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Research Progress on Mineral and Bone Metabolism Disorders in Chronic Kidney Disease

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DOI: 10.23977/medsc.2022.030802 | Downloads: 9 | Views: 431

Author(s)

Wenjing Wang 1, Yiying Wu 1, Lei Xu 1, Hang Li 1, Yanlong Zhao 2

Affiliation(s)

1 Shaanxi University of Chinese Medicine, Xianyang, Shaanxi, 712046, China
2 Hemodialysis Room of Nephropathy Hospital of Shaanxi Provincial Hospital of Traditional Chinese Medicine, Xi'an, Shaanxi, 710003, China

Corresponding Author

Yanlong Zhao

ABSTRACT

Abnormal mineral and bone metabolism (MBD) is one of the most common complications in patients with chronic kidney disease (CKD), and an important factor in the occurrence of cardiovascular events and increased mortality in CKD patients. Abnormal calcium, phosphorus, parathyroid hormone (PTH), vitamin D metabolism, bone turnover, and vascular calcification are its abnormal manifestations. This article aims to review the research progress of CKD-MBD in recent years, to provide a reference for the clinical treatment of CKD-MBD.

KEYWORDS

Chronic Kidney Disease, Mineral and Bone Metabolism, FGF-23, Treatment

CITE THIS PAPER

Wenjing Wang, Yiying Wu, Lei Xu, Hang Li, Yanlong Zhao, Research Progress on Mineral and Bone Metabolism Disorders in Chronic Kidney Disease . MEDS Clinical Medicine (2022) Vol. 3: 13-20. DOI: http://dx.doi.org/10.23977/medsc.2022.030802.

