ACUTE KIDNEY INJURY: ETIOLOGY AND TREATMENT

1144

ResearchBib IF - 11.01, ISSN: 3030-3753, Volume 2 Issue 3

ACUTE KIDNEY INJURY: ETIOLOGY AND TREATMENT

Mansurov Sardor Vali o’g’li

Asian International University, Bukhara, Uzbekistan.

https://doi.org/10.5281/zenodo.15070424

Abstract.

Acute kidney injury (AKI), previously called acute renal failure (ARF), denotes

a sudden and often reversible reduction in kidney function, as measured by glomerular filtration

rate (GFR). AKI is part of a range of conditions summarized as acute kidney diseases and

disorders (AKD), in which slow deterioration of kidney function or persistent kidney dysfunction

is associated with an irreversible loss of kidney cells and nephrons, which can lead to chronic

kidney disease (CKD). New biomarkers to identify injury before function loss await clinical

implementation. AKI and AKD are a global concern. In low-income and middle-income

countries, infections and hypovolaemic shock are the predominant causes of AKI. In high-

income countries, AKI mostly occurs in elderly patients who are in hospital, and is related to

sepsis, drugs or invasive procedures. Infection and trauma-related AKI and AKD are frequent in

all regions. The large spectrum of AKI implies diverse pathophysiological mechanisms. AKI

management in critical care settings is challenging, including appropriate volume control,

nephrotoxic drug management, and the timing and type of kidney support. Fluid and electrolyte

management are essential. As AKI can be lethal, kidney replacement therapy is frequently

required. AKI has a poor prognosis in critically ill patients. Long-term consequences of AKI and

AKD include CKD and cardiovascular morbidity. Thus, prevention and early detection of AKI

are essential.

Keywords:

Acute kidney injury, glomerular filtration rate, chronic kidney disease,

hypovolaemic shock, high-income countries, pathophysiological mechanisms.

ОСТРОЕ ПОВРЕЖДЕНИЕ ПОЧЕК: ЭТИОЛОГИЯ И ЛЕЧЕНИЕ

Аннотация.

Острое повреждение почек (ОПП), ранее называвшееся острой

почечной недостаточностью (ОПН), означает внезапное и часто обратимое снижение

функции почек, измеряемое по скорости клубочковой фильтрации (СКФ). ОПН является

частью ряда состояний, обобщенных как острые заболевания и расстройства почек

(ОПН), при которых медленное ухудшение функции почек или стойкая дисфункция почек

связаны с необратимой потерей почечных клеток и нефронов, что может привести к

хронической болезни почек (ХБП). Новые биомаркеры для определения повреждения до

потери функции ожидают клинического внедрения. ОПН и ОПН являются глобальной

проблемой. В странах с низким и средним уровнем дохода основными причинами ОПН

являются инфекции и гиповолемический шок. В странах с высоким уровнем дохода ОПН

чаще всего возникает у пожилых пациентов, находящихся в больнице, и связано с

1145

ResearchBib IF - 11.01, ISSN: 3030-3753, Volume 2 Issue 3

сепсисом, приемом лекарств или инвазивными процедурами. ОПН и ОПН, связанные с

инфекцией и травмой, часто встречаются во всех регионах. Широкий спектр ОПН

подразумевает разнообразные патофизиологические механизмы. Лечение ОПН в условиях

интенсивной терапии является сложной задачей, включая надлежащий контроль объема,

управление нефротоксичными препаратами, а также выбор времени и типа поддержки

почек. Управление жидкостью и электролитами имеет важное значение. Поскольку

ОПН может быть летальным, часто требуется заместительная почечная терапия.

ОПН имеет плохой прогноз у пациентов в критическом состоянии. Долгосрочные

последствия ОПН и ОБП включают ХБП и сердечно-сосудистую заболеваемость. Таким

образом, профилактика и раннее выявление ОПН имеют важное значение.

Ключевые слова:

острое повреждение почек, скорость клубочковой фильтрации,

хроническое заболевание почек, гиповолемический шок, страны с высоким уровнем дохода,

патофизиологические механизмы.

