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BIOCHEMICAL STUDY OF THE DEVELOPMENT OF CHRONIC VIRAL
HEPATITIS WITH COMORBID COURSE OF CHRONIC
GLOMERULONEPHRITIS
Ismatova Rano Ahadovna
Candidate of Technical Sciences, PhD, Director
of the Academic Lyceum No. 1 at the
Bukhara State Medical Institute
email: lyuba-ali-1988@mail.ru
https://doi.org/10.5281/zenodo.11194608
Аннотация.
Вторичные клубочковые поражения при вирусных
гепатитах протекают медленно, однако у трети больных процесс
неуклонно прогрессирует и проявляется нефротическим синдромом,
ухудшает состояние больного с проявлениями почечной недостаточности.
Цель данного исследования изучить клинические и биохимические
аспекты поражения функционального состояния почек при хроническом
вирусном гепатите В и С. В исследование включено 198 пациентов с
положительными серологическими маркерами ВГВ и ВГС и клинико--
лабораторными синдромами поражения почек.
Ключевые слова:
Хронический гломерулонефрит, хронический
гепатит В и С.
Annotation.
Secondary glomerular lesions in viral hepatitis occur slowly,
but in a third of patients the process progresses steadily and manifests as
nephrotic syndrome, worsening the patient's condition with manifestations of
renal failure. The purpose of this study is to study the clinical and biochemical
aspects of the damage to the functional state of the kidneys in chronic viral
hepatitis B and C.The study included 198 patients with positive serological
markers of HBV and HCV and clinical-renal syndrome of kidney damage.
Key words:
Chronic glomerulonephritis, chronic hepatitis B and C.
Relevance.
Chronic viral hepatitis B, C, which occupies a dominant place
among all liver diseases, is one of the most important problems of modern
hepatology due to its widespread distribution and high incidence rate. According
to WHO, there are about 15% of carriers of hepatitis B virus (HBV) in the world
and 10% of carriers of viral hepatitis C (HCV) of the entire population of the
globe [2,5].
In the pathogenesis of parenteral hepatitis, course and outcomes, the
leading role is given to immune mechanisms. The characteristic “escape” of
hepatitis viruses from “immune surveillance”, due to the inferiority of the
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immune response, determines the persistence of the pathogen and the
formation of a chronic course of infection. Circulating immune complexes in
chronic viral liver pathology can cause the appearance of extrahepatic lesions of
organs and systems.
It is believed that the hepatitis B virus may play a role in the development
of glomerulonephritis. As evidence of this position, the following are considered:
an increased frequency of detection of markers of infection with the hepatitis B
virus, and primarily HBsAg, among patients with various forms of
glomerulonephritis; detection of HBsAg deposits in the glomeruli of the kidneys
and immune complexes HBsAg - anti-HBs, which are of primary importance in
kidney damage. According to some researchers, HBsAg carriage is regarded as a
risk factor for the development of glomerulonephritis [6].
Among patients with hepatitis B with the presence of glomerulonephritis,
its morphological variants are recorded: membranous, membranous-
proliferative, endo - and extracapillary, etc.
The mechanism of renal damage associated with viral hepatitis B has not
been fully determined. Several assumptions have been made related to: the
direct effect of the HBsAg-anti-HBs immunocomplexes; immunocomplexes
containing anti-HBc, HBeAg, anti-HBe; with the action of components of
destroyed hepatocytes and autoantibodies produced on them during the disease
process.
In the structure of renal pathology, one of the leading places belongs to
glomerulonephritis (GN), due to the severity of complications, difficulties of
diagnosis, imperfect therapy, and poor prognosis of most of its chronic forms.
GN today is a kidney disease, which, in addition to the primary one, often
acquires the significance of a secondary lesion that develops within the
framework of a certain systemic or metabolic-endocrine pathology, the
spectrum of which is extremely wide. The systemic nature of the process
involving the kidneys is inherent in blood-borne viral hepatitis, in particular
HBV and HCV.
