Semegen-Bodak K. Features of the risk factors and clinical course of stable forms of coronary heart disease in chronic kidney disease nondiabetic origin

Українська версія

Thesis for the degree of Candidate of Sciences (CSc)

State registration number

0414U000979

Applicant for

Specialization

  • 14.01.02 - Внутрішні хвороби

03-04-2014

Specialized Academic Board

Д 35.600.05

Danylo Halytsky Lviv National Medical University

Essay

Thesis is devoted to optimizing the diagnosis and treatment of stable forms of chronic heart disease (CHD) in patients with chronic kidney disease (CKD) nondiabetic origin based on the study features of the clinical course, risk factors and their relationship, depending on the glomerular filtration rate (GFR) and pathological changes in coronary arteries (CA). It was analyzed 559 cases of patients with chronic glomerulonephritis (CGN) and examined 118 patients with stable CHD and nondiabetic CKD. It was found that the stable CHD in patients with CKD nondiabetic origin characterized by a predominance of atypical pain (55,1%), the prevalence of which increases with a decrease in GFR. In that patients, there are marked proatherogenic metabolic disorders, increase in systemic inflammation and lipid peroxidation (LPO), which are associated with a decrease in GFR. In 30% of patients recorded moderate increase in the level of HbA1c (6,5-7,3%) on the background of normal values of glycemia and glucose tolerant test. In patients with stable CHD and nondiabetic CKD were CGN at coronarography study mostly found stenoses of the distal small branches CA, while hypertensive nephropathy - multiple of proximal stenoses and pathological sinuosity. Addition of atorvastatin in the complex therapy of patients with stable CHD and nondiabetic CKD not only significantly reduces the level of atherogenic lipid fractions, uricemia - by 12,5%, HbA1c - 4,5% , C-reactive protein - by 51,4 %, but also further reduces the systolic and pulse pressure by 4,5 mm Hg and 4,8 mm Hg respectively, and also exhibits nephroprotective effect, the consequence of which is to increase GFR of 6,75 ml/min.

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