.
  37. Koenig KG, Lindberg JS, Zerwekh JE, et al. Free and total 1,25-dihydroxyvitamin D levels in subjects with renal disease. Kidney Int 1992; 41:161.
  38. Wilson L, Felsenfeld A, Drezner MK, Llach F. Altered divalent ion metabolism in early renal failure: role of 1,25(OH)2D. Kidney Int 1985; 27:565.
  39. Gutiérrez OM, Isakova T, Andress DL, et al. Prevalence and severity of disordered mineral metabolism in Blacks with chronic kidney disease. Kidney Int 2008; 73:956.
  40. Saito H, Kusano K, Kinosaki M, et al. Human fibroblast growth factor-23 mutants suppress Na+-dependent phosphate co-transport activity and 1alpha,25-dihydroxyvitamin D3 production. J Biol Chem 2003; 278:2206.
  41. Shimada T, Hasegawa H, Yamazaki Y, et al. FGF-23 is a potent regulator of vitamin D metabolism and phosphate homeostasis. J Bone Miner Res 2004; 19:429.
  42. Urakawa I, Yamazaki Y, Shimada T, et al. Klotho converts canonical FGF receptor into a specific receptor for FGF23. Nature 2006; 444:770.
  43. Hsu CH, Patel SR, Young EW, Vanholder R. The biological action of calcitriol in renal failure. Kidney Int 1994; 46:605.
  44. Silver J, Naveh-Many T, Mayer H, et al. Regulation by vitamin D metabolites of parathyroid hormone gene transcription in vivo in the rat. J Clin Invest 1986; 78:1296.
  45. Malluche HH, Mawad H, Koszewski NJ. Update on vitamin D and its newer analogues: actions and rationale for treatment in chronic renal failure. Kidney Int 2002; 62:367.
  46. Brumbaugh PF, Hughes MR, Haussler MR. Cytoplasmic and nuclear binding components for 1alpha25-dihydroxyvitamin D3 in chick parathyroid glands. Proc Natl Acad Sci U S A 1975; 72:4871.
  47. Denda M, Finch J, Brown AJ, et al. 1,25-dihydroxyvitamin D3 and 22-oxacalcitriol prevent the decrease in vitamin D receptor content in the parathyroid glands of uremic rats. Kidney Int 1996; 50:34.
  48. Usatii M, Rousseau L, Demers C, et al. Parathyroid hormone fragments inhibit active hormone and hypocalcemia-induced 1,25(OH)2D synthesis. Kidney Int 2007; 72:1330.
  49. Slatopolsky E, Weerts C, Thielan J, et al. Marked suppression of secondary hyperparathyroidism by intravenous administration of 1,25-dihydroxy-cholecalciferol in uremic patients. J Clin Invest 1984; 74:2136.
  50. Dusso AS, Pavlopoulos T, Naumovich L, et al. p21(WAF1) and transforming growth factor-alpha mediate dietary phosphate regulation of parathyroid cell growth. Kidney Int 2001; 59:855.
  51. Cozzolino M, Lu Y, Finch J, et al. p21WAF1 and TGF-alpha mediate parathyroid growth arrest by vitamin D and high calcium. Kidney Int 2001; 60:2109.
  52. Fukuda N, Tanaka H, Tominaga Y, et al. Decreased 1,25-dihydroxyvitamin D3 receptor density is associated with a more severe form of parathyroid hyperplasia in chronic uremic patients. J Clin Invest 1993; 92:1436.
  53. Patel SR, Ke HQ, Vanholder R, et al. Inhibition of calcitriol receptor binding to vitamin D response elements by uremic toxins. J Clin Invest 1995; 96:50.
  54. Block GA, Hulbert-Shearon TE, Levin NW, Port FK. Association of serum phosphorus and calcium x phosphate product with mortality risk in chronic hemodialysis patients: a national study. Am J Kidney Dis 1998; 31:607.
  55. Floege J, Kim J, Ireland E, et al. Serum iPTH, calcium and phosphate, and the risk of mortality in a European haemodialysis population. Nephrol Dial Transplant 2011; 26:1948.
