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РецензированоEN2025

PATHOPHYSIOLOGY OF HEPATORENAL SYNDROME: A COMPREHENSIVE REVIEW

D.R. Abdullayeva,I.Sh. Bobojonov (Urgench Branch of Tashkent Medical Academy, Urgench, Uzbekistan,Urgench Branch of Tashkent Medical Academy, Urgench, Uzbekistan)

Научный информационный бюллетень · 163-170 · 2025

Аннотация

Hepatorenal Syndrome (HRS) is a grave complication of advanced liver disease, characterized by functional renal failure in the absence of underlying structural kidney pathology. The pathogenesis of HRS is multifactorial and deeply intertwined with the complex hemodynamic changes that occur in cirrhosis. The hallmark features include splanchnic arterial vasodilation, systemic circulatory dysfunction, renal vasoconstriction, and impaired renal autoregulation. Neurohormonal activation, particularly the renin-angiotensin-aldosterone system (RAAS), sympathetic nervous system (SNS), and non-osmotic vasopressin release, plays a pivotal role. Emerging evidence highlights the role of systemic inflammation, bacterial translocation, and immune dysregulation in the progression of renal dysfunction in cirrhosis. This article explores the detailed pathophysiology of HRS, from its historical development to molecular mechanisms, and discusses how this understanding informs clinical management and therapeutic development.

Доказательный фрагмент

«Hepatorenal Syndrome (HRS) is a grave complication of advanced liver disease, characterized by functional renal failure in the absence of underlying structural kidney pathology.»

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Демо-превью

Hepatorenal Syndrome (HRS) is a grave complication of advanced liver disease, characterized by functional renal failure in the absence of underlying structural kidney pathology. Полный текст публикации CiteX не хранит — доступ к первоисточнику открывается по DOI согласно лицензии издателя и выбранному плану.

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Тип
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Узбекистан
Ключевые слова
Hepatorenal syndrome, Pathophysiology, Cirrhosis, Renal vasoconstriction, Splanchnic vasodilation, Systemic inflammation, Portal hypertension, Neurohormonal activation, Nitric oxide, RAAS, AKI in cirrhosis.
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