Introduction

Acute kidney injury (AKI) is a syndrome. It is an important complication in patients

admitted to hospital (15–20% of all hospitalisations) and in patients in the intensive care unit

(ICU) where its prevalence can sometimes exceed 55%. Despite its complexity, AKI is

traditionally seen as a single disease or classified according to semianatomical categories (pre-

renal, intrinsic, and postrenal AKI) in reference to the kidney.

This simplistic taxonomy is now giving way to more specific syndromic descriptions

including among others hepatorenal, cardiorenal, nephrotoxic, and sepsis-associated AKI. This

increased specificity is because of increasing evidence that these syndromes have a unique

pathophysiology and treatment.

Etiology

The impetus for glomerular filtration is the pressure difference between the glomerulus

and Bowman's space. This pressure gradient is affected by the renal blood flow and is under the

direct control of the combined resistances of afferent and efferent vascular pathways. For most

causes of AKI, renal blood flow reduction is a common pathologic pathway for declining GFR.

The pathophysiology of AKI has traditionally been divided into three categories: prerenal,

intrinsic renal, and postrenal. Each of these categories has many different associated causes, and

some causative factors of AKI have overlapping mechanisms of injury.

The prerenal form of AKI is due to any cause of reduced blood flow to the kidney. This

may be part of systemic hypoperfusion resulting from hypovolemia or due to selective

hypoperfusion of the kidneys, such as resulting from renal artery stenosis or aortic dissection.

1146

ResearchBib IF - 11.01, ISSN: 3030-3753, Volume 2 Issue 3

However, tubular and glomerular function tends to be initially normal. A few examples of

prerenal AKI mechanisms are listed below:

1.

Hypovolemia: hemorrhage, severe burns, and gastrointestinal fluid losses such as

diarrhea, vomiting, and high ostomy output.

2.

Hypotension from decreased cardiac output: cardiogenic shock, massive pulmonary

embolism, acute coronary syndrome.

3.

Hypotension from systemic vasodilation: septic shock, anesthesia administration.

4.

Renal vasoconstriction: NSAIDs, amphotericin B, calcineurin inhibitors, hepatorenal

syndrome.

5.

Glomerular efferent arteriolar vasodilation (causing intraglomerular hypotension): ACE

inhibitors, angiotensin receptor blockers.

Intrinsic renal causes include conditions that affect the glomerulus or tubule, such as

acute tubular necrosis and acute interstitial nephritis. This underlying glomerular or tubular

injury is associated with the release of vasoconstrictors from the renal efferent pathways.

Prolonged renal ischemia, sepsis, and nephrotoxins are the most common causes. It is

worth mentioning that prerenal injury can convert into a renal injury if the offending factor's

exposure is prolonged enough to cause cellular damage. A few examples of this mechanism are

listed below:

1.

Acute tubular necrosis (ATN): ischemia from prolonged prerenal injury; drugs such as

aminoglycosides, amphotericin B, and pentamidine; iodinated contrast; rhabdomyolysis;

intravascular hemolysis

2.

Acute interstitial nephritis (AIN): Drugs such as beta-lactam antibiotics, penicillins, NSAIDs,

proton pump inhibitors (PPIs), and 5-ASA; infection; autoimmune conditions (systemic lupus

erythematosus [SLE], IgG-related disease); and hereditary AIN.

3.

Glomerulonephritis: anti-glomerular basement membrane disease, immune complex-mediated

diseases (post-infectious glomerulonephritis, cryoglobulinemia, IgA nephropathy, IgA vasculitis).

4.

Intratubular obstruction: monoclonal gammopathy, hemolytic anemia, and toxins such as

ethylene glycol.

Postrenal etiology for AKI includes obstructive causes, which lead to congestion and

urinary backflow of the filtration system, leading to a shift in the filtration driving forces. A

noteworthy fact is that a unilateral obstruction may not always present as AKI, especially if the

obstruction is gradual, because a normal working contralateral kidney may compensate for the

function of the affected kidney.

Pathological disturbances can occur within 2 hours of obstruction, starting with decreased

filtration at the level of the glomerulus due to increased upper urinary tract pressure. This results

1147

ResearchBib IF - 11.01, ISSN: 3030-3753, Volume 2 Issue 3

in decreased renal perfusion, inflammation, tubular atrophy, and interstitial fibrosis. Eventually,

bladder atony, periglomerular fibrosis, chronic interstitial nephritis can develop. The most

common etiology of postrenal AKI is bladder outlet obstruction, which is often due to prostatic

hypertrophy in older men, pelvic masses in older women, and nephrolithiasis in younger patients.

