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– 2003. – Vol. 124 (6). – P. 2093–2097.40. Anand I.S. Pathogenesis of anemia in cardiorenal disease. // Rev Cardiovasc Med. –2005. – Vol. 6 (Suppl 3). – P.13–21.41. Angela Yee-Moon Wang, Kar-Neng Lai. Use of Cardiac Biomarkers in End-StageRenal Disease. // J Am Soc Nephrol. – 2008. – Vol. 19.
– Р. 1643–1652.12942. Baker J.F., Krishnan E., Chen L. et al. Serum uric acid cardiovascular disease:recent developments, and where do they leave us? // Am. J. Med. – 2005. – Vol. 118.– P. 816–826.43. Bash L.D., Erlinger T.P., Coresh J. et al. Inflammation, hemostasis, and the risk ofkidney function decline in the atherosclerosis risk in communities (ARIC) study. //Am J Kidney Dis. – 2009.
– Vol. 53 (4). – P. 596–605.44. Bock J.S., Gottlieb S.S. Cardiorenal syndrome: new perspectives. // Circulation.–2010 – Vol. 121 (23). – P. 2592–2600.45. Bolton C.H., Downs L.G., Victory J.G. et al. Endothelial dysfunction in chronicrenal failure: roles of lipoprotein oxidation and pro-inflammatory cytokines. //Nephrol Dial Transplant. – 2001.
– Vol. 16 (6). – P. 1189–1197.46. Bongartz L.G., Cramer M.J., Doevendans P.A. et al. The severe cardiorenalsyndrome: ‘Guyton revisited’. // Eur Heart J. – 2005. – Vol. 26 (1). – P. 11–17.47. Brutsaert D.L. Diagnosing primary diastolic heart failure. // Eur Heart J. – 2000. –Vol. 21. – Р. 94–96.48. Castello-Boerrigter L.C., Boerrigter G., Redfield M. M. et al. Amino-terminal proB-type natriuretic peptide an B-natriuretic peptide in the general community:determaintion and detection of left vetricular disfunction.
// J Am Coll Cardiol. –2006.– Vol. 47. – Р. 345-353.49. Chen S., Law C.S., Olsen K, Gardner D.G. A role for the cell cycle phosphataseCdc25a in vitamin D-dependent inhibition of adult rat vascular smooth muscle cellproliferation. // J Steroid Biochem Mol Biol. – 2010. – Vol. 122. – P. 326–332.50. Cheng X.W., Obata K., Kuzuya M. et al. Elastolytic cathepsin induction/ activationsystem exists in myocardium and is upregulated in hypertensive heart failure.
//Hypertension. – 2006. – Vol. 48 (5). – P. 979–987.51. Cohn J.N. Structural basis for heart failure: ventricular remodeling and itspharmacological inhibition. // Circulation. – 1995. – Vol. 91 (10). – P. 2504-2507.52. Danesh J., Collins R., Appleby P., Peto R. Association of fibrinogen, C-reactiveprotein, albumin, or leucocyte count with coronary heart disease. // JAMA. – 1998. –Vol.
279 (18). – P. 1477-1482.13053. Davis S., Kümpers P., Seidler V. et al. Diagnostic value of N-terminal proB-typenatriuretic peptide (NT-proBNP) for left ventricular dysfunction in patients withchronic kidney disease stage 5 on haemodialysis. // Nephrol. Dial. Transplant. –2008. – Vol. 23.
– P.1370–1377.54. Dervisoglu E., Kozdag G., Etiler N., Kalender B. Association of glomerularfiltration rate and inflammation with left ventricular hypertrophy in chronic kidneydisease patients. // Hippokratia 2012. – Vol. 16 (2). – P. 137–142.55. Dhaun N., Goddard J., Webb D.J. The endothelin system and its antagonism inchronic kidney disease. // J Am Soc Nephrol. – 2006. – Vol.
17 (4). – P. 943–955.56. Dollery C.M., McEwan J.D., Henney A.M. Matrix metalloproteinase andcardiovascular disease. // Circ Res. – 1995. – Vol. 77 (5). – P. 863-868.57. Donald G. Vidt. Inflammation in Renal Disease. // Am J Cardiol. – 2006. – Vol. 97(1). – P. 20–27.58. Dounousi Е., Koliousi Е., Papagianni А. et al. Mononuclear leukocyte apoptosis andinflammatory markers in patients with Chronic Kidney Disease. // Am J Nephrol. –2012. – Vol. 36. – P. 531–536.59.
