Роль регуляторов фосфорно-кальциевого обмена в развитии кардиоренального синдрома
https://doi.org/10.24884/1682-6655-2024-23-3-12-18
Аннотация
Кардиоренальный синдром – сложное состояние, относящееся к категории острой или хронической патологии почек, вызывающих сердечно-сосудистые заболевания, и, наоборот, острых или хронических заболеваний сердца, провоцирующих дисфункцию почек. Взаимосвязь патологии сердечно-сосудистой системы и почек обусловлена общностью факторов риска патологии обеих систем. В последние годы доказана связь регуляторов минерального обмена – витамина D, паратиреотропного гормона, эндокринных факторов роста фибробластов 19, 21, 23, белка Клото – с развитием сердечной недостаточности,мерцательной аритмии, гипертрофии левогожелудочка сердца, а также с прогрессированием хронической болезни почек. Ранними маркерами хронической болезни почек и сердечно-сосудистых заболеваний признаны повышенный уровень фактора роста фибробластов-23 и снижение растворимой фракции белка Клото в плазме крови. Дальнейшее изучение влияния регуляторов минерального обмена на кардиоренальный синдром создает новое направление в лечении сердечно-сосудистых заболеваний и хронической болезни почек.
Об авторах
Н. Н. Смирнова
ФГБОУ ВО «Первый Санкт-Петербургский государственный медицинский университет имени академика И. П. Павлова» Министерства здравоохранения Российской Федерации
Россия
Россия
Смирнова Наталия Николаевна – д-р мед. наук, профессор, зав. кафедрой педиатрии,
197022, Санкт-Петербург, ул. Льва Толстого, д. 6-8.
Н. Б. Куприенко
ФГБОУ ВО «Первый Санкт-Петербургский государственный медицинский университет имени академика И. П. Павлова» Министерства здравоохранения Российской Федерации
Россия
Россия
Куприенко Наталья Борисовна – канд. мед. наук, доцент,
197022, Санкт-Петербург, ул. Льва Толстого, д. 6-8.
Список литературы
1. House AA, Anand I, Bellomo R et al. Definition and classification of Cardio-Renal Syndromes: workgroup statements from the 7th ADQI Consensus Conference. Nephrol Dial Transpl ant. 2010;25(5):1416-1420.
2. Hatamizadeh P, Fonarow GC, Budoff MJ, Darabian S, Kovesdy CP, Kalantar-Zadeh K. Cardiorenal syndrome: pathophysiology and potential targets for clinical management. Nat Rev Nephrol. 2013;9(2):99-111. Doi: 10.1038/nrneph.2012.279.
3. Waziri B, Duarte R, Naicker S. Chronic kidney disease–mineral and bone disorder (CKD-MBD): Current perspectives. Int J Nephrol Renovasc Dis. 2019;12:263-276. Doi: 10.2147/IJNRD.S191156.
4. de Albuquerque Suassuna PG, Sanders-Pinheiro H, De Paula RB. Uremic cardiomyopathy: A new piece in the chronic kidney disease-mineral and bone disorder puzzle. Front Med (Lausanne). 2018;5:206. Doi: 10.3389/fmed.2018.00206.
5. Rroji M, Figurek A, Spasovski G. Should we consider the cardiovascular system while evaluating CKD-MBD? Toxins. 2020;12(3):140. Doi: 10.3390/toxins12030140.
6. Navarro-García JA, Fernández-Velasco M, Delgado C, Delgado JF, Kuro-O M, Ruilope LM et al. PTH, vitamin D, and the FGF-23–klotho axis and heart: Going beyond the confines of nephrology. Eur J Clin Invest. 2018;48(4):e12902. Doi: 10.1111/eci.12902.
7. Куприенко Н.Б., Смирнова Н.Н. Витамин D, ожирение и риск кардиоренальных нарушений у детей // Артер. гипертензия. – 2015. – Т. 21, № 1. – С. 48–58. [Kuprienko NB, Smirnova NN. Vitamin D, obesity and cardiorenal disorders risk in children. Arter Hypertens. 2015;21(1):48-58. (in Russ.)].
8. Громова О.А., Торшин И.Ю. Витамин D – смена парадигмы. – М.: ГЭОТАР-Медиа, 2021. – 736 с. [Gromova OA, Torshin IYu. Vitamin D – smena paradigmy. Moscow, GEOTAR-Media, 2021:736. (in Russ.)].