In adults, secondary glomerular lesions due to viral hepatitis proceed
slowly, but in a third of patients the process steadily progresses, may manifest as
nephrotic syndrome, worsen the patient’s condition with manifestations of renal
failure, is difficult to respond to anti-inflammatory therapy, and requires the use
of extracorporeal methods of treating immune complex pathology
(plasmopharesis, hemosorption) [1,2].
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The purpose of this study is to study the clinical and biochemical aspects of
damage to the functional state of the kidneys in chronic viral hepatitis B and C.
Material and methods.
The present study included 198 patients with
positive serological markers of HBV and HCV and clinical and laboratory
syndromes of kidney damage (glomerulonephritis). Among them, men
accounted for 47.8% (95 people), women 52.2% (103 people). The average age
of those examined was 52±3.7 years.
To compare the course of the disease, glomerulonephritis associated with
chronic viral hepatitis, the examination included 32 patients with
glomerulonephritis who were not found to be infected with hepatitis viruses.
The study was conducted in the nephrology department of the Bukhara
Regional Multidisciplinary Medical Center.
When examining patients, anamnestic data was collected, anthropometric
indicators were measured, div type was determined, the condition of organs
and systems was assessed, and blood pressure was measured.
All subjects underwent a functional examination, a biochemical blood test
with determination of the level of ALT, AST, bilirubin and its fractions, total
protein and its fractions, the level of urea and creatinine, the glomerular
filtration rate of GFR was determined (according to the SKD-EPI equation), a
general urinalysis, with the determination daily proteinuria. In all those
examined, markers of hepatitis B and C were determined using ELISA and also
ultrasound examination of the kidneys and liver.
The diagnosis of chronic glomerulonephritis (CGn) was established on the
basis of anamnestic and clinical-biochemical data: edema syndrome, high blood
pressure, changes in the fundus characteristic of nephrogenic hypertension,
increased urea and creatinine in the blood serum, hypoproteinemia,
dysproteinemia, proteinuria (more than 1g/day ) characteristic urinary
sediment (hematuria, cylindruria) [3].
The examination of patients was carried out in accordance with the
recommendations of WHO experts for the healthcare system [WHO, Geneva,
2012]. When carrying out our research, we complied with all ethical principles
of medical research involving human subjects adopted by the Declaration of
Helsinki of the World Medical Association in 1964 (latest addition at the 59th
General Assembly of the World Medical Association in 2008 in Seoul).
Processing of the obtained data was carried out by the method of
nonparametric statistics using a computer program. Correlations with p < 0.05
were considered statistically significant.
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Results and discussion.
The results of our survey showed the following
data: the detection rate of chronic hepatitis B was 47%, chronic hepatitis C was
41.4%. 11.6% were found to be infected with a mixed infection, and markers of
hepatitis B and C were determined (Table 1).
1 table
Frequency of detection of types of chronic hepatitis in patients with
chronic glomerulonephritis (CGn)
1 group
CGn with HBV
n=93
2nd group
CGn with HCV
n=82
3 group
CGn with VG
B+S n=23
Patients with
and without
chronic viral
hepatitis
n=32
Age
44,1±3,1
38,3 ±4,2
33,7±7
48,4±8,5
Man
Woman
52
41
40
42
14
9
11
21
Duration
Currents(years):
HGn, HVG
6,8±0,7
4,6±0,5
7,2±0,8
4,2±0,5
6,9±1,4
3,9±0,8
7,1±1,2
When analyzing the results of clinical and laboratory studies, the frequency
of detection and severity of clinical symptoms of chronic glomerulonephritis and
the level of laboratory markers of this disease in all groups of patients were
studied. At the same time, the clinical manifestation of the disease was
characterized by the development of nephrotic syndrome, hematuria, and
arterial hypertension. We paid attention to pronounced peripheral edema, the
presence of free fluid in the abdominal and pleural cavities, the level of
increased blood pressure, and the severity of splenomegaly [4].
