RENAL FUNCTION AND CARDIOVASCULAR RISK IN PATIENTS WITH ARTERIAL HYPERTENSION AND OBESITY: THE ROLE OF LEPTIN AND ADIPONEKTIN

THE AIM: to evaluate the role of laboratory obesity markers in the progression of chronic kidney disease (CKD) and the development of cardiovascular complications in patients with arterial hypertension (AH) and obesity.

PATIENTS AND METHODS. 120 patients with AH stage II-III aged  from 45 to 70 years with unachieved target blood pressure values  (BP) were divided into four comparable in sex, age, frequency of  smoking occurrence, hypertension duration, the level of office  systolic AD (SBP) and diastolic blood pressure (DBP) groups  depending on the body mass index (BMI). We performed physical  examination, evaluated the renal function, laboratory markers of  obesity, analyzed the combined risk of CKD progression and the  development of cardiovascular complications.

RESULTS. There was a significant increase in the level of proteinuria (PU) and albuminuria (AU) among the patients in groups 3 and 4  compared with group 1 (301.3 [138.1, 691.0] and 305.7 [139.4,  646.9] vs 101.3 [47.9, 116.9] mg/g; 91.0 [65.9, 273.5] and 119.2  [91.0, 291.2 vs 42.2 [41.3; 51.1] mg/g, respectively), as well as a  statistically significant decrease in the glomerular filtration rate  (GFR) in patients of groups 3 and 4 compared with patients in group 1 (63,53,73 and 61,22,71 vs 72 [ 64; 98] mL / min / 1.73 m2).  Serum leptin concentration increased from group 1 to group 4 (significant differences were found between groups 2,3,4 in  comparison with group 1 and between group 4 in comparison with group 2), while the concentration of adiponectin decreased from  group 1 to group 4 (the differences were significant between groups  2,3,4 in comparison with group 1). A statistically significant inverse  correlation between GFR and leptin concentration (r = -0.42), a direct correlation between the concentration of adiponectin and GFR (r = 0.36), the inverse relationship between the concentration of adiponectin and PU (r = -0.33), AU (r = -0.24) were found.

CONCLUSION. The study showed a statistically significant  progressive deterioration in the renal function, as well as an increase in the combined risk of progression of CKD and the development of  cardiovascular complications in AH patients with an increase in  obesity with comparable values of office SAP and office DAP among  the studied groups. The revealed reliable correlation interrelations  between the parameters of renal function and obesity markers  testify to the important pathogenetic role of leptin and adiponectin in the development and progression of CKD in patients with AH and obesity.

1. Шляхто ЕВ, Недогода СВ, Конради АО. Национальные клинические рекомендации «Диагностика, лечение, профилактика ожирения и ассоциированных с ним заболеваний». СПб., 2017;1-164 [Shlyakhto EV, Nedogoda SV, Konradi AO. National clinical recommendations «Diagnosis, treatment, prevention of obesity and associated diseases». St. Petersburg, 2017;1-164]

2. World Health Organization Media Centre. Obesity and overweight. Fact sheet no Geneva: World Health Organization; 2013.

3. Hall ME, do Carmo JM, da Silva AA et al. Obesity, hypertension, and chronic kidney disease. Int J Nephrol Renovasc Dis 2014:18(7):75-88. Doi: 10.2147/IJNRD.S39739

4. Недогода СВ, Барыкина ИН, Саласюк АС. Национальные клинические рекомендации по ожирению: концепция и перспективы. Вестник Волгоградского государственного медицинского университета 2017: 1 (61):134-140 [Nedogoda SV, Barykina IN, Salasyuk AS. National clinical recommendations for obesity: concept and perspectives. Vestnik Volgogradskogo gosudarstvennogo meditsinskogo universiteta 2017: 1 (61):134-140]

5. Levey AS, Stevens LA, Schmid CH et al. A new equation to estimate glomerular filtration rate. Ann Intern Med 2009; 150: 604-612

6. Рабочая группа Российского кардиологического общества, Научного общества нефрологов России, Российской ассоциации эндокринологов, Российского медицинского общества по артериальной гипертонии, Национального общества по изучению атеросклероза, Российского научного медицинского общества терапевтов. Национальные рекомендации. Сердечно-сосудистый риск и хроническая болезнь почек: стратегии кардио-нефропротекции. Российский кардиологический журнал 2014; 8(112): 7-37 [Russian National Guidelines. Cardiovascular risk and chronic kidney disease: cardio-nephroprotection strategy. Rossiyskiy kardiologicheskiy zhurnal 2014; 8 (112): 7-37].