REFERENCES

[1] Gal-Moscovici, A., and Sprague, S.M. (2007) Bone Health in Chronic Kidney Disease-Mineral and Bone Disease. Adv Chronic Kidney Dis, 14(1), 27-36.
[2] Jadoul, M., et al. (2006) Incidence And Risk Factors For Hip or Other Bone Fractures Among Hemodialysis Patients in the Dialysis Outcomes and Practice Patterns Study. Kidney Int, 70(7), 1358-66.
[3] Moe, S., Et Al. (2006) Definition, Evaluation, and Classification of Renal Osteodystrophy: A Position Statement from Kidney Disease: Improving Global Outcomes (KDIGO). Kidney Int, 69(11), 1945-53.
[4] Cunningham, J., Locatelli, F., and Rodriguez, M., (2011) Secondary Hyperparathyroidism: Pathogenesis, Disease Progression, and Therapeutic Options. Clin J Am Soc Nephrol, 6(4), 913-21.
[5] Goodman, W.G. and Quarles, L.D. (2008) Development and Progression of Secondary Hyperparathyroidism in Chronic Kidney Disease: Lessons from Molecular Genetics. Kidney Int, 74(3), 276-88.
[6] Moe, S.M., Et Al. (2007) Chronic Kidney Disease-Mineral-Bone Disorder: A New Paradigm. Adv Chronic Kidney Dis, 14(1), 3-12.
[7] Evenepoel, J.B., and Urena, T.P. (2016) Parathyroid Hormone Metabolism And Signaling In Health And Chronic Kidney Disease. Kidney Int, 90(6), 1184-1190.
[8] Johansen, K.L. and Chertow, G.M. (2007) Chronic Kidney Disease Mineral Bone Disorder and Health-Related Quality Of Life among Incident End-Stage Renal-Disease Patients. J Ren Nutr, 17(5), 305-13.
[9] Mittalhenkle, A., D.L. Gillen and Stehman-Breen, C.O. (2004) Increased Risk of Mortality Associated with Hip Fracture in the Dialysis Population. Am J Kidney Dis, 44(4), 672-9.
[10] Hampson, G., Et Al. (2021) A Review and Perspective on the Assessment, Management and Prevention of Fragility Fractures In Patients with Osteoporosis and Chronic Kidney Disease. Endocrine, 73(3), 509-529.
[11] Li, Y.B. and Zhang, L. (2016) The Interpretation of the Updated Opinion Draft of KDIGO Chronic Kidney Disease Bone And Mineral Disorder Guidelines In 2016 Chinese Journal Of Practical Internal Medicine, 36 (12), 1040-1043.
[12] Heaf, J.G. (2015) Chronic Kidney Disease-Mineral Bone Disorder in the Elderly Peritoneal Dialysis Patient. Perit Dial Int, 35(6), 640-4.
[13] Zawierucha, J., Et Al. (2016)[Contemporary Opinions on the Diagnosis and Treatment of Secondary Hyperparathyroidism]. Przegl Lek, 73(7), 497-503.
[14] Silver, J. and Naveh-Many, T. (2013) FGF-23 and Secondary Hyperparathyroidism in Chronic Kidney Disease. Nat Rev Nephrol, 9(11), 641-9.
[15] Danese, M.D., Et Al. (2006) PTH and the Risks for Hip, Vertebral, and Pelvic Fractures among Patients on Dialysis. Am J Kidney Dis, 47(1), 149-56.
[16] Lindberg, I., Et Al. (2015) FGF23 Is Endogenously Phosphorylated In Bone Cells. J Bone Miner Res, 30(3), 449-54.
[17] Saito, H., Et Al. (2003) Human Fibroblast Growth Factor-23 Mutants Suppress Na+-Dependent Phosphate Co-Transport Activity and 1alpha, 25-Dihydroxyvitamin D3 Production. J Biol Chem, 278(4), 2206-11.
[18] Moe, S.M., Et Al. (2009) A Rat Model of Chronic Kidney Disease-Mineral Bone Disorder. Kidney Int, 75(2), 176-84.
[19] O'Neill, W.C. and Lomashvili, K.A. (2010) Recent Progress in the Treatment of Vascular Calcification. Kidney Int, 78(12), 1232-9.
[20] O'Neill, W.C., Et Al. (2011) Treatment with Pyrophosphate Inhibits Uremic Vascular Calcification. Kidney Int, 79(5), 512-7.
[21] Jovanovich, A., Et Al. (2013) Fibroblast Growth Factor 23, Bone Mineral Density, and Risk of Hip Fracture among Older Adults: The Cardiovascular Health Study. J Clin Endocrinol Metab, 98(8), 3323-31.
[22] Rodriguez, M., Et Al. (2012) FGF23 and Mineral Metabolism, Implications in CKD-MBD. Nefrologia, 32(3), 275-8.
[23] Schafer, C., Et Al. (2003) The Serum Protein Alpha 2-Heremans-Schmid Glycoprotein/Fetuin-A Is A Systemically Acting Inhibitor Of Ectopic Calcification. J Clin Invest, 112(3), 357-66.
[24] Bennett, B.J., Et Al. (2006) Osteoprotegerin Inactivation Accelerates Advanced Atherosclerotic Lesion Progression and Calcification in Older Apoe-/- Mice. Arterioscler Thromb Vasc Biol, 26(9), 2117-24.
[25] Lim, K., Et Al. (2012) Vascular Klotho Deficiency Potentiates the Development of Human Artery Calcification and Mediates Resistance to Fibroblast Growth Factor 23. Circulation, 125(18), 2243-55.
