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Morphological Features of Placentas in Chronic Arterial Hypertension and Associated Preeclampsia

https://doi.org/10.52420/umj.25.1.7

EDN: LSEVEN

Abstract

 Introduction. Preeclampsia (PE) is serious complication of gestation, the central place in the pathogenesis of which is placental dysfunction. The similarity of the pathogenetic mechanisms of chronic arterial hypertension (CAH) and PE determines interest in studying the morphological features of placentas in these patients.

Materials and methods. Histological and immunohistochemical (IHC) study of placentas was performed, assessing expression levels of VEGF, PlGF, angiotensinogen. Group 1 included placentas from women with CAH (n = 24), Group 2 — from women with CAH and PE (SPE) (n = 26), and Group 3 included placentas from patients without hypertensive disorders of pregnancy (HDP) (n = 20).

Results. Histological examination revealed statistically significant increase in the incidence of decidual arteriopathy (p = 0.007) and villous edema (p = 0.005) in Group 2 compared with Group 1. Group 1 had significantly higher incidence of villous necrosis (p = 0.005) and fibrinoid deposition (p = 0.016) compared with Group 3. When assessing expression level of IHC markers, highest levels of VEGF and PlGF expression were observed in group of patients without HDP (p1 : 3 < 0.0001 and p2 : 3 < 0.0001), while level of angiotensinogen expression, in contrast, was lower in pregnant women from Group 3 (p1 : 3 < 0.0001 and p2 : 3 < 0.0001). The expression levels of VEGF, PlGF, and angiotensinogen were statistically significantly higher in Group 2 compared to Group 1 (p < 0.0001).

Discussion. This study demonstrates different morphological profiles of placental tissue in CAH and SPE: isolated CAH is characterized by signs of chronic placental insufficiency, while SPE is dominated by markers of acute endotheliopathy and impaired placentation. IHC data demonstrate dysregulated angiogenesis and vasoconstriction in placenta, as well as significant endothelial dysfunction in HDP. 

About the Authors

E. A. Azarenkova
Ural Research Institute for Maternal and Child Health
Russian Federation

Evgeniia A. Azarenkova  — Head of the Educational and Methodological Department 

Ekaterinburg 


Competing Interests:

The author declare the absence of obvious or potential conflict of interest. 



Y. A. Semenov
Ural State Medical University
Russian Federation

Yuriy A. Semenov — Doctor of Sciences (Medicine), Associate Professor, Rector

Ekaterinburg 


Competing Interests:

Yuriy A. Semenov is the editor-in-chief of Ural Medical Journal; he did not participate in reviewing the material, as well as in making a decision on its publication.  



V. N. Antonov
South Ural State Medical University
Russian Federation

Vladimir N. Antonov — Doctor of Sciences (Medicine), Associate Professor, Professor of the Department of Therapy, Institute of Continuing Professional Education 

Chelyabinsk 


Competing Interests:

The author declare the absence of obvious or potential conflict of interest. 



G. V. Sychugov
South Ural State Medical University; Chelyabinsk Regional Pathological Anatomy Bureau
Russian Federation

Gleb V. Sychugov — Candidate of Sciences (Medicine), Associate Professor of the Department of Pathological Anatomy and Forensic Medicine named after Professor V. L. Kovalenko; Deputy Chief Physician for Medical Affairs 

Chelyabinsk 


Competing Interests:

The author declare the absence of obvious or potential conflict of interest. 



A. G. Sychugov
Ural Research Institute for Maternal and Child Health
Russian Federation

Aleksandr G. Sychugov — Head of the Department of Pathomorphology and Cytodiagnostics 

Ekaterinburg 


Competing Interests:

The author declare the absence of obvious or potential conflict of interest. 



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Review

For citations:


Azarenkova EA, Semenov YA, Antonov VN, Sychugov GV, Sychugov AG. Morphological Features of Placentas in Chronic Arterial Hypertension and Associated Preeclampsia. Ural Medical Journal. 2026;25(1):7–17. (In Russ.) https://doi.org/10.52420/umj.25.1.7. EDN: LSEVEN

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