Renal calculi can present in the renal calyces, renal pelvis, bladder. Size and location are

the determining factors of AKI, and this is a significant etiology in those with a solitary kidney.

Struvite and cystine stones grow especially rapidly and commonly cause obstruction.

Tumors, blood clots, and neurogenic bladder cause mechanical ureteral outlet obstruction.

Blood clots can be a result of bladder or urinary tract malignancy.

Urethral obstruction is the most common cause of prostate enlargement in older men. The

obstruction can also be caused by retroperitoneal fibrosis, pregnancy, fecal impaction, pelvic

organ prolapse.

Clinical presentation

Kidney disease is usually a silent condition. Except for urinary tract obstruction, it does

not cause pain or any specific signs or symptoms. Patients can therefore present in two ways.

First, a patient might present with an acute illness such as sepsis,or be exposed to a

condition known to be associated with AKI such as major surgery.Importantly, such patients

might not present to the ICU and it is therefore essential that clinicians working outside the ICU

are aware of the clinical presentation of kidney disease and specifically AKI. In ideal

circumstances, a premorbid assessment of kidney function within the past 4 months might be

available and changes from this baseline state can be detected by measuring serum creatinine or

urinary output.

Second, a patient might present with abnormal kidney function of unknown duration and

the clinician has to then decide if the condition is AKI, CKD, or both. This scenario can pose a

substantial clinical dilemma particularly if the patient’s medical history, including baseline renal

function, is not well documented. Indeed, baseline renal function often has to be inferred using

various sources of information including the medical history, kidney size using imaging,

presence or absence of albuminuria, and the history of serum measurements of serum creatinine

over time. A decrease in serum creatinine after hospital admission might indicate that AKI had

occurred before admission.

Prevention of AKI

The first principle of AKI prevention is to treat its cause or trigger. The second principle

is to ensure that further insults are avoided.

Systemic haemodynamics should be optimised so that, irrespective of the trigger, further

damage does not occur and adequate renal perfusion and perfusion pressure are maintained. If

1148

ResearchBib IF - 11.01, ISSN: 3030-3753, Volume 2 Issue 3

intravascular volume is compromised, it must be rapidly restored by administration of

intravenous fluids.

Avoidance of other nephrotoxic drugs is another important step in preventing AKI or

shortening its course. However, no specific drug-based intervention has been consistently and

reproducibly shown to be kidney protective. Thus, there is no established pharmacotherapy for

AKI. Among patients undergoing cardiac surgery, off-pump coronary artery bypass grafting has

been shown to attenuate renal injury. However, the magnitude of effect is small and the inferior

quality of grafting is a major concern.

Treatment

Many cases overlap between prerenal and ATN types of AKI. The best way to determine

if the AKI is prerenal or not is a fluid challenge. If there is no contraindication, all patients with

acute renal dysfunction should receive a fluid challenge. This requires close monitoring of urine

output and renal function. If the renal function improves with fluid, this indicates prerenal AKI.

Acute tubular necrosis and other intrarenal causes are often slow to recover and can take

weeks to months for complete recovery of renal function. Diuretics may be required during the

oliguric phase of ATN if significant volume overload develops. It is also important to avoid

further kidney insults, such as nephrotoxic drugs. In addition, many medications must be renally

adjusted once a patient develops AKI. Dietary ingestion of potassium and phosphorus should

also be monitored.

If hyperkalemia develops, it needs to be managed expeditiously. Approaches to lower

potassium in the div include:

Dietary restriction

Insulin, IV dextrose, and beta-agonists

Potassium-binding resins

Calcium gluconate to stabilize the cardiac membrane if EKG changes are present

Dialysis for nonresponsive hyperkalemia

Some AKI patients tend to develop volume overload, which should be corrected as early

as possible to avoid pulmonary and cardiac complications. Euvolemic state can be achieved with

the help of diuretics, which is a cornerstone in managing such patients. Usually, high doses of IV

furosemide are needed to correct volume overload in AKI patients; however, it plays no role in

converting oliguric AKI to non-oliguric AKI.