  56. Moe SM, Seifert MF, Chen NX, et al. R-568 reduces ectopic calcification in a rat model of chronic kidney disease-mineral bone disorder (CKD-MBD). Nephrol Dial Transplant 2009; 24:2371.
  57. Rodriguez M, Nemeth E, Martin D. The calcium-sensing receptor: a key factor in the pathogenesis of secondary hyperparathyroidism. Am J Physiol Renal Physiol 2005; 288:F253.
  58. Li YC, Amling M, Pirro AE, et al. Normalization of mineral ion homeostasis by dietary means prevents hyperparathyroidism, rickets, and osteomalacia, but not alopecia in vitamin D receptor-ablated mice. Endocrinology 1998; 139:4391.
  59. Panda DK, Miao D, Bolivar I, et al. Inactivation of the 25-hydroxyvitamin D 1alpha-hydroxylase and vitamin D receptor demonstrates independent and interdependent effects of calcium and vitamin D on skeletal and mineral homeostasis. J Biol Chem 2004; 279:16754.
  60. Gogusev J, Duchambon P, Hory B, et al. Depressed expression of calcium receptor in parathyroid gland tissue of patients with hyperparathyroidism. Kidney Int 1997; 51:328.
  61. Yano S, Sugimoto T, Tsukamoto T, et al. Association of decreased calcium-sensing receptor expression with proliferation of parathyroid cells in secondary hyperparathyroidism. Kidney Int 2000; 58:1980.
  62. Cañadillas S, Canalejo A, Santamaría R, et al. Calcium-sensing receptor expression and parathyroid hormone secretion in hyperplastic parathyroid glands from humans. J Am Soc Nephrol 2005; 16:2190.
  63. Brown AJ, Ritter CS, Finch JL, Slatopolsky EA. Decreased calcium-sensing receptor expression in hyperplastic parathyroid glands of uremic rats: role of dietary phosphate. Kidney Int 1999; 55:1284.
  64. Nagano N. Pharmacological and clinical properties of calcimimetics: calcium receptor activators that afford an innovative approach to controlling hyperparathyroidism. Pharmacol Ther 2006; 109:339.
  65. Levi R, Ben-Dov IZ, Lavi-Moshayoff V, et al. Increased parathyroid hormone gene expression in secondary hyperparathyroidism of experimental uremia is reversed by calcimimetics: correlation with posttranslational modification of the trans acting factor AUF1. J Am Soc Nephrol 2006; 17:107.
  66. Rodriguez ME, Almaden Y, Cañadillas S, et al. The calcimimetic R-568 increases vitamin D receptor expression in rat parathyroid glands. Am J Physiol Renal Physiol 2007; 292:F1390.
  67. Liu S, Gupta A, Quarles LD. Emerging role of fibroblast growth factor 23 in a bone-kidney axis regulating systemic phosphate homeostasis and extracellular matrix mineralization. Curr Opin Nephrol Hypertens 2007; 16:329.
  68. Liu S, Quarles LD. How fibroblast growth factor 23 works. J Am Soc Nephrol 2007; 18:1637.
  69. Lavi-Moshayoff V, Wasserman G, Meir T, et al. PTH increases FGF23 gene expression and mediates the high-FGF23 levels of experimental kidney failure: a bone parathyroid feedback loop. Am J Physiol Renal Physiol 2010; 299:F882.
  70. López I, Rodríguez-Ortiz ME, Almadén Y, et al. Direct and indirect effects of parathyroid hormone on circulating levels of fibroblast growth factor 23 in vivo. Kidney Int 2011; 80:475.
  71. Quinn SJ, Thomsen AR, Pang JL, et al. Interactions between calcium and phosphorus in the regulation of the production of fibroblast growth factor 23 in vivo. Am J Physiol Endocrinol Metab 2013; 304:E310.
  72. Imanishi Y, Inaba M, Nakatsuka K, et al. FGF-23 in patients with end-stage renal disease on hemodialysis. Kidney Int 2004; 65:1943.
  73. Larsson T, Nisbeth U, Ljunggren O, et al. Circulating concentration of FGF-23 increases as renal function declines in patients with chronic kidney disease, but does not change in response to variation in phosphate intake in healthy volunteers. Kidney Int 2003; 64:2272.
