Авторы

  • Сафронбек Султанов
    Ташкентской медицинской академии Докторант 1-го года обучения

DOI:

https://doi.org/10.71337/inlibrary.uz.ejmns.128161

Ключевые слова:

Артериальная гипертензия дисфункция почек скорость клубочковой фильтрации.

Аннотация

Артериальная гипертензия негативно влияет на ряд систем организма человека и может нанести значительный ущерб, особенно таким важным жизненно важным органам, как почки и сердце. Артериальная гипертензия обычно поражает все органы в организме через высокое кровяное давление, но почки являются одним из наиболее чувствительных органов к высокому давлению. Это состояние приводит к функциональным и структурным изменениям в почках и сердце из-за длительной гипертонии и отсутствия своевременного применения контрмер.


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EURASIAN JOURNAL OF MEDICAL AND

NATURAL SCIENCES

Innovative Academy Research Support Center

IF = 7.921

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Volume 5 Issue 7, July 2025 ISSN 2181-287X

Page 7

STRUCTURAL AND FUNCTIONAL STATE OF THE KIDNEYS

AND HEART IN THE DEVELOPMENT OF RENAL

DYSFUNCTION IN PATIENTS WITH ARTERIAL

HYPERTENSION

Sultanov Safronbek Safarboy o’g’li

Tashkent Medical Academy 1st year PhD doctoral student

https://doi.org/10.5281/zenodo.15854594

ARTICLE INFO

ABSTRACT

Received: 02

nd

July 2025

Accepted: 09

th

July 2025

Online: 10

th

July 2025

,

Arterial hypertension negatively affects a number of systems in
the human div, and can cause significant damage, especially to
important vital organs such as the kidneys and heart. Arterial
hypertension usually affects all organs in the div through high
blood pressure, but the kidneys are one of the most sensitive
organs to high pressure. This condition leads to functional and
structural changes in the kidneys and heart due to the long
duration of hypertension and the lack of timely application of
countermeasures.[2,4]

KEYWORDS

Arterial

hypertension,

renal

dysfunction,

glomerular filtration rate.

СТРУКТУРНО-ФУНКЦИОНАЛЬНОЕ СОСТОЯНИЕ ПОЧЕК И СЕРДЦА ПРИ

РАЗВИТИИ ПОЧЕЧНОЙ ДИСФУНКЦИИ У ПАЦИЕНТОВ С АРТЕРИАЛЬНОЙ

ГИПЕРТЕНЗИЕЙ

Султанов Сафронбек Сафарбой уғли

Ташкентской медицинской академии

Докторант 1-го года обучения

https://doi.org/10.5281/zenodo.15854594

ARTICLE INFO

ABSTRACT

Received: 02

nd

July 2025

Accepted: 09

th

July 2025

Online: 10

th

July 2025

,

Артериальная гипертензия негативно влияет на ряд
систем организма человека и может нанести
значительный ущерб, особенно таким важным жизненно
важным органам, как почки и сердце. Артериальная
гипертензия обычно поражает все органы в организме
через высокое кровяное давление, но почки являются
одним из наиболее чувствительных органов к высокому
давлению. Это состояние приводит к функциональным и
структурным изменениям в почках и сердце из-за
длительной гипертонии и отсутствия своевременного
применения контрмер.

KEYWORDS

Артериальная
гипертензия,
дисфункция

почек,

скорость клубочковой
фильтрации.

ARTERIAL GIPERTENZIYALI BEMORLARDA BUYRAKLAR DISFUNKSIYASI

RIVOJLANISHIDA BUYRAKLARNING VA YURAKNING STRUKTUR-

FUNKSIONAL HOLATI

Sultanov Safronbek Safarboy o’g’li

Toshkent Tibbiyot Akademiyasi 1-bosqich PHD doktaranti

https://doi.org/10.5281/zenodo.15854594

ARTICLE INFO

ABSTRACT

Received: 02

nd

July 2025

Accepted: 09

th

July 2025

,


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EURASIAN JOURNAL OF MEDICAL AND

NATURAL SCIENCES

Innovative Academy Research Support Center

IF = 7.921

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Volume 5 Issue 7, July 2025 ISSN 2181-287X

Page 8

Online: 10

th

July 2025

Arterial gipertenziya inson organizmidagi bir qator tizimlarga
salbiy ta’sir ko‘rsatadi, va ayniqsa buyraklar va yurak kabi
muhim hayotiy organlarga sezilarli darajada zarar yetkazishi
mumkin. Arterial gipertenziya, odatda, qon tomirlarining
yuqori bosimi orqali organizmdagi barcha organlarga ta’sir
qiladi, ammo buyraklar yuqori bosimga eng sezgir organlardan
biridir. Bu holat gipertenziyaning uzoq davomiyligi va unga
qarshi choralarning o‘z vaqtida qo‘llanilmasligi tufayli
buyraklar hamda yurakning funktsional va struktural
o‘zgarishlariga olib keladi.