9. Naveh-Many T, Volovelsky O. Parathyroid Cell Proliferation in Secondary Hyperparathyroidism of Chronic Kidney Disease. Int J Mol Sci. 2020;21(12):4332. Doi: 10.3390/ijms21124332.
10. Anis KH, Pober D, Rosas SE. Vitamin D Analogues and Coronary Calcification in CKD Stages 3 and 4: a Randomized Controlled Trial of Calcitriol Versus Paricalcitol. Kidney Med. 2020;2(4):450-458. Doi: 10.1016/j.xkme.2020.05.009.
11. Leifheit-Nestler M, Grabner A, Hermann L, Richter B, Schmitz K, Fischer DC. Vitamin D treatment attenuates cardiac Fgf23/Fgfr4 signaling and hypertrophy in uremic rats. Nephrol Dial Transplant. 2017;32(9):1493-1503. Doi: 10.1093/ndt/gfw454.
12. Tamayo M, Martín-Nunes L, Val-Blasco A, G M-Piedras MJ, Navarro-García JA, Lage E. Beneficial effects of paricalcitol on cardiac dysfunction and remodelling in a model of established heart failure. Br J Pharmacol. 2020;177(14):32733290. Doi: 10.1111/bph.15048.
13. Molina P, Molina MD, Pallardó LM, Torralba J, Escudero V, Álvarez L et al. Disorders in bone-mineral parameters and the risk of death in persons with chronic kidney disease stages 4 and 5: the Pecera study. J Nephrol. 2021;34(4):11891199. Doi: 10.1007/s40620-020-00916-9.
14. Bacchetta J, Bernardor J, Garnier C, Naud C, Ranchin B. Hyperphosphatemia and Chronic Kidney Disease: a Major Daily Concern Both in Adults and in Children. Calcif Tissue Int. 2020;108(1):116-127. Doi: 10.1007/s00223-020-00665-8.
15. Moon H, Chin HJ, Na KY, Joo KW, Kim YS, Kim S et al. Hyperphosphatemia and risks of acute kidney injury, end-stage renal disease, and mortality in hospitalized patients. BMC Nephrol. 2019;20(1):362. Doi: 10.1186/s12882-019-1556-y.
16. Cozzolino M, Ciceri P, Galassi A, Mangano M, Carugo S, Capelli I et al. The Key Role of Phosphate on Vascular Calcification. Toxins. 2019;11(4):213. Doi: 10.3390/toxins11040213.
17. Zou J, Yu Y, Wu P, Lin F J, Yao Y, Xie Y. Serum phosphorus is related to left ventricular remodeling independent of renal function in hospitalized patients with chronic kidney disease. Int J Cardiol. 2016;221:134-140. Doi: 10.1016/j.ijcard.2016.06.181.
18. Vogt I, Haffner D, Leifheit-Nestler M. FGF23 and phosphate–cardiovascular toxins in CKD. Toxins (Basel). 2019; 11(11):647. Doi: 10.3390/toxins11110647.
19. Zangerolamo L, Carvalho M, Velloso LA, Helena CL Barbosa. Endocrine FGFs and their signaling in the brain: Relevance for energy homeostasis. Eur J Pharmacol. 2024; 963:176248. Doi: 10.1016/j.ejphar.2023.176248.
20. Hao Y, Zhou J, Zhou M et al. Serum levels of fibroblast growth factor 19 are inversely associated with coronary artery disease in Chinese individuals. PLoS One. 2013;8(8):e72345. Doi: 10.1371/journal.pone.0072345.
21. Flippo KH, Potthoff MJ. Metabolic Messengers: FGF21. Nat Metab. 2021;3(3):309-317. Doi: 10.1038/s42255021-00354-2.
22. Кузник Б.И, Хавинсон В.Х, Линькова Н.С. и др. Факторы роста фибробластов FGF19, FGF21, FGF23 как эндокринные регуляторы физиологических функций и геропротекторы. Эпигенетические механизмы регуляции // Успехи соврем. биол. – 2017. – T. 131, № 1. – C. 84–99. [Kuznik BI, Khavinson VKh, Linkova NS, Ryzhak GA, Sall’ TS, Trofimova SV. Faktory rosta fibroblastov FGF19, FGF21, FGF23 kak endokrinnyye regulyatory fiziologicheskikh funktsiy i geroprotektory. Epigeneticheskiye mekhanizmy regulyatsii. Uspekhi sovremennoy biologii. 2017;131(1):84-99. (in Russ.)].