  74. Mace ML, Gravesen E, Hofman-Bang J, et al. Key role of the kidney in the regulation of fibroblast growth factor 23. Kidney Int 2015; 88:1304.
  75. Miyamoto K, Ito M, Tatsumi S, et al. New aspect of renal phosphate reabsorption: the type IIc sodium-dependent phosphate transporter. Am J Nephrol 2007; 27:503.
  76. Dhayat NA, Ackermann D, Pruijm M, et al. Fibroblast growth factor 23 and markers of mineral metabolism in individuals with preserved renal function. Kidney Int 2016; 90:648.
  77. Taal MW, Thurston V, McIntyre NJ, et al. The impact of vitamin D status on the relative increase in fibroblast growth factor 23 and parathyroid hormone in chronic kidney disease. Kidney Int 2014; 86:407.
  78. Ben-Dov IZ, Galitzer H, Lavi-Moshayoff V, et al. The parathyroid is a target organ for FGF23 in rats. J Clin Invest 2007; 117:4003.
  79. Komaba H, Goto S, Fujii H, et al. Depressed expression of Klotho and FGF receptor 1 in hyperplastic parathyroid glands from uremic patients. Kidney Int 2010; 77:232.
  80. Canalejo R, Canalejo A, Martinez-Moreno JM, et al. FGF23 fails to inhibit uremic parathyroid glands. J Am Soc Nephrol 2010; 21:1125.
  81. Kuro-o M. Klotho as a regulator of fibroblast growth factor signaling and phosphate/calcium metabolism. Curr Opin Nephrol Hypertens 2006; 15:437.
  82. Asai O, Nakatani K, Tanaka T, et al. Decreased renal α-Klotho expression in early diabetic nephropathy in humans and mice and its possible role in urinary calcium excretion. Kidney Int 2012; 81:539.
  83. Hu MC, Shi M, Zhang J, et al. Klotho deficiency causes vascular calcification in chronic kidney disease. J Am Soc Nephrol 2011; 22:124.
  84. de Seigneux S, Courbebaisse M, Rutkowski JM, et al. Proteinuria Increases Plasma Phosphate by Altering Its Tubular Handling. J Am Soc Nephrol 2015; 26:1608.
  85. Gutiérrez OM, Mannstadt M, Isakova T, et al. Fibroblast growth factor 23 and mortality among patients undergoing hemodialysis. N Engl J Med 2008; 359:584.
  86. Isakova T, Xie H, Yang W, et al. Fibroblast growth factor 23 and risks of mortality and end-stage renal disease in patients with chronic kidney disease. JAMA 2011; 305:2432.
  87. Faul C, Amaral AP, Oskouei B, et al. FGF23 induces left ventricular hypertrophy. J Clin Invest 2011; 121:4393.
  88. Andrukhova O, Smorodchenko A, Egerbacher M, et al. FGF23 promotes renal calcium reabsorption through the TRPV5 channel. EMBO J 2014; 33:229.
  89. Andrukhova O, Slavic S, Smorodchenko A, et al. FGF23 regulates renal sodium handling and blood pressure. EMBO Mol Med 2014; 6:744.
  90. Scialla JJ, Lau WL, Reilly MP, et al. Fibroblast growth factor 23 is not associated with and does not induce arterial calcification. Kidney Int 2013; 83:1159.
  91. Rodriguez M, Felsenfeld AJ, Llach F. Calcemic response to parathyroid hormone in renal failure: role of calcitriol and the effect of parathyroidectomy. Kidney Int 1991; 40:1063.
  92. Slatopolsky E, Finch J, Clay P, et al. A novel mechanism for skeletal resistance in uremia. Kidney Int 2000; 58:753.
  93. Indridason OS, Heath H 3rd, Khosla S, et al. Non-suppressible parathyroid hormone secretion is related to gland size in uremic secondary hyperparathyroidism. Kidney Int 1996; 50:1663.
  94. Grzela T, Chudzinski W, Lasiecka Z, et al. The calcium-sensing receptor and vitamin D receptor expression in tertiary hyperparathyroidism. Int J Mol Med 2006; 17:779.
