Please use this identifier to cite or link to this item: http://repo.tma.uz/xmlui/handle/1/4162
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dc.contributor.authorNazarova N.O-
dc.date.accessioned2026-06-09T08:39:40Z-
dc.date.available2026-06-09T08:39:40Z-
dc.date.issued2026-
dc.identifier.urihttp://repo.tma.uz/xmlui/handle/1/4162-
dc.description.abstractAtherosclerotic renal artery disease (ARAD) is a major cause of secondary hypertension and ischemic nephropathy. Angiotensinogen (AGT), as the precursor of angiotensin peptides in the renin-angiotensin-aldosterone system (RAAS), is central to many of the pathophysiologic mechanisms in ARAD. In this review, we examine clinical studies on AGT gene polymorphisms, outcomes of RAAS blockade, and the impact of AGT-fo cused therapies in ARAD. The aim is to clarify what is known, what remains controversial, and which areas merit further investigationen_US
dc.language.isoen_USen_US
dc.publisherO'zbekiston, Toshkent ( O‘ZBEKISTON TIBBIYOT AXBOROTNOMASI JURNALI )en_US
dc.subjectchronic kidney disease, renal artery atherosclerosis, urea, creatinine, cystatin C, endothelin1, proteinuriaen_US
dc.titleTHE ROLE OF ANGIOTENSINOGEN (AGT) IN ATHEROSCLEROTIC RENAL ARTERY DISEASEen_US
dc.typeArticleen_US
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