23. Itoh N, Ohta H, Konishi M. Endocrine FGFs: evolution, physiology, pathophysiology, and pharmacotherapy. Front Endocrinol (Lausanne). 2015;6:154. Doi: 10.3389/fendo.2015.00154.
24. Vázquez-Sánchez S, Poveda J, Navarro-García JA, González-Lafuente L, Rodríguez-Sánchez E, Ruilope LM, Ruiz-Hurtado G. An Overview of FGF-23 as a Novel Candidate Biomarker of Cardiovascular Risk. Front Physiol. 2021; 12:632260. Doi: 10.3389/fphys.2021.632260.
25. Fukumoto S. FGF23-FGF receptor/Klotho pathway as a new drug target for disorders of bone and mineral metabolism. Calcified Tissue Int. 2016;98(4):334-340. Doi: 10.1007/s00223-015-0029-y.
26. Silva AP, Mendes F, Carias E, Gonçalves RB, Fragoso A, Dias C et al. Plasmatic Klotho and FGF23 Levels as Biomarkers of CKD-Associated Cardiac Disease in Type 2 Diabetic Patients. Int J Mol Sci. 2019;20(7):1536. Doi: 10.3390/ijms20071536.
27. Cheng N, He Y, Dang A, Lv N, Wang X, Li H. Association between plasma fibroblast growth factor 23 and left ventricular mass index in patients with Takayasu arteritis. Clin Rheumatol. 2020;39(5):1591-1599. Doi: 10.1007/s10067-01904895-6.
28. Patel RB, Ning H, de Boer IH, Kestenbaum B, Lima JAC, Mehta R et al. Fibroblast growth factor 23 and long-term cardiac function: the multi-ethnic study of atherosclerosis. Circ Cardiovasc Imaging. 2020;13(11):e011925. Doi: 10.1161/CIRCIMAGING.120.011925.
29. Silva AP, Mendes F, Carias E, Gonçalves RB, Fragoso A, Dias C. Plasmatic Klotho and FGF23 Levels as Biomarkers of CKD-Associated Cardiac Disease in Type 2 Diabetic Patients. Int J Mol Sci. 2019;20(7):1536. Doi: 10.3390/ijms20071536.
30. Böckmann I, Lischka J, Richter B, Deppe J, Rahn A, Fischer DC. FGF23-Mediated Activation of Local RAAS Promotes Cardiac Hypertrophy. Int J Mol Sci. 2019;20(18):21-24. Doi: 10.3390/ijms20184634.
31. Son T, Fu Y, Wang Y, Li W, Zhao J, Wang X. FGF23 correlates with endocrine and metabolism dysregulation, worse cardiac and renal function, inflammation level, stenosis degree, and independently predicts in-stent restenosis risk in coronary heart disease patients underwent drug-eluting-stent PCI. BMC Cardiovasc Disord. 2021;21(1):24. Doi: 10.1186/s12872-020-01839-w.
32. Nayor M, Larson MG, Wang N, Santhanakrishnan R, Lee DS, Tsao CW et al. The association of chronic kidney disease and microalbuminuria with heart failure with preserved vs. reduced ejection fraction. Eur J Heart Fail. 2017; 19(5):615-623. Doi: 10.1002/ejhf.778.
33. Kanagala P, Arnold JR, Khan JN, Singh A, Gulsin GS, Eltayeb M et al. Fibroblast-growth-factor-23 in heart failure with preserved ejection fraction: relation to exercise capacity and outcomes. ESC Heart Fail. 2020;7(6):4089-4099. Doi: 10.1002/ehf2.13020.
34. Roy C, Lejeune S, Slimani A, de Meester C, Ahn As SA, Rousseau MF. Fibroblast growth factor 23: a biomarker of fibrosis and prognosis in heart failure with preserved ejection fraction. ESC Heart Fail. 2020;7(5):2494-2507. Doi: 10.1002/ehf2.12816.
35. Chua W, Purmah Y, Cardoso VR, Gkoutos GV, Tull SP, Neculau G et al. Data-driven discovery and validation of circulating blood-based biomarkers associated with prevalent atrial fibrillation. Eur Heart J. 2019;40(16):1268-1276. Doi: 10.1093/eurheartj/ehy815.
36. Dong Q, Li S, Wang W, Han L, Xia Z, Wu Y. FGF23 regulates atrial fibrosis in atrial fibrillation by mediating the STAT3 and SMAD3 pathways. J Cell Physiol. 2019;234(11):1950219510. Doi: 10.1002/jcp.28548.
