Pathological changes of myocardium in the model of chronic renal insufficiency at application of low-protein diet

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.