Conclusion

1149

ResearchBib IF - 11.01, ISSN: 3030-3753, Volume 2 Issue 3

AKI is undergoing substantial evolution in terms of definition and classification,

understanding of pathophysiological mechanisms, and interaction with other disciplines and

organ systems. Epidemiology describes an increasing incidence partly due to a more thorough

clinical evaluation and detection.The management of patients with AKI has improved together

with the improvements in hospital and intensive care quality, supported in part by sophisticated

technology of extracorporeal organ support, a more personalised pharmacological therapy, and a

standardised and protocolised management of physiological endpoints. In many areas,

controversies still exist but consensus has been reached in several protocols and treatments so

that true benchmarking and quality control are possible.

REFERENCES

1.

Vali o’g’li, M. S. KIDNEY CANCER: EPIDEMIOLOGY AND TREATMENT.

2.

Valiyevich, M. S. (2024). Specific Morphofunctional Characteristics of the Kidney Caused

by Brain Damage in Various Emergency Situations. Research Journal of Trauma and

Disability Studies, 3(4), 286-289.

3.

PROSTATE CANCER: PATHOLOGY AND TREATMENT. (2024). International Bulletin

of Medical Sciences and Clinical Research, 4(11), 65-70. https://doi.org/10.37547/

4.

MUSHAKLARNING

TARAQQIYOTI.

MUSHAKLARNING

YORDAMCHI

APPARATI.

TADQIQOTLAR. UZ

,

40

(3), 94-100.

5.

Narzulaeva,

U.

(2023).

Pathogenetic

Mechanisms

of

Microcirculation

disorders.

International Bulletin of Medical Sciences and Clinical Research

,

3

(10), 60-65.

6.

Narzullaeva, U. R., Samieva, G. U., & Samiev, U. B. (2020). The importance of a healthy

lifestyle in eliminating risk factors in the early stages of hypertension.

Journal Of

Biomedicine And Practice

, 729-733

7.

Abdurashitovich,

Z.

F.

(2024).

APPLICATION

OF

MYOCARDIAL

CYTOPROTECTORS IN ISCHEMIC HEART DISEASES.

ОБРАЗОВАНИЕ НАУКА И

ИННОВАЦИОННЫЕ ИДЕИ В МИРЕ

,

39

(5), 152-159.

8.

Abdurashitovich, Z. F. (2024). SIGNIFICANCE OF BIOMARKERS IN METABOLIC

SYNDROME.

EUROPEAN JOURNAL OF MODERN MEDICINE AND PRACTICE

,

4

(9),

409-413.

9.

Zikrillaev, F. A. (2024). Cardiorehabilitations from Physiotherapeutic Treatments in

Cardiovascular Diseases.

American Journal of Bioscience and Clinical Integrity

,

1

(10), 96-

102.

10.

Abdurashitovich, Z. F. (2024). Cardiovascular System. Heart. Aorta. Carotid Artery.

1150

ResearchBib IF - 11.01, ISSN: 3030-3753, Volume 2 Issue 3

11.

Abdurashitovich, Z. F. (2024). MORPHO-FUNCTIONAL ASPECTS OF THE DEEP

VEINS OF THE HUMAN BRAIN.

ОБРАЗОВАНИЕ НАУКА И ИННОВАЦИОННЫЕ

ИДЕИ В МИРЕ

,

36

(6), 203-206.

12.

Abdurashitovich, Z. F. (2024).

ASTRAGAL O’SIMLIGINING TIBBIYOTDAGI MUHIM

AHAMIYATLARI

VA

SOG’LOM

TURMUSH

TARZIGA

TA’SIRI.

Лучшие

интеллектуальные исследования

,

14

(4), 111-119.

13.

Abdurashitovich,

Z.

F.

(2024).

ODAM

ANATOMIYASI

FANIDAN

SINDESMOLOGIYA

BO’LIMI

HAQIDA

UMUMIY

MALUMOTLAR.

ОБРАЗОВАНИЕ НАУКА И ИННОВАЦИОННЫЕ ИДЕИ В

МИРЕ

,

41

(4), 37-45.

14.

Abdurashitovich, Z. F. (2024). THE IMPORTANCE OF THE ASTRAGAL PLANT IN

MEDICINE AND ITS EFFECT ON A HEALTHY LIFESTYLE.