37. Mathew JS, Sachs MC, Katz R, Patton KK, Heckbert SR, Hoofnagle AN et al. Fibroblast growth factor-23 and incident atrial fibrillation: the Multi-Ethnic Study of Atherosclerosis (MESA) and the Cardiovascular Health Study (CHS). Circulation. 2014;130(4):298-307. Doi: 10.1161/circulationaha.113.005499.
38. Eisner DA, Caldwell JL, Kistamás K, Trafford AW. Calcium and excitation-contraction coupling in the heart. Circ Res. 2017;121(2):181-195. Doi: 10.1161/CIRCRESAHA.117.310230.
39. Pescatore LA, Gamarra LF, Liberman M. Multifaceted mechanisms of vascular calcification in aging. Arterioscler Thromb Vasc Biol. 2019;39(7):1307-1316. Doi: 10.1161/atvbaha.118.311576.
40. Donate-Correa J, Martín-Núñez E, Hernández-Carballo C, Ferri C, Tagua VG, Delgado-Molinos A et al. Fibroblast growth factor 23 expression in human calcified vascular tissues. Aging. 2019;11(18):7899-7913. Doi: 10.18632/aging.102297.
41. Vázquez-Sánchez S, Poveda J, Navarro-García JA, González-Lafuente L, Rodríguez-Sánchez E, Ruilope LM, Ruiz-Hurtado G. An Overview of FGF-23 as a Novel Candidate Biomarker of Cardiovascular Risk. Front Physiol. 2021; 12:632260. Doi: 10.3389/fphys.2021.632260.
42. Vergara N, de Mier MVPR, Rodelo-Haad C, Revilla-González G, Membrives C, Díaz-Tocados JM, Martínez-Moreno JM, Torralbo AI, Herencia C, Rodríguez-Ortiz ME, López-Baltanás R, Richards WG, Felsenfeld A, Almadén Y, Martin-Malo A, Ureña J, Santamaría R, Soriano S, Rodríguez M, Muñoz-Castañeda JR. The direct effect of fibroblast growth factor 23 on vascular smooth muscle cell phenotype and function. Nephrol Dial Transplant. 2023;38(2):322-343. Doi: 10.1093/ndt/gfac220.
43. Guo Y, Zhuang X, Huang Z, Zou J, Yang D, Hu X et al. Klotho protects the heart from hyperglycemia-induced injury by inactivating Ros and Nf-κB-mediated inflammation both in vitro and in vivo. Biochim Biophys Acta Mol Basis Dis. 2018;1864(1):238-251. Doi: 10.1016/j.bbadis.2017.09.029.
44. Drew DA, Katz R, Kritchevsky S, Ix J, Shlipak M, Gutiérrez OM. Association between Soluble Klotho and Change in Kidney Function: the Health Aging and Body Composition Study. J Am Soc Nephrol. 2017;28(6):1859-1866. Doi: 10.1681/ASN.2016080828.
45. Chen Y, Chen YX, Huang C, Duan ZB, Xu CY. The Clinical Value of Klotho and FGF23 in Cardiac Valve Calcification Among Patients with Chronic Kidney Disease. Int J Gen Med. 2021;14:857-866. Doi: 10.2147/IJGM.S299197.
46. Leifheit-Nestler M, Richter B, Basaran M, Nespor J, Vogt I, Alesutan I. Impact of Altered Mineral Metabolism on Pathological Cardiac Remodeling in Elevated Fibroblast Growth Factor 23. Front Endocrinol (Lausanne). 2018;9:333. Doi: 10.3389/fendo.2018.00333.
47. Navarro-García JA, Rueda A, Romero-García T, Aceves-Ripoll J, Rodríguez-Sánchez E, González-Lafuente L. Enhanced Klotho availability protects against cardiac dysfunction induced by uraemic cardiomyopathy by regulating Ca. Br J Pharmacol. 2020;177(20):4701-4719. Doi: 10.1111/bph.15235.
Рецензия
Для цитирования:
Смирнова Н.Н., Куприенко Н.Б. Роль регуляторов фосфорно-кальциевого обмена в развитии кардиоренального синдрома. Регионарное кровообращение и микроциркуляция. 2024;23(3):12-18. https://doi.org/10.24884/1682-6655-2024-23-3-12-18
For citation:
Smirnova N.N., Kuprienko N.B. Role of phosphorus-calcium metabolism regulators in cardiorenal syndrome development. Regional blood circulation and microcirculation. 2024;23(3):12-18. (In Russ.) https://doi.org/10.24884/1682-6655-2024-23-3-12-18
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