Rostov State Medical University; Rostov-on-Don, the Russian Federation
*Corresponding author: Liliya I. Rudenko, PhD. Rostov State Medical University, Rostov-on-Don, Russia. E-mail: email@example.com
Published: March 16, 2016. DOI: 10.21103/Article6(1)_OA4
The aim of the present study was the integrated assessment of the role of non-traditional factors (inflammation, malnutrition, calcium-phosphorus disorder and imbalance in the concentration of inducers and inhibitors of calcification) in forming cardiovascular calcification (CVC) and the structural-functional rearrangement of LV myocardium in patients with chronic kidney disease (CKD) receiving hemodialysis (HD).
Materials and Methods: The present study included 84 HD patients with CKD 5D stage. We evaluated 3 components of the Dialysis Malnutrition Score (DMS), according to which body mass index (BMI), the level of serum albumin, and the percent saturation of transferrin with iron were determined. We also analyzed CRP, fibrinogen, and beta-2 microglobulin, and calculated the number of points (from zero to 2) according to the Glasgow Prognostic Score (GPS), which allowed us to combine indicators of inflammation and make a common prognostic assessment.
The serum levels of protein alpha-Klotho и FGF-23 were determined by enzyme immunoassay. Echocardiographic measurements were performed using B-mode, M-mode and Doppler-mode. Different patterns of LV geometry were identified according to Ganau et al. (1992).
The severity of calcification was estimated by a semi-quantitative scale for assessing the degree of calcification of heart structures according to the National recommendations for CKD-MBD (2010).
Results: The increased risk for development of CVC, LVH, and diastolic dysfunction was associated with markers of malnutrition, anemia, and inflammation in HD patients. Reduced serum alpha-Klotho level, hypoalbuminemia and a high level of FGF-23 had a prognostic value in CVC formation.
- Moody W.E. Arterial disease in chronic kidney disease. Heart 2013; 99; 6: 365-72.
- Foley R. Serum phosphorus levels associate with coronary atherosclerosis in young adults. J Am Soc Nephrol 2009; 20: 397–404.
- Block G.A. Mineral metabolism, mortality, and morbidity in maintenance hemodialysis. J Am Soc Nephrol 2004; 15; 2208–2218.
- Ganesh S.K. Association of elevated serum PO(4), Ca × PO(4) product, and parathyroid hormone with cardiac mortality risk in chronic hemodialysis patients. J Am Soc Nephrol 2001; 12; 2131–2138.
- Forrest L.M. A prospective longitudinal study of performance status, an inflammation-based score (GPS) and survival in patients. Br J Cancer 2005; 92; 10; 1834–1836.
- Kauppila LI, Polak JF, Cupples LA, et al. New indices to classify location, severity and progression of calcific lesions in the abdominal aorta: a 25-year follow-up study. Atherosclerosis. 1997;132:245–250.
- Rambod M. Association of Malnutrition-Inflammation Score with quality of life and mortality in hemodialysis patients: a 5-year prospective cohort study 2009; 53 (2); 298-309.
- Fouque D. Use of a renal-specific oral supplement by haemodialysis patients with low protein intake does not increase the need for phosphate binders and may prevent a decline in nutritional status and quality of life. Nephrol Dial Transplant 2008; 18 (9); 2902–2910.
- Stenvinkel P. Inflammation in end-stage renal disease: sources, consequences, and therapy 2002; 15; №5; 329-337.
- Rudenko L.I., Batjushin M.M., Kastanajan A.A., Vorob'ev B.I. Cardio-vascular calcification risk prognosis in patients receiving chronic hemodialysis. Nefrologija 2015; 19; №5; 72-76
- Yan L. Calgranulin-mediated inflammation accelerates left ventricular hypertrophy and aortic valve sclerosis in chronic kidney disease in a receptor for advanced glycation end products-dependent manner 2014; 34(7); 1399-411.
- Barry SP. What causes a broken heart--molecular insights into heart failure. Int Rev Cell Mol Biol 2010; 284; 113–179.
- Lee JK, Lin HH, Tsai CT, Chen JJ, Kuo CC, et al. (2012) Differential association of proinflammatory cytokines with left ventricular diastolic dysfunction in subjects with and without continuous ambulatory peritonealdialysis. Nutr Metab Cardiovasc Dis 22:974–980
- Smeets PJ, Teunissen BE, Planavila A, de Vogel-van den Bosch H, Willemsen PH, van der Vusse GJ, et al. Inflammatory pathways are activated during cardiomyocyte hypertrophy and attenuated by peroxisome proliferator-activated receptors PPARalpha and PPARdelta.J Biol Chem. 2008 Oct 24;283(43):29109-18.
- Wang AY, Wang M, Woo J, Lam CW, Lui SF, Li PK, et al. Inflammation, residual kidney function, and cardiac hypertrophy are interrelated and combine adversely to enhance mortality and cardiovascular death risk of peritoneal dialysis patients. J Am Soc Nephrol; 2004; 15 (8); 2186-94.\
- Masuda M, Ishimura E, Ochi A, Tsujimoto Y, Tahahra H, Okuno S, Tabata T, Nishizawa Y, Inaba M.Serum β2-microglobulin correlates positively with left ventricular hypertrophy in long-term hemodialysis patients. Nephron Clin Pract. 2014;128(1-2):101-6.
- Aronow WS, Ahn C, Kronzon I. Association of mitral annular calcium with symptomatic peripheral arterial disease in older persons. Am J Cardiol.; 2001; 88 (3); 333–4.
- Hu MC, Shi M, Zhang J, Quiñones H, Griffith C, Kuro-o M, et al. Klotho deficiency causes vascular calcification in chronic kidney disease.J Am Soc Nephrol. 2011 Jan;22(1):124-36.
- Rudenko L.I., Batjushin M.M., Kastanajan A.A., Vorob'ev B.I., Sarvilina I. V. The serum alpha-Klotho, FGF-23 and their participation in cardiovascular calcification. Klinicheskaja nefrologija 2015; №1; 23-26.
- Nasrallah MM, El-Shehaby AR, Salem MM, Osman NA, El Sheikh E, Sharaf El, et al. Fibroblast growth factor-23 (FGF-23) is independently correlated to aortic calcification in haemodialysis patients. Nephrol Dial Transplant; 2010; 25(8); 2679–85.
- Gutierrez OM, Mannstadt M, Isakova T, Rauh-Hain JA, Tamez H, Shah A, Smith K, Lee H, Thadhani R, Juppner H, Wolf M: Fibroblast growth factor 23 and mortality among patients undergoing hemodialysis. N Engl J Med 359: 584–592, 2008
- Ix JH, Shlipak MG, Wassel CL, Whooley MA: Fibroblast growth factor-23 and early decrements in kidney function: The Heart and Soul Study. Nephrol Dial Transplant 25: 993–997, 2010
- Kanbay M, Nicoleta M, Selcoki Y, Ikizek M, Aydin M, Eryonucu B, Duranay M, Akcay A, Armutcu F, Covic A: Fibroblast growth factor 23 and fetuin A are independent predictors for the coronary artery disease extent in mild chronic kidney disease. Clin J Am Soc Nephrol 5: 1780–1786, 2010
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