ОБРАЗОВАНИЕ

НАУКА И ИННОВАЦИОННЫЕ ИДЕИ В МИРЕ

,

41

(4), 88-95.

15.

Abdurashitovich, Z. F. (2024). Department of Syndesmology from the Science of Human

Anatomy General Information About.

Research Journal of Trauma and Disability

Studies

,

3

(3), 158-165.

16.

Abdurashitovich, Z. F. (2024). THE COMPLEXITY OF THE FUSION OF THE BONES

OF THE FOOT.

JOURNAL OF HEALTHCARE AND LIFE-SCIENCE RESEARCH

,

3

(5),

223-230.

17.

Abdurashitovich, Z. F. (2024). ANATOMICAL COMPLEXITIES OF JOINT BONES OF

THE HAND.

EUROPEAN JOURNAL OF MODERN MEDICINE AND PRACTICE

,

4

(4),

198-206.

18.

Зикриллаев, Ф. А. (2024). АНАТОМИЧЕСКОЕ СТРОЕНИЕ ОРГАНОВ ДЫХАНИЯ

И ЕГО ЛИЧНЫЕ ХАРАКТЕРИСТИКИ.

TADQIQOTLAR. UZ

,

40

(3), 86-93.

19.

Abdurashitovich, Z. F., & Komoliddinovich, S. J. (2024).

DIGESTIVE SYSTEM.

ANATOMY OF THE STOMACH.

TADQIQOTLAR. UZ

,

40

(3), 78-85.

20.

Abdurashitovich,

Z.

F.

(2024).

UMURTQA

POG’ONASI

BIRLASHUVLARI.

TADQIQOTLAR. UZ

,

40

(3), 40-47.

21.

Rakhmatova, D. B., & Zikrillaev, F. A. (2022). DETERMINE THE VALUE OF RISK

FACTORS FOR MYOCARDIAL INFARCTION.

FAN, TA'LIM, MADANIYAT VA

INNOVATSIYA JURNALI| JOURNAL OF SCIENCE, EDUCATION, CULTURE AND

INNOVATION

,

1

(4), 23-28.

22.

Abdurashitovich, Z. F. (2024). MIOKARD INFARKTI UCHUN XAVF OMILLARINING

AHAMIYATINI ANIQLASH.

ОБРАЗОВАНИЕ НАУКА И ИННОВАЦИОННЫЕ

ИДЕИ В МИРЕ

,

36

(5), 83-89.

1151

ResearchBib IF - 11.01, ISSN: 3030-3753, Volume 2 Issue 3

23.

Abdurashitovich, Z. F. (2024). THE RELATIONSHIP OF STRESS FACTORS AND

THYMUS.

ОБРАЗОВАНИЕ НАУКА И ИННОВАЦИОННЫЕ ИДЕИ В МИРЕ

,

36

(6),

188-196.

24.

Toxirovna, E. G. (2024). QALQONSIMON BEZ KASALLIKLARIDAN HASHIMOTO

TIREODIT KASALLIGINING MORFOFUNKSIONAL O’ZIGA XOSLIGI.

Modern

education and development

,

16

(7), 120-135.

25.

Toxirovna,

E.

G.

(2024).

REVMATOID

ARTRIT:

BO’G'IMLAR

YALLIG'LANISHINING SABABLARI, KLINIK BELGILARI, OQIBATLARI VA

ZAMONAVIY

DAVOLASH

YONDASHUVLARI.

Modern

education

and

development

,

16

(7), 136-148.

26.

Эргашева, Г. Т. (2024). ОЦЕНКА КЛИНИЧЕСКОЙ ЭФФЕКТИВНОСТИ

ОРЛИСТАТА

У

БОЛЬНЫХ

ОЖИРЕНИЕМ

И

АРТЕРИАЛЬНОЙ

ГИПЕРТЕНЗИЕЙ.

Modern education and development

,

16

(7), 92-105.

27.

Ergasheva, G. T. (2024). THE SPECIFICITY OFAUTOIMMUNE THYROIDITIS IN

PREGNANCY.

European Journal of Modern Medicine and Practice

,

4

(11), 448-453.

28.

Эргашева, Г. Т. (2024). ИССЛЕДОВАНИЕ ФУНКЦИИ ЩИТОВИДНОЙ ЖЕЛЕЗЫ

ПРИ ТИРЕОИДИТЕ ХАШИМОТО.

