Як цитувати

Muminov, S. (2021). FUNCTIONAL STATE OF KIDNEYS IN PATIENTS WITH IHD. InterConf, (49), 469-476.


The aim of the study: to study the functional state of the kidneys in patients with ischemic heart disease (IHD) in the long-term period after myocardial revascularization. Material and research methods. The study included 160 patients with ischemic heart disease (IHD), hospitalized for coronary angiography and decisions on the appropriateness and choice of revascularization technique. The study did not include patients with eGFR less than 60 ml/min. All patients were prescribed standard IHD therapy. On the second day after the endovascular procedure, coronary angiography/percutaneous coronary intervention (CAG/PCI), all patients underwent determination of the blood creatinine concentration to identify patients who developed contrast-induced nephropathy (CIN). In dynamics, three months later, at the end of the first and second years of observation after revascularization, all patients underwent determination of the functional state of the kidneys: the concentration of blood creatinine, with the calculation of GFR, the concentration of parathyroid hormone, phosphorus, uric acid in the peripheral blood. According to the results of coronary angiography, 21 patients underwent surgical revascularization (coronary artery bypass grafting CABG) within a month after CAG. Endovascular revascularization (stenting of the coronary arteries) was performed in 139 patients. CIN in the early period after endovascular intervention was observed in 37 patients. The study showed that during 2 years of follow-up after coronary revascularization, there was a progressive decrease in eGFR: by the 3rd month, eGFR decreased by -17.39 ± 1.17%, by the end of the 1st year - by -43.62 ± 1.28%, by the end of the second year of follow-up - by -46.50 ± 1.79% The decrease in eGFR was significantly more pronounced in the group of patients who had CIN in the early period after endovascular intervention (37 patients): (-39 , 82 ± 2.02% by the end of the 3rd month, -54.61 ± 2.94% by the end of the 1st year and -60.10 ± 3.99% by the end of the 2nd year of follow-up versus -10, 65 ± 0.57%, -40.32 ± 1.27% and -42.41 ± 1.85% in patients with CIN, respectively, p <0.001). By the third month of follow-up, the dynamics of eGFR in the groups, depending on the revascularization method, did not differ (-16.36 ± 3.30% and -17.55 ± 1.25%, respectively). By the end of the 1st year of follow-up, in patients who underwent surgical revascularization, the decrease in eGFR was significantly more pronounced than in patients who underwent coronary artery stenting (-51.80 ± 3.51% versus -42.39 ± 1.35%, p <0.05), and the differences increased even more during the second year of observation (-57.99 ± 4.75% versus -44.76 ± 1.89%, p <0.05). Violation of the functional state of the kidneys was manifested by an increase in the concentration of blood phosphorus, parathyroid hormone and uric acid. The concentration of these markers increased during observation in parallel with a decrease in eGFR. The concentration of these substances was higher in patients after CIN. compared with patients with an uncomplicated postprocedural period. The concentration of uric acid was initially higher in the group of patients who underwent CABG compared with patients who underwent percutaneous coronary intervention PTCI. Conclusion. In patients with IHD after revascularization, there is a significant decrease in the glomerular filtration function of the kidneys by the 3rd month after the endovascular procedure and lasts at least 2 years. The most significant decrease was observed in patients with diabetes mellitus, as well as in patients who underwent CIN in the early period after endovascular intervention. The progression of CKD continues to be accompanied by an increase in the concentration of parathyroid hormone, uric acid and blood phosphates.


American Diabetes Association. Standards of medical care in dia¬betes – 2014 // Diabetes Care. – 2014. –V. 37. – Suppl. 1. – P. 14-80.

Azzalini L1, Spagnoli V1, Ly HQ2. Contrast-Induced Nephropathy: From Pathophysiology to Preventive Strategies. //Can J Cardiol. 2016 Feb;32(2):247-55.

Chrysohoou C, Bougatsos G, Magkas N, Skoumas J, Kapota A, Kopelias J, Bliouras N. et al. Peritoneal dialysis as a therapeutic solution in elderly patients with cardiorenal syndrome and heart failure: A case-series report. Hellenic J Cardiol. 2019

De Vecchis R., Baldi C. Cardiorenal syndrome type 2: from diagnosis to optimal management. Ther. Clin. Risk Manag. 2014;10:949–961.

Di Lullo L, Reeves PB, Bellasi A, Ronco C. Cardiorenal Syndrome in Acute Kidney Injury. Semin Nephrol. 2019;39(1):31–40.

Eliseev M.S. Chronic kidney disease: the role of hyperuricemia and the possibility of urate-lowering therapy. Modern Rheumatology Journal. 2018;12(1):60-65. (In Russ.)

Fliser D., Laville M., Covic A. et al., “A European Renal Best Practice (ERBP) position statement on the Kidney Disease Improving Global Outcomes (KDIGO) clinical practice guidelines on acute kidney injury: part 1: definitions, conservative management and contrast-induced nephropathy,” Nephrology Dialysis Transplantation, vol. 27, no. 12, pp. 4263–4272, 2012.

Hadjiphilippou S, Kon SP. Cardiorenal syndrome: review of our current understanding. J R Soc Med. 2016;109(1):12–17.

Iyngkaran P., Thomas M., Majoni W., Anavekar N.S., Ronco C. Comorbid Heart Failure and Renal Impairment: Epidemiology and Management. Cardiorenal Med. 2017;2:281–297.

Ji L, Su X, Qin W, Mi X, Liu F, Tang X, Li Z, Yang L. Novel risk score of contrast-induced nephropathy after percutaneous coronary intervention.//Nephrology (Carlton). 2015 Aug;20(8):544-51. doi: 10.1111/nep.12429.

Lim SS, Vos T, Flaxman AD, Danaei G, Shibuya K, Adair-Rohani H, et al. A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990-2010: a systematic analysis for the global burden of disease study 2010. Lancet. 2012;380:2224–60.

Mann D.L., Hassenfuss G. Pathophysiology of Heart Failure in part IV Heart Failure of Braunwald’s Heart Diseases. Edn Mann DL, Zipes DP, Libby P. Bonow, RO: Elsevier Saunders; 2015.

Creative Commons License

Ця робота ліцензується відповідно до Creative Commons Attribution 4.0 International License.


Дані завантаження ще не доступні.

| Переглядів: 18 | Завантажень: 9 |