The functional capacity of the kidneys was assessed by serum creatinine
levels and glomerular filtration rate. Kidney function is assessed by glomerular
filtration rate (GFR). Calculation of GFR is mandatory. The most rational and
reliable way to determine GFR is its automatic calculation in biochemical
laboratories, which should produce two results - serum creatinine concentration
and estimated GFR. We calculated GFR using the CKD-EPI method, taking into
account the level of creatinine in the blood serum, race, gender and age of the
patient.
The clinical picture of liver damage in the examined patients was assessed
taking into account the syndromes of cytolysis (increased activity of ALT and
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AST), cholestasis (increased levels of GGT, alkaline phosphatase, bilirubin),
jaundice (increased total bilirubin due to its direct fraction). The results of urine
analysis, the level and severity of proteinuria, hematuria in all groups were
analyzed (table 2).
Table 2.
Clinical and laboratory parameters of patients with CG on the
background of CVH
Indicators
1 group
CGn
with
HBV n=93
2nd group
CGn
with
HCV n=82
3 group
CGn
with
VG
B+S
n=23
Patients with
and without
chronic viral
hepatitis
n=32
Peripheral edema
(%)
65,6
41,2
90
58,3
Ascites (%)
29,1
33,6
46,7
12,6
Arterial
hypertension (%)
25,3
26,6
31,2
41,3
Splenomegaly (%) 34,6
39,5
47,8
20,3
Proteinuria
(g/day)
4,1±0.3
3,9±0.2
5,9±0.2
4,3±0.3
Total protein (g/l) 57,6±1.1
52,3±1.3
46,1±1.4
52,5±1.5
Albumin(g/l)
39,9±1.3
38,3±1.2
25,7±1.4
39,7±1.3
GFR ml
66,6±2.3
62,9±2.2
50,7±2.6
69.3±1.8
ALT (IU/l)
46,2±2.1
47,7±2.9
51,9±3.5
53,5±3.3
AST (IU/l)
48,4±1.2
49,1±1.8
61,2±1.5
40,4±1.9
Analysis of the results shows that the occurrence of clinical symptoms of
chronic glomerulonephritis increases in patients with CGN-associated CVH. The
severity of edema syndrome is more common in the group of CG patients with
hepatitis B+C (90%). In patients in this group, the incidence of arterial
hypertension also predominates in other groups [5-6].
The incidence of splenomegaly syndrome is greater in patients with CGN
associated CVH (47.8%) than in patients with glomerulonephritis not infected
with hepatitis B and C viruses (20.3%).
The analyzed results of biochemical tests show that the level of liver
damage (according to the results of ALT and AST levels) is higher in patients
with CGN-associated chronic hepatitis than in patients with glomerulonephritis
not infected with hepatitis B and C viruses. Accordingly, one can see the level of
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kidney damage. Since GFR indicators are low in patients with CGN associated
CVH.
Conclusion. In CGN associated with CVH, a significant decrease in protein
metabolism, GFR, and increased liver damage are observed in comparison with
similar indicators for CGN without CVH association.
Comparison of blood protein metabolism indicators, the level of GFR and
daily proteinuria revealed the following features of CGN associated with CVH:
the most severe changes that contribute to the progression of CGN
(hypoproteinemia, proteinuria, decreased GFR) are more typical for patients
with CGN with the association of CGN C and B+C, in comparison with CHVG B
and CHVG C.
In conclusion, it should be noted that kidney damage associated with the course
of chronic viral hepatitis is quite common and may have different development
mechanisms and diverse clinical and morphological manifestations. It is obvious
that the awareness of infectious disease doctors and nephrologists in this field of
medicine, their closer interaction in this direction is necessary for the diagnosis
and treatment of this complex associated pathology.
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