Modern education and development

,

16

(7), 106-119.

29.

Toxirovna, E. G. (2024). GIPOFIZ ADENOMASINI NAZORAT QILISHDA

KONSERVATIV JARROHLIK VA RADIATSIYA TERAPIYASINING UZOQ

MUDDATLI SAMARADORLIGI.

Modern education and development

,

16

(7), 79-91.

30.

ERGASHEVA, G. T. (2024). OBESITY AND OVARIAN INSUFFICIENCY.

Valeology:

International Journal of Medical Anthropology and Bioethics

,

2

(09), 106-111.

31.

Ergasheva, G. T. (2024). Modern Methods in the Diagnosis of Autoimmune

Thyroiditis.

American Journal of Bioscience and Clinical Integrity

,

1

(10), 43-50.

32.

Tokhirovna, E. G. (2024). COEXISTENCE OF CARDIOVASCULAR DISEASES IN

PATIENTS WITH TYPE 2 DIABETES.

TADQIQOTLAR. UZ

,

40

(3), 55-62.

33.

Toxirovna, E. G. (2024). DETERMINATION AND STUDY OF GLYCEMIA IN

PATIENTS

WITH

TYPE

2

DIABETES

MELLITUS

WITH

COMORBID

DISEASES.

TADQIQOTLAR. UZ

,

40

(3), 71-77.

34.

Toxirovna, E. G. (2024). XOMILADORLIKDA QANDLI DIABET KELTIRIB

CHIQARUVCHI

XAVF

OMILLARINI

ERTA

ANIQLASH

USULLARI.

TADQIQOTLAR. UZ

,

40

(3), 63-70.

35.

Toxirovna, E. G. (2024). QANDLI DIABET 2-TIP VA KOMORBID KASALLIKLARI

BO’LGAN BEMORLARDA GLIKEMIK NAZORAT.

TADQIQOTLAR. UZ

,

40

(3), 48-54.

1152

ResearchBib IF - 11.01, ISSN: 3030-3753, Volume 2 Issue 3

36.

Tokhirovna, E. G. (2024). MECHANISM OF ACTION OF METFORMIN (BIGUANIDE)

IN TYPE 2 DIABETES.

JOURNAL OF HEALTHCARE AND LIFE-SCIENCE

RESEARCH

,

3

(5), 210-216.

37.

Tokhirovna, E. G. (2024). THE ROLE OF METFORMIN (GLIFORMIN) IN THE

TREATMENT OF PATIENTS WITH TYPE 2 DIABETES MELLITUS.

EUROPEAN

JOURNAL OF MODERN MEDICINE AND PRACTICE

,

4

(4), 171-177.

38.

Эргашева, Г. Т. (2024). Эффект Применения Бигуанида При Сахарным Диабетом 2

Типа И Covid-19.

Research Journal of Trauma and Disability Studies

,

3

(3), 55-61.

39.

Toxirovna, E. G. (2024). QANDLI DIABET 2 TUR VA YURAK QON TOMIR

KASALLIKLARINING BEMOLARDA BIRGALIKDA KECHISHI.

ОБРАЗОВАНИЕ

НАУКА И ИННОВАЦИОННЫЕ ИДЕИ В МИРЕ

,

38

(7), 202-209.

40.

Эргашева, Г. Т. (2024). СОСУЩЕСТВОВАНИЕ ДИАБЕТА 2 ТИПА И СЕРДЕЧНО-

СОСУДИСТЫХ ЗАБОЛЕВАНИЙ У ПАЦИЕНТОВ.

ОБРАЗОВАНИЕ НАУКА И

ИННОВАЦИОННЫЕ ИДЕИ В МИРЕ

,

38

(7), 219-226.

41.

Эргашева, Г. Т. (2024).

СНИЖЕНИЕ РИСКА ОСЛОЖНЕНИЙ У БОЛЬНЫХ САХАРНЫМ

ДИАБЕТОМ 2 ТИПА И СЕРДЕЧНО-СОСУДИСТЫМИ ЗАБОЛЕВАНИЯМИ.

Образование

Наука И Инновационные Идеи В Мире

,

38

(7), 210-218.

42.