[26] Grabner, A., Et Al. (2017) FGF23/FGFR4-Mediated Left Ventricular Hypertrophy Is Reversible. Sci Rep, 7(1), 1993.
[27] Faul, C., Et Al. (2011) FGF23 Induces Left Ventricular Hypertrophy. J Clin Invest, 121(11), 4393-408.
[28] Cannata, Andia, J.J.V. (2014) Torregrosa, Spanish Nephrologists and the Management of Mineral and Bone Metabolism Disorders in Chronic Kidney Disease. Nefrologia, 34(2), 175-88.
[29] Razzaque, M.S., Et Al. (2006) Premature Aging-Like Phenotype in Fibroblast Growth Factor 23 Null Mice Is A Vitamin D-Mediated Process. FASEB J, 20(6), 720-2.
[30] Sitara, D., Et Al. (2006) Genetic Ablation of Vitamin D Activation Pathway Reverses Biochemical and Skeletal Anomalies in Fgf-23-Null Animals. Am J Pathol, 169(6), 2161-70.
[31] Shimada, T., Et Al. (2004) FGF-23 Is A Potent Regulator Of Vitamin D Metabolism And Phosphate Homeostasis. J Bone Miner Res, 19(3), 429-35.
[32] Kato, Y., Et Al. (2000) Establishment of the Anti-Klotho Monoclonal Antibodies and Detection of Klotho Protein in Kidneys. Biochem Biophys Res Commun, 267(2), 597-602.
[33] Urakawa, I., Et Al. (2006) Klotho Converts Canonical FGF Receptor into A Specific Receptor for FGF23. Nature, 444(7120), 770-4.
[34] Nakano, C., Et Al. (2012) Combined Use of Vitamin D Status And FGF23 for Risk Stratification of Renal Outcome. Clin J Am Soc Nephrol, 7(5), 810-9.
[35] Nitta, K., Nagano, N., and Tsuchiya, K. (2014) Fibroblast Growth Factor 23/Klotho Axis in Chronic Kidney Disease. Nephron Clin Pract, 128(1-2), 1-10.
[36] Guan, X., Et Al. (2014) Klotho Suppresses Renal Tubulo-Interstitial Fibrosis by Controlling Basic Fibroblast Growth Factor-2 Signalling. J Pathol, 234(4), 560-72.
[37] Doi, S., Et Al. (2011) Klotho Inhibits Transforming Growth Factor-Beta1 (TGF-Beta1) Signaling And Suppresses Renal Fibrosis And Cancer Metastasis In Mice. J Biol Chem, 286(10), 8655-8665.
[38] Zhou, L., Et Al. (2013) Loss of Klotho Contributes To Kidney Injury by Derepression of Wnt/Beta-Catenin Signaling. J Am Soc Nephrol, 24(5), 771-85.
[39] Yuan, Q., Et Al. (2022) A Klotho-Derived Peptide Protects Against Kidney Fibrosis by Targeting TGF-Beta Signaling. Nat Commun, 13(1), 438.
[40] Hu, M.C., Et Al. (2010) Klotho Deficiency Is An Early Biomarker Of Renal Ischemia-Reperfusion Injury and Its Replacement Is Protective. Kidney Int, 78(12), 1240-51.
[41] Kim, J.H., Et Al. (2017) Klotho May Ameliorate Proteinuria By Targeting TRPC6 Channels In Podocytes. J Am Soc Nephrol, 28(1), 140-151.
[42] Meng, D.M., and Li, W. (2019) Research Progress on the Effect and Mechanism of Calcium and Phosphorus Metabolism Disorder on Chronic Kidney Disease. Guangxi Medical Journal, 41 (13), Page 1684-1688.
[43] Boaz, M., and Smetana, S. (1996) Regression Equation Predicts Dietary Phosphorus Intake From Estimate of Dietary Protein Intake. J Am Diet Assoc, 96(12), 1268-70.
[44] Li, H., Et Al. (2011) Effect Of Short-Term Low-Protein Diet Supplemented With Keto Acids On Hyperphosphatemia In Maintenance Hemodialysis Patients. Blood Purif, 31(1-3), 33-40.
[45] Finn, W.F. (2006) Lanthanum Carbonate versus Standard Therapy for the Treatment of Hyperphosphatemia: Safety and Efficacy in Chronic Maintenance Haemodialysis Patients. Clin Nephrol, 65(3), 191-202.
[46] Gao, X.F. (2020) Observation on the Effect of Carvellam Carbonate in the Treatment of Hemodialysis Patients with Hyperphosphatemia. Huaihai Medical Journal, 38 (04), 338-340.
[47] Ketteler, M., Et Al. (2017) Executive Summary Of The 2017 KDIGO Chronic Kidney Disease-Mineral And Bone Disorder (CKD-MBD) Guideline Update: What's Changed And Why It Matters. Kidney Int, 92(1), 26-36.
[48] Toussaint, N.D., Et Al. (2011) Attenuation of Aortic Calcification with Lanthanum Carbonate versus Calcium-Based Phosphate Binders in Haemodialysis: A Pilot Randomized Controlled Trial. Nephrology (Carlton), 16(3), 290-8.
[49] Chertow, G.M., Et Al. (2004) Determinants of Progressive Vascular Calcification in Haemodialysis Patients. Nephrol Dial Transplant, 19(6), 1489-96.
[50] Finch, J.L., Et Al. (2013) Phosphate Restriction Significantly Reduces Mortality in Uremic Rats with Established Vascular Calcification. Kidney Int, 84(6), 1145-53.

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