KEYWORDS

Arterial

gipertenziya,

buyraklar dinfunksiyasi,
koptokchalar filtratsiya
tezligi.


Arterial hypertension is a disease characterized by persistently high blood pressure in the

arteries. In Western countries, approximately 30-45% of the population suffers from high blood
pressure. However, in Uzbekistan, this number is difficult to calculate accurately, but national
studies have shown that it may be about 25-30% among adults. According to statistics, kidney
dysfunction affects millions of people worldwide. Approximately 700,000 people suffer from
chronic kidney disease every year. Women are more likely to suffer from this disease than men.

The kidneys play an important role in performing their main functions, namely, removing

toxins from the div, maintaining fluid balance and ensuring the correct distribution of
electrolytes. Therefore, the effect of arterial hypertension on the kidneys can lead to the
development of renal failure and kidney diseases. [1,3]

Purpose of the study:

To study the effect of arterial hypertension on the development of

renal dysfunction.

Materials and methods:

Our research is based on the results of laboratory and

instrumental examinations of 80 patients with renal dysfunction and 30 healthy control groups.
A group of patients with and without arterial hypertension, with renal dysfunction, was
included in the study. All patients included in the study underwent laboratory and instrumental
examinations. 80 patients included in the study were divided into 2 main groups on the basis
of a “case-control” design.

1 – group. No arterial hypertension, group with advanced renal dysfunction (n=40). Male

n=10 (25%), female n=21 (75%), average age -35.5

Group 2 – group. Group with arterial hypertension, group with advanced renal

dysfunction (n=40). Male n=15 (37.5%), female n=25 (62.5%), average age -47.2

All patients with advanced renal dysfunction, with and without arterial hypertension who

were included in the study underwent instrumental examinations such as glomerular filtration
rate(GFR), renal vascular dopplerography (RVD), and echocardiography (ExoKG).

Results and their analysis:

The functional state of the kidneys was studied by GFR, renal

vascular dopplerography and the functional state of the heart was studied by echocardiography
(ExoKG) among the patients in groups 1 and 2. In the groups studied, renal hemodynamics and
GFR were evaluated. Accordingly, when comparing groups 1 and 2, a decrease in GFR was
observed in patients in group 2, a significant decrease in the functional state of the kidneys was
observed, respectively 90.14±3.17- 46.9±72.55. In the renal vascular doppler examination, the
initial systolic velocity (Vmax), final diastolic velocity (Vmin), resistance index, i.e. vascular


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resistance (RI), pulse index (PI) and systolic-diastolic index (S/D) of interstitial blood flow were
studied. Accordingly, when comparing groups 1 and 2, it was observed that renal blood flow
was significantly reduced in patients in group 2. RI 0.63±0.01-0.75±0.01* PI, RI 1.59±0.02-
1.70±0.01* PI was positively correlated (r=0.28). End-diastolic velocity, pulse index and
systolic-diastolic index were significantly negatively correlated (r=-0.45, r=-0.27). Renal
vascular resistance index (RI) and pulse index (PI) were significantly positively correlated with
left ventricular end-diastolic volume (LVEDV) and left ventricular end-diastolic diameter
(LVEDD) (r=0.25, r=0.33- r=0.25, r=0.32). Table 1.

Table 1

Renal vascular dopplerography

1-group

2-group

Age

35,5±0,83

47,2±2,85

Vmax

0,85±0.02

0,79±0.02*

Vmin

0,26±0.01

0,24±0.03

RI

0,63±0.01

0,75±0.01*

PI

1,59±0.02

1,70±0.01*

S/D

3,52±0.06

3,85±0.06*

*Statistically significant (p<0.05)

