Effect of aldosterone on collagen formation markers in patients with myocardial infarction and renal dysfunction

Authors

  • K .V. Tashchuk “Bukovinіan State Medical University”, Chernivtsi, Ukraine,
  • O. S. Polianska “Bukovinіan State Medical University”, Chernivtsi, Ukraine,
  • O. I. Gulaga “Bukovinian State Medical University”, Chernivtsi, Ukraine,

DOI:

https://doi.org/10.14739/2310-1210.2018.4.135791

Keywords:

myocardial infarction, aldosterone, chronic renal diseases

Abstract

 

Aim. To investigate the level of aldosterone, angiotensin-converting enzyme and the blood proteolytic system activity in patients with acute myocardial infarction on the background of chronic kidney disease.

Materials and methods. The observation group consisted of 106 patients who underwent in-patient treatment for acute Q-myocardial infarction. Patients were divided into 2 groups depending on the glomerular filtration rate (GFR): Group I consisted of patients with GFR ≤90 ml / h, Group II – with GFR >90 ml / h.

Results. It was found that in patients with AMI of Group I the level of aldosterone was significantly higher than in the Group II patients (P < 0.05). The concentration of angiotensin-converting enzyme in patients of the Group I was significantly higher than in the comparison group (P < 0.05). The increase in blood serum proteolytic activit was observed in the Group I patients: azoalbumin (P > 0.05), azocasein (P < 0.05) and azocollagen (P > 0.05). A highly probable negative correlation of aldosterone level with proteolysis activity when tested on azocollagen (P < 0.01) was revealed, and it confirms the role of aldosterone in the processes of collagen formation. The pathogenetically substantiated classification of myocardial fibrosis proposed by the authors should be up for discussion: 1. replacement fibrosis: - local (with aneurysm of the left ventricle or without it); diffuse (with a left ventricular preserved ejection fraction – more than 40 % or with a decrease in the left ventricular ejection fraction – less than 40 %); 2. interstitial fibrosis; 3. endomyocardial fibrosis.

Conclusions. In patients with acute myocardial infarction at the stage II of chronic kidney disease a significant increase in the aldosterone and angiotensin-converting enzyme levels has been found, which could result in heart failure progression. An increase in the serum proteolytic activity by the level of azocasein lysis and a highly probable negative correlation between aldosterone level and activity of proteolysis when tested on azocollagen (r-0,36; P < 0.01) indicate an unfavorable course of myocardial infarction in patients with renal dysfunction.

 

References

Martinez-Martínez, N. E., Ibarrola, J., Fernandez-Celis, A., Santamaria, E., Fernandez-Irigoyen, J., Rossignol, P., et al. // (2017). Differential Proteomics Identifies Reticulocalbin-3 as a Novel Negative Mediator of Collagen Production in Human Cardiac Fibroblasts. Sci. Rep., 7(1), 121–192. doi: 10.1038/s41598-017-12305-7.

Mahalias, V. M., Mixieiev, A. O., Rohovyi, Yu. Ye., Shcherbinina, A. V., Turchynets, T. N., & Chipko, T. M. (2001). Suchasni metodyky eksperymentalnykh ta klinichnykh doslidzhen Centralnoi naukovo-doslidnoi laboratorii [Modern methods of experimental and clinical research of the Central Research Laboratory]. Chernivtsi: BDMA. [in Ukrainian].

Rossi, G. P., Seccia, T. M., Barton, M., Danser, A. H., de Leeuw, P. W., Dhaun, N., et al. (2018). Endothelial factors in the pathogenesis and treatment of chronic kidney disease Part I: General mechanisms: a joint consensus statement from the European Society of Hypertension Working Group on Endothelin and Endothelial Factors and The Japanese Society of Hypertension. J. Hypertens, 36(3), 451–461. doi: 10.1097/HJH.0000000000001599.

Hyndman, K. A., Mironova, E. V., Giani, J. F., Dugas, C., Collins, J., McDonough, A. A., et al. (2017). Collecting Duct Nitric Oxide Synthase 1Я Activation Maintains Sodium Homeostasis During High Sodium Intake Through Suppression of Aldosterone and Renal Angiotensin II Pathways. J Am Heart Assoc.,6(10), pii: e006896. doi: 10.1161/JAHA.117.006896.

Brown, N. J. (2013). Contribution of aldosterone to cardiovascular and renal inflammation and fibrosis. Nat Rev Nephrol., 9(8), 459–69. doi: 10.1038/nrneph.2013.110.

Park, E. J., Jung, H. J., Choi, H. J., Cho, J. I., Park, H. J., & Kwon, T. H. (2018). MiR-34c-5p and CaMKII are involved in aldosterone-induced fibrosis in kidney collecting duct cells. Am J Physiol Renal Physiol., 314(3), F329–F342. doi: 10.1152/ajprenal.00358.2017.

Azibani, F., Fazal, L., Chatziantoniou, C., Samuel, J., & Delcayre, C. (2013). Aldosterone mediates cardiac fibrosis in the setting of hypertension patients. Curr Hypertens Rep, 15(4), 395–400. doi: 10.1007/s11906-013-0354-3.

Tian, J., An, X., & Niu, L. (2017). Myocardial fibrosis in congenital and pediatric heart disease. Exp. Ther. Med., 13(5), 1660–1664. doi: 10.3892/etm.2017.4224.

Donderski, R., Strozecki, P., Sulikowska, B., Grajewska, M., Miskowiec, I., Stefaсska, et al. (2017) Aldosterone antagonist therapy and its relationship with inflammation, fibrosis, thrombosis, mineral-bone disorder and cardiovascular complications in peritoneal dialysis (PD) patients. Int. Urol. Nephrol., 49(10), 1867–1873. doi: 10.1007/s11255-017-1655-2.

Hulaha, O. I., Tashchuk, V. K., Polianska, O. S., (patentee) (2011). Patent №63277 Ukraina МПК A61B 5/00. Sposib prohnozuvannia perebihu infarktu miokarda za pokaznykom kolahenolitychnoi aktyvnosti [Patent №63277 Ukraine МПК A61B 5/00. Method of forecasting the course of myocardial infarction on the indicator of collagenolytic activity]. Bіuleten, 19. [in Ukrainian].

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How to Cite

1.
Tashchuk K .V., Polianska OS, Gulaga OI. Effect of aldosterone on collagen formation markers in patients with myocardial infarction and renal dysfunction. Zaporozhye medical journal [Internet]. 2018Jul.13 [cited 2024Apr.27];(4). Available from: http://zmj.zsmu.edu.ua/article/view/135791

Issue

No. 4 (2018)

Section

Original research

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