Tokhirovna, E. G. (2024). CLINICAL AND MORPHOLOGICAL ASPECTS OF THE

COURSE

OF

ARTERIAL

HYPERTENSION.

Лучшие

интеллектуальные

исследования

,

12

(4), 234-243.

43.

Tokhirovna, E. G. Studying the Causes of the Relationship between Type 2 Diabetes and

Obesity.

Published in International Journal of Trend in Scientific Research and

Development (ijtsrd), ISSN

, 2456-6470.

44.

Toxirovna, E. G. (2024). ARTERIAL GIPERTENZIYA KURSINING KLINIK VA

MORFOLOGIK JIHATLARI.

Лучшие интеллектуальные исследования

,

12

(4), 244-253.

45.

Эргашева, Г. Т. (2024). НОВЫЕ АСПЕКТЫ ТЕЧЕНИЕ АРТЕРИАЛЬНОЙ

ГИПЕРТОНИИ

У

ВЗРОСЛОГО

НАСЕЛЕНИЕ.

Лучшие

интеллектуальные

исследования

,

12

(4), 224-233.

46.

Эргашева, Г. Т. (2024). ФАКТОРЫ РИСКА РАЗВИТИЯ САХАРНОГО ДИАБЕТА 2

ТИПА.

ОБРАЗОВАНИЕ НАУКА И ИННОВАЦИОННЫЕ ИДЕИ В МИРЕ

,

36

(5), 70-74.

47.

Эргашева, Г. Т. (2024). ОСЛОЖНЕНИЯ САХАРНОГО ДИАБЕТА 2 ТИПА

ХАРАКТЕРНЫ ДЛЯ КОГНИТИВНЫХ НАРУШЕНИЙ.

TADQIQOTLAR. UZ

,

30

(3),

112-119.

48.

Эргашева, Г. Т. (2023). Исследование Причин Связи Диабета 2 Типа И

Ожирения.

Research Journal of Trauma and Disability Studies

,

2

(12), 305-311.

1153

ResearchBib IF - 11.01, ISSN: 3030-3753, Volume 2 Issue 3

49.

Tokhirovna, E. G. (2024). Risk factors for developing type 2 diabetes

mellitus.

ОБРАЗОВАНИЕ НАУКА И ИННОВАЦИОННЫЕ ИДЕИ В МИРЕ

,

36

(5), 64-69.

50.

Toxirovna, E. G. (2024). QANDLI DIABET 2-TUR VA O’LIMNI KELTIRIB

CHIQARUVCHI SABABLAR.

Лучшие интеллектуальные исследования

,

14

(4), 86-93.

51.

Tokhirovna, E. G. (2023). Study of clinical characteristics of patients with type 2 diabetes

mellitus in middle and old age.

Journal of Science in Medicine and Life

,

1

(4), 16-19.

52.

Toxirovna, E. G. (2024). GIPERPROLAKTINEMIYA KLINIK BELGILARI VA

BEPUSHTLIKKA SABAB BO’LUVCHI OMILLAR.

Лучшие интеллектуальные

исследования

,

14

(4), 168-175.

53.

Toxirovna, E. G. (2023). QANDLI DIABET 2-TUR VA SEMIZLIKNING O’ZARO

BOG’LIQLIK

SABABLARINI

O’RGANISH.

Ta'lim

innovatsiyasi

va

integratsiyasi

,

10

(3), 168-173.

54.

Saidova, L. B., & Ergashev, G. T. (2022). Improvement of rehabilitation and rehabilitation

criteria for patients with type 2 diabetes.

55.

Эргашева, Г. Т. (2023). Изучение Клинических Особенностей Больных Сахарным

Диабетом 2 Типа Среднего И Пожилого Возраста.

Central Asian Journal of Medical

and Natural Science

,

4

(6), 274-276.

56.

Toxirovna, E. G. (2023). O’RTA VA KEKSA YOSHLI BEMORLARDA 2-TUR

QANDLI

DIABET

KECHISHINING

KLINIKO-MORFOLOGIK

XUSUSIYATLARI.

ОБРАЗОВАНИЕ НАУКА И ИННОВАЦИОННЫЕ ИДЕИ В

МИРЕ

,

33

(1), 164-166.

57.

Ergasheva, G. T. (2022). QANDLI DIABET BILAN KASALLANGANLARDA

REABILITATSIYA

MEZONLARINI

TAKOMILASHTIRISH.