Thus, an increase in renal vascular resistance leads to the development of renal

dysfunction. The structural and functional state of the heart was examined in the studied
groups. When comparing groups 1 and 2, left ventricular systolic dysfunction was observed,
that is, the left ventricular end-diastolic volume and end-systolic volume significantly differed
in group 2 compared to group 1, respectively 109.04±4.44 -139.13±6.60*. At the same time, the
left ventricular end-diastolic size and end-systolic size and the ejection fraction (EF) were also
significantly different in group 2 compared to group 1, respectively 3.13±0.07-3.63±0.11*,
4.80±0.08-5.31±0.11*, 59.25±1.17-54.03±1.14*. The increase in heart size and dimensions,
namely left ventricular end-diastolic size, left ventricular end-systolic size, formed a significant
positive correlation with ventricular interventricular wall thickness, left ventricular myocardial
mass and ventricular myocardial mass, respectively (r=0.36, r=0.34), (r=0.71, r=0.68), (r=0.61,
r=0.57). Left ventricular end-diastolic size was positively correlated with left ventricular end-
systolic diameter (LVESD). However, left ventricular volume and size were significantly
negatively correlated with ejection fraction, respectively (r=-0.39, r=-0.70), (r=0.37, r=0.69).
The development of arterial hypertension increases the volume, size, and myocardial mass of
the heart, which causes cardiac remodeling and the development of cardiorenal syndrome.
Enlargement of the heart chambers and a decrease in ejection fraction lead to stagnation of
blood in the kidneys and the development of renal dysfunction. Left ventricular end-diastolic
volume, left ventricular end-systolic volume and left ventricular end-diastolic volume, left
ventricular end-systolic volume formed a significant negative correlation with glomerular
filtration rate, respectively (r=-0.37, r=-0.36), (r=-0.36, r=-0.34). An increase in cardiac output
decreases glomerular filtration rate in the kidney, which leads to the development of renal
dysfunction Table 2.




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Table 2

EXOKG results

1-group

2-group

Age

35,5±0,83

47,2±2,85

LV EDD

109,04±4,44

139,13±6,60*

LV ESD

39,03±2,27

56,53±3,78*

LV EDV

4,80±0,08

5,31±0,11*

LV ESV

3,13±0,07

3,63±0,11*

LVM

220,05±15,22

245,98±13,92

Ind.mass

160,95±12,56

177,05±10,67

SV

70,00±3,20

79,89±3,80*

EF

59,25±1,17

54,03±1,14*

*Statistically significant (p<0.05)

Conclusion:

According to the results of the scientific research, taking into account the

proportional damage to the kidneys and heart in patients with arterial hypertension with
advanced renal dysfunction, that is, the pathogenetic mechanisms of cardiorenal syndrome,
timely examination of hemodynamic disorders in the heart, as well as renal vascular
dopplerography and EXOKG examinations, allows for early assessment of early changes in renal
dysfunction in patients, thereby helping to prevent further exacerbation of the existing disease
in patients.

References:

1.

Turaev, I.A., & Abdujabborov, B.A. (2021). "Arterial gipertenziya va buyrak faoliyati."

Uzbekistan Tibbiyot Jurnali, 43(2), 56-60.
2.

Guan, Z., Intapad, S., Palygin, O., and Sullivan, J. C. (2022). Hypertension and chronic kidney

injury or failure, volume II. Front. Physiology 2479.
3.

Ku, E., Lee, B. J., Wei, J., and Weir, M. R. (2019). Hypertension in CKD: Core curriculum

2019. Am. J. Kidney Dis. 74, 120–131. doi:10.1053/j.ajk2018.12.044
4.

Sanchez, O. A., Ferrara, L. K., Rein, S., Berglund, D., Matas, A. J., and Ibrahim, H. N. (2018).

Hypertension after kidney donation: Incidence, predictors, and correlates. Am. J. Transpl. 18,
2534–2543. doi:10.1111/ajt.14713 Sata, Y., Burke, S. L., Watson, A. M., Jha, J. C., Gueguen, C.,
Eikelis, N

Библиографические ссылки

Turaev, I.A., & Abdujabborov, B.A. (2021). "Arterial gipertenziya va buyrak faoliyati." Uzbekistan Tibbiyot Jurnali, 43(2), 56-60.

Guan, Z., Intapad, S., Palygin, O., and Sullivan, J. C. (2022). Hypertension and chronic kidney injury or failure, volume II. Front. Physiology 2479.

Ku, E., Lee, B. J., Wei, J., and Weir, M. R. (2019). Hypertension in CKD: Core curriculum 2019. Am. J. Kidney Dis. 74, 120–131. doi:10.1053/j.ajk2018.12.044

Sanchez, O. A., Ferrara, L. K., Rein, S., Berglund, D., Matas, A. J., and Ibrahim, H. N. (2018). Hypertension after kidney donation: Incidence, predictors, and correlates. Am. J. Transpl. 18, 2534–2543. doi:10.1111/ajt.14713 Sata, Y., Burke, S. L., Watson, A. M., Jha, J. C., Gueguen, C., Eikelis, N