Eckardt K.-U., Clyne N., Drueke T. et al. Variables of left ventricular geometry andfunction in patients enrolled in the create trial. // In ERA-EDTA XXXIX Congress,Copenhagen. – 2002. – Abstract 136.60. Fabbian F., Cantelli S., Molino C. et al. Pulmonary hypertension in dialysis patients:a cross-sectional Italian study.
// Int J Nephrol. – 2010. – Vol. 2011. – P. 283- 475.61. Fenster B.E, Lasalvia L., Schroeder J.D. et al. Cystatin C: a potential biomarker forpulmonary arterial hypertension. // Respirology. – 2014. – Vol. 19 (4). – P. 583-589.62. Ferdinandy P., Schultz R. Nitric oxide, superoxide and peroxinitrite in myocardialischemiareperfusion injure and preconditioning. // Br J Pharmacol. – 2003.
– Vol.138 (4).– P. 532-542.63. Foley R.N., Curtis B.M., Randell E.W. et al. Left ventricular hypertrophy in newhemodialysis patients without symptomatic cardiac disease. // Clin. J Am. Soc.Nephrol.– 2010. – Vol. 5 (5). – P. 805–813.13164. Foley R.N., Parfrey P.S., Harnett J.D. et al. Clinical and echocardiographic diseasein patients starting end-stage renal disease therapy. // Kidney Int. – 1995.
– Vol. 47(1). – P. 186-192.65. Fried L, Solomon C, Shlipak M et. Al. Inflammatory and prothrombotic markersand the progression of renal disease in elderly individuals. // J Am Soc Nephrol. –2004.– Vol. 15 (12). – P. 3184–3191.66.
Gan C.T., McCann G.P., Marcus J.T. et al. NT-proBNP reflects right ventricularstructure and function in pulmonary hypertension. // Eur Respir J. – 2006. – Vol. 28(6). – P. 1190–1194.67. Ganguly P.K. Catecholamines and cardiovascular disorders: pathophysiologicconsiderations. // Am Heart J. – 1989. – Vol. 118. – P. 868-872.68. Garg A.X., Clark W.F., Haynes R.B., House A.A. Moderate renal insufficiency andthe risk of cardiovascular mortality: results from the NHANES I.
// Kidney Int. –2002. – Vol. 61 (4). – P. 1486-1494.69. Gerdes A.M., Capasso J.M. Structural remodeling and mechanical dysfunction ofcardiac myocytes in heart failure. // J Mol Cell Cardiol. – 1995. – Vol. 27. – P. 84985670. Go A.S., Chertow G.M., Fan D. et al. Chronic kidney disease and the risks of death,cardiovascular events, and hospitalization. // N Engl J Med.
– 2004. – Vol. 351(13).– P. 1296-1305.71. Guazzi M. Alveolar gas diffusion abnormalities in heart failure. // J Card Fail. –2008. – Vol. 14 (8). – P. 695–702.72. Guyton A.C. The surprising kidney-fluid mechanism for pressure control – itsinfinite gain! // Hypertension. – 1990. – Vol. 16 (6). – P. 725–730.73. Hajjar V., Schreiber M.J. Does measuring natriuretic peptides have a role in patintswith chronic kidney disease? // Cleveland clinic journal of medicine.
– 2009. – Vol.76. – P. 476–478.74. Hall A., Håkansson K., Mason R.W. et al. Structural basis for the biologicalpecificity of cystatin C. // Journal of Biological Chemistry. – 1995. – Vol. 270(10). – P. 5115-5121.13275. Hallan S.I., Stevens P. Screening for chronic kidney disease: which strategy? //J Nephrol.
– 2010. – Vol. 23 (2). – P. 147-155.76. Havlucu Y., Kursat S., Ekmekci C. et al. Pulmonary hypertension in patients withchronic renal failure. // Respiration. – 2007. – Vol. 74 (5). – P. 503–510.77. Herget-Rosenthal S., Bökenkam A., Hofmann W. How to estimate GFR – serumcreatinine, serum cystatin C or equations? // Clin Biochem. – 2007. – Vol.
