Pathological changes of myocardium in the model of chronic renal insufficiency at application of low-protein diet
- Authors: Shved N.V1, Baykov V.V2
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Affiliations:
- Moscow City Oncology Hospital № 62
- I.P. Pavlov the First Saint-Petersburg State Medical University
- Issue: Vol 14, No 4 (2019)
- Pages: 61-65
- Section: Articles
- URL: https://genescells.ru/2313-1829/article/view/122210
- DOI: https://doi.org/10.23868/201912033
- ID: 122210
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Abstract
Myocardial damage in patients with chronic renal failure histologically manifests as hypertrophy of cardiomyocytes, intramyocardial artery walls, development of diffuse sclerosis and a change in the number of capillaries. One of the components in the complex treatment of this category of patients is a low-protein diet, however, to date there is no data on the effect of a low-protein diet on structural changes in the myocardium. The aim of the work was to assess the effect of low protein diet on myocardial structural changes in the experimental model of chronic renal failure. To reproduce the experiment of chronic renal failure, a standardized 5/6 nephrectomy model was used in wistar rats. To determine the effect of a low-protein diet on structural changes in the myocardium, two types of diet were used - a standard one and a low-protein diet (Ketosteril). The animals were sacrificed 4 months after nephrectomy. For a comparative assessment of the effect of low-protein diet on structural changes in the myocardium, histological methods of investigation and morphometry were used. The use of low-protein diet was accompanied by a less pronounced violation of biochemical blood parameters (creatinine, urea, calcium, phosphorus), as well as maintaining normal blood pressure, myocardial mass and left ventricular wall thickness. Histologically, this was manifested by a decrease in the severity of dystrophic changes in cardiomyocytes, the degree of their hypertrophy, a decrease in the area of nuclei, and a decrease in the nuclear-cytoplasmic ratio. Indices of perivascular and diffuse sclerosis were lower compared with the control group. Also, when using low-protein diet in animals with a chronic renal failure model, a decrease in the total cross-sectional area of capillaries was noted with an increase in their number in comparison with animals of the control group. Thus, the use of a low-protein diet in an experimental model of chronic renal failure has a cardioprotective effect by reducing the severity of uremia and stabilizing biochemical parameters.
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About the authors
N. V Shved
Moscow City Oncology Hospital № 62
Email: nika2485@yandex.ru
Moscow, Russia
V. V Baykov
I.P. Pavlov the First Saint-Petersburg State Medical University
Email: nika2485@yandex.ru
Saint-Petersburg, Russia
References
- Segurа J., García-Donаire J.A., Praga M. et аl. Chronic kidney diseаse as a situation of high аdded risk in hypertensive patients. J. Am. Soc. Nеphrol. 2006; 17(4): 136-40.
- Folеy R.N., Murrаy A.M., Li S. et al. Chronic kidnеy disease аnd the risk fоr cardiovasculаr diseаse, renаl replаcement, and deаth in the United Stаtes Medicаre populаtion, 1998 to 1999. J. Am. Soc. Nephrol. 2005; 16(2): 489-95.
- Londоn G.M., Guerin A.P., Mаrchais S.J. et al. Pаthophysiology of left ventriculаr hypertrophy in diаlysis pаtients. Bloоd Purif. 1994; 12(4-5): 277-83.
- Konstаm M.A., Krаmer D.G., Pаtel A.R. et al. Left vеntricular remodеling in heart failurе. JACC Cаrdiovasc. Imаging. 2011; 4(1): 98-108.
- Blаntz R.С., Deng A., Lortie M. et al. The complеx role of nitric oxidе in the rеgulation of glomеrular ultrаfiltration. Kidney Int. 2002; 61(3): 782-85.
- Maschiо G., Oldrizzi L., Tessitоre N. et al. Effects of dietary prоtein and phоsphorus restrictiоn on the progressiоn of early renal fаilure. Kidney Int. 1982; 22: 371-76.
- Isakovа T., Wolf M.S. FGF23 or PTH: which comеs first in CKD? Kidnеy Int. 2010; 78(10): 947-49.
- Bongartz L.G., Braam B., Gaillard C.A. et al. Target organ cross talk in cardiorenal syndrome: animal models. Am. J. Physiol. Renal. Physiol. 2012; 303(9): 1253-63.
- Nozynski J., Zakliczynski M., Konecka-Mrowka D. et al. Differences in antiapoptotic, proliferative activities and morphometry in dilated and ischemic cardiomyopathy: study of hearts explanted from transplant recipients. Transplant Proc. 2009; 41(8): 3171-78.
- Hatori N., Havu N., Hofman-Bang C. et al. Myocardial morphology and cardiac function in rats with renal failure. Jap. Circ. J. 2000; 64(8): 606-10.
- Dyck J.R., Hopkins T.A., Bonnеt S. Absеnce of malonyl coеnzyme A decarboxylasе in mice increasеs cardiac glucosе oxidation and protеcts the heart from ischеmic injury. Circulation. 2006; 114(16): 1721-28.
- Eghbali M., Weber K.T. Collagen and the myocardium: fibrillar structure, biosynthesis and degradation in relation to hypertrophy and its regression. Mol. Cell Biochem. 1990; 96(1): 1-14.
- Amann K., Ritz E., Wiest G. et al. A role of parathyroid hormone for the activation of cardiac fibroblasts in uremia. J. Am. Soc. Nephrol. 1994; 4(10): 1814-19.
- Cachofeiro V., Goicochea M., Vinuesa S.G. et al. Oxidative stress and inflammation, a link between chronic kidney disease and cardiovascular disease. Kidney Int Suppl. 2006; 74: 4-9.
- Franco F., Thomas G.D., Giroir B. et al. Magnetic resonance imaging and invasive evaluation of development of heart failure in transgenic mice with myocardial expression of tumor necrosis factor-alpha. Circulation. 1999; 99(3): 448-54.
- Mohammadi М.М., Badder K., Grund A. et al. The transcription factor GATA4 promotes myocardial regeneration in neonatal mice. EMBO Mol Med. 2017; 9(2): 265-279.
- Leferavich J.M., Bedelbaeva K., Samulewicz S. et al. Heart regeneration in MRL mice. PNAS USA. 2001; 98: 9830-9835.
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