  95. Arnold A, Brown MF, Ureña P, et al. Monoclonality of parathyroid tumors in chronic renal failure and in primary parathyroid hyperplasia. J Clin Invest 1995; 95:2047.
  96. Drüeke TB. The pathogenesis of parathyroid gland hyperplasia in chronic renal failure. Kidney Int 1995; 48:259.
  97. Moorthi RN, Moe SM. CKD-mineral and bone disorder: core curriculum 2011. Am J Kidney Dis 2011; 58:1022.
  98. Delanaye P, Dubois BE, Jouret F, et al. Parathormone and bone-specific alkaline phosphatase for the follow-up of bone turnover in hemodialysis patients: is it so simple? Clin Chim Acta 2013; 417:35.
  99. Sprague SM, Bellorin-Font E, Jorgetti V, et al. Diagnostic Accuracy of Bone Turnover Markers and Bone Histology in Patients With CKD Treated by Dialysis. Am J Kidney Dis 2016; 67:559.
  100. Bakkaloglu SA, Wesseling-Perry K, Pereira RC, et al. Value of the new bone classification system in pediatric renal osteodystrophy. Clin J Am Soc Nephrol 2010; 5:1860.
  101. National Kidney Foundation. K/DOQI clinical practice guidelines for bone metabolism and disease in chronic kidney disease. Am J Kidney Dis 2003; 42:S1.
  102. D'Haese PC, Spasovski GB, Sikole A, et al. A multicenter study on the effects of lanthanum carbonate (Fosrenol) and calcium carbonate on renal bone disease in dialysis patients. Kidney Int Suppl 2003; :S73.
  103. Changsirikulchai S, Domrongkitchaiporn S, Sirikulchayanonta V, et al. Renal osteodystrophy in Ramathibodi Hospital: histomorphometry and clinical correlation. J Med Assoc Thai 2000; 83:1223.
  104. Moe SM, Drüeke TB. A bridge to improving healthcare outcomes and quality of life. Am J Kidney Dis 2004; 43:552.
  105. Felsenberg D, Boonen S. The bone quality framework: determinants of bone strength and their interrelationships, and implications for osteoporosis management. Clin Ther 2005; 27:1.
  106. Malluche HH, Porter DS, Monier-Faugere MC, et al. Differences in bone quality in low- and high-turnover renal osteodystrophy. J Am Soc Nephrol 2012; 23:525.
  107. Martin KJ, Olgaard K, Coburn JW, et al. Diagnosis, assessment, and treatment of bone turnover abnormalities in renal osteodystrophy. Am J Kidney Dis 2004; 43:558.
  108. Sherrard DJ, Hercz G, Pei Y, et al. The spectrum of bone disease in end-stage renal failure--an evolving disorder. Kidney Int 1993; 43:436.
  109. Ferreira A, Frazão JM, Monier-Faugere MC, et al. Effects of sevelamer hydrochloride and calcium carbonate on renal osteodystrophy in hemodialysis patients. J Am Soc Nephrol 2008; 19:405.
  110. Barreto FC, Barreto DV, Moysés RM, et al. K/DOQI-recommended intact PTH levels do not prevent low-turnover bone disease in hemodialysis patients. Kidney Int 2008; 73:771.
  111. Malluche HH, Mawad HW, Monier-Faugere MC. Renal osteodystrophy in the first decade of the new millennium: analysis of 630 bone biopsies in black and white patients. J Bone Miner Res 2011; 26:1368.
  112. Spasovski GB, Bervoets AR, Behets GJ, et al. Spectrum of renal bone disease in end-stage renal failure patients not yet on dialysis. Nephrol Dial Transplant 2003; 18:1159.
  113. Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD Work Group. KDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD). Kidney Int Suppl 2009; :S1.
  114. Qunibi WY. Cardiovascular calcification in nondialyzed patients with chronic kidney disease. Semin Dial 2007; 20:134.
  115. Chertow GM, Burke SK, Raggi P, Treat to Goal Working Group. Sevelamer attenuates the progression of coronary and aortic calcification in hemodialysis patients. Kidney Int 2002; 62:245.
  116. Qunibi W, Moustafa M, Muenz LR, et al. 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. Am J Kidney Dis 2008; 51:952.