TA'LIM

VA

RIVOJLANISH TAHLILI ONLAYN ILMIY JURNALI

,

2

(12), 335-337.

58.

Ergasheva, G. (2024). METHODS TO PREVENT SIDE EFFECTS OF DIABETES

MELLITUS IN SICK PATIENTS WITH TYPE 2 DIABETES.

Журнал академических

исследований нового Узбекистана

,

1

(2), 12-16.

59.

ГТ, Э., & Саидова, Л. Б. (2022). СОВЕРШЕНСТВОВАНИЕ РЕАБИЛИТАЦИОННО-

ВОССТАНОВИТЕЛЬНЫХ КРИТЕРИЕВ БОЛЬНЫХ С СД-2 ТИПА.

TA'LIM VA

RIVOJLANISH TAHLILI ONLAYN ILMIY JURNALI

,

2

(12), 206-209.

60.

Saloxiddinovna, X. Y. (2024). Modern Views on the Effects of the Use of Cholecalciferol

on the General Condition of the Bod.

JOURNAL OF HEALTHCARE AND LIFE-SCIENCE

RESEARCH

,

3

(5), 79-85.

1154

ResearchBib IF - 11.01, ISSN: 3030-3753, Volume 2 Issue 3

61.

Халимова, Ю. С., & Хафизова, М. Н. (2024). МОРФО-ФУНКЦИОНАЛЬНЫЕ И

КЛИНИЧЕСКИЕ АСПЕКТЫ СТРОЕНИЯ И РАЗВИТИЯ ЯИЧНИКОВ (ОБЗОР

ЛИТЕРАТУРЫ).

TADQIQOTLAR. UZ

,

40

(5), 188-198.

62.

Халимова, Ю. С. (2024). Морфологические Особенности Поражения Печени У

Пациентов С Синдромом Мэллори-Вейса.

Journal of Science in Medicine and Life

,

2

(6),

166-172.

63.

Xalimova, Y. S. (2024). Morphology of the Testes in the Detection of Infertility.

Journal

of Science in Medicine and Life

,

2

(6), 83-88.

64.

KHALIMOVA, Y. S. (2024). MORPHOFUNCTIONAL CHARACTERISTICS OF

TESTICULAR AND OVARIAN TISSUES OF ANIMALS IN THE AGE

ASPECT.

Valeology: International Journal of Medical Anthropology and Bioethics

,

2

(9),

100-105.

65.

Salokhiddinovna, K. Y. (2024). IMMUNOLOGICAL CRITERIA OF REPRODUCTION

AND VIABILITY OF FEMALE RAT OFFSPRING UNDER THE INFLUENCE OF

ETHANOL.

EUROPEAN JOURNAL OF MODERN MEDICINE AND PRACTICE

,

4

(10),

200-205.

66.

Salokhiddinovna, K. Y., Saifiloevich, S. B., Barnoevich, K. I., & Hikmatov, A. S. (2024).

THE INCIDENCE OF AIDS, THE DEFINITION AND CAUSES OF THE

DISEASE.

ОБРАЗОВАНИЕ НАУКА И ИННОВАЦИОННЫЕ ИДЕИ В МИРЕ

,

55

(2),

195-205.

67.

Nematilloevna, K. M., & Salokhiddinovna, K. Y. (2024).

IMPORTANT FEATURES IN

THE

FORMATION

OF

DEGREE

OF

COMPARISON

OF

ADJECTIVES

IN

LATIN.

ОБРАЗОВАНИЕ НАУКА И ИННОВАЦИОННЫЕ ИДЕИ В МИРЕ

,

55

(2), 150-157.

68.

Saloxiddinovna, X. Y., & Ne’matillaevna, X. M. (2024).

FEATURES OF THE

STRUCTURE

OF

THE

REPRODUCTIVE

ORGANS

OF

THE

FEMALE

BODY.

ОБРАЗОВАНИЕ НАУКА И ИННОВАЦИОННЫЕ ИДЕИ В МИРЕ

,

55

(2), 179-183.

69.

Khalimova, Y. (2025). MORPHOLOGY OF PATHOLOGICAL FORMS OF

PLATELETS.

Modern Science and Research

,

4

(2), 749-759.