40 (3-4).–P. 153–61.78. Hirota H., Yoshida K., Kishimoto Т., Taga T. Continuous activation of gp130 asignal-transduction receptor component for interleukin 6-related cytokines, causesmyocardial hypertrophy in mice. // Proc Natl Acad USA. – 1995. – Vol. 92. – P.4862-4866.79. Hirsch A.T., Pinto Y.M., Schunkert H., Dzau V.J. Potential role of the tissue reninangiotensin system in the pathophysiology of congestive heart failure. // Am JCardiol.
– 1990. – Vol. 66. – P. 22D–30D.80. Humbert M., Sitbon O., Simonneau G. Treatment of pulmonary arterialhypertension. // N Engl J Med. – 2004. – Vol. 351 (14). – P. 1425–1436.81. Hutchison J.A. Vascular calcification in dialysis patients. // Prilozi. – 2007. – Vol.28 (1). – P. 215-224.82. Hüting J. Course of left ventricular hypertrophy and function in end-stage renaldisease after renal transplantation. // Am J Cardiol. – 1992.
– Vol. 70. – P. 14811484.83. Irani K. Oxidant signaling in vascular cell growth, death and survival. // Circ Res. –2000. – Vol. 87. – P. 179-190.84. Irish A. CVD, fibrinogen and acute phase response; association with lipid and BP inpatients with chronic renal disease. // Atherosclerosis. – 1998. – Vol. 137. – P. 133139.85. Iwanaga Y., Nishi I., Furuichi S.
et al. B-type natriuretic peptide strongly reflectsdiastolic wall stress in patient with chronic heart failure: comparison betweensystolic and diastolic heart failure. // J Am Coll Cardiol. – 2006. – Vol. 47 (4). – Р.742-748.13386. Ix J.H., Shlipak M.G., Chertow G.M., Ali S. et al. Cystatin C, left ventricularhypertrophy, and diastolic dysfunction: data from the Heart and Soul Study. //J Cardiac Fail.
– 2006. – Vol. 12. – P. 601– 607.87. Jernberg T., Lindahl B., James S. et al. Cystatin C – A novel predictor of outcome insuspected or confirmed non-STelevation acute coronary syndromes. // Circulation. –2004. – Vol. 110 (16). – P. 2342–2348.88. Joachim H. Cystatin C, left ventricular hypertrophy, and diastolic dysfunction: DataFrom the Heart and Soul Study. // Journal of Cardiac Failure. – 2006. – Vol. 12 (8).–P.
601-607.89. Kang D.H., Nakagawa T., Feng L. et al. A role for uric acid in the progression ofrenal disease. // J. Am. Soc. Nephrol. – 2002. – Vol. 13(12). – P. 2888–2897.90. Khan I.A., Fink J., Nass C. et al. N-terminal pro-B-type natriuretic peptide and Btype natriuretic peptide for identifying coronary artery disease and left ventricularhypertrophy in ambulatory chronic kidney disease patients.
// Am J Cardiol. – 2006.– Vol. 97. – P. 1530–1534.91. Kielstein J.T., Bode-Boger S.M., Klein G. et al. Endogenous nitric oxide synthaseinhibitors and renal perfusion in patients with heart failure. // Eur J Clin Invest. –2003. – Vol. 33 (5). – P. 370–375.92. Kinnunen P., Vuolteenaho O., Ruskoaho H. Mechanisms of atrial and brainnatriuretic peptide release from rat ventricular myocardium: effect of stretching.
//Endocrinology. – 1993. – Vol. 132 (5). – P. 1961–1970.93. Kiyosue A., Hirata Y., Ando J. et al. Plasma cystatin C concentration reflects theseverity of coronary artery disease in patients without chronic kidney disease. //Circ J. – 2010. – Vol. 74. – P. 2441–2447.94. Kramer H., Toto R., Peshock R. et al. Association between chronic kidney diseaseand coronary artery calcification: the DALLAS Heart Study. // J Am Soc Nephrol.