7. Стаценко МЕ, Деревянченко МВ, Шилина НН и др. Функциональное состояние почек у больных с сердечно- сосудистыми заболеваниями и ожирением Нефрология 2016;20(5):43-49 [Statsenko ME, Derevyanchenko MV, Shilina NN i dr. Renal function in patients with cardiovascular disease and obesity. Nephrology (Saint-Petersburg) 2016;20(5):43-49. (In Russ)]

8. Yusuf S, Hawken S, Ounpuu S et al. Obesity and the risk of myocardial infarction in 27,000 participants from 52 countries: a case-control study. Lancet 2005;366:1640–1649

9. Britton KA, Massaro JM, Murabito JM et al. Body fat distribution, incident cardiovascular disease, cancer, and all-cause mortality. J Am Coll Cardiol 2013;62:921–925

10. Стаценко МЕ, Деревянченко МВ, Пастухова ОР. Влияние комбинированной антигипертензивной терапии на суточный профиль артериального давления и показатели метаболизма у больных сахарным диабетом 2 типа. Кардиология 2014;54(11):20-24 [Statsenko ME, Derevyanchenko MV, Pastuhova OR. Effect of combined antihypertensive therapy on circadian blood pressure profile and metabolic parameters in patients with type 2 diabetes. Kardiologiya 2014; 54 (11): 20-24]

11. Стаценко МЕ, Деревянченко МВ. Кардионефропротекция – важнейшая задача антигипертензивной терапии у больных сахарным диабетом 2 типа. Кардиология 2015;55(8):43-48 [Statsenko ME, Derevyanchenko MV. Cardio-nephroprotection is the most important task of antihypertensive therapy in patients with type 2 diabetes. Kardiologiya 2015; 55 (8): 43-48]

12. Стаценко МЕ, Туркина СВ, Тыщенко ИА и др. Висцеральное ожирение как маркер риска мультиорганного поражения. Вестник Волгоградского государственного медицинского университета 2017; 1(61):10-15 [Statsenko ME, Turkina SV, Tyshchenko IA. Visceral obesity as a marker of multi-organ damage risk. Vestnik Volgogradskogo gosudarstvennogo meditsinskogo universiteta 2017; 1 (61): 10-15]

13. Hall JE, do Carmo JM, da Silva AA et al. Obesity-induced hypertension: interaction of neurohumoral and renal mechanisms. Circ Res 2015;116(6):991-1006. doi: 10.1161/CIRCRESAHA.116.305697

14. Chalmers L, Kaskel FJ, Bangbola O. The role of obesity and its bioclinical correlates in the progression of chronic kidney disease. Adv Chronic Kidney Dis 2006;13:352–364

15. Nasrallah MP, Ziyadeh FN. Overview of the physiology and pathophysiology of leptin with special emphasis on its role in the kidney. Semin Nephrol 2013 33(1):54-65. Doi: 10.1016/j.semnephrol.2012.12.005

16. Beltowski J. Leptin and the regulation of renal sodium handling and renal Na- transporting ATPases: role in the pathogenesis of arterial hypertension. Curr Cardiol Rev 2010;6:31–40

17. Zha D, Wu X, Gao P. Adiponectin and Its Receptors in Diabetic Kidney Disease: Molecular Mechanisms and Clinical Potential. Endocrinology 2017 158(7):2022-2034. Doi: 10.1210/en.2016-1765

18. Christou GA, Kiortsis DN. The role of adiponectin in renal physiology and development of albuminuria. J Endocrinol 2014 221(2):R49-61