Authors :
Syed Muhammad Ali; Liu Zhen; Doctor Sadia Hassan; Rexidan; Nida Aslam
Volume/Issue :
Volume 9 - 2024, Issue 3 - March
Google Scholar :
https://tinyurl.com/y8s26dbu
Scribd :
https://tinyurl.com/zek8dmvb
DOI :
https://doi.org/10.38124/ijisrt/IJISRT24MAR1868
Note : A published paper may take 4-5 working days from the publication date to appear in PlumX Metrics, Semantic Scholar, and ResearchGate.
Abstract :
Chronic kidney disease (CKD) is a global
health concern associated with significant morbidity and
mortality. Albuminuria, a hallmark of kidney damage, is
a strong predictor of CKD progression and adverse
outcomes. Recent research has focused on understanding
the correlation between urinary angiotensinogen (AGT)
levels, a component of the renin-angiotensin system
(RAS), and albuminuria in CKD patients. This review
article synthesizes evidence from various studies
exploring this correlation and elucidates its mechanistic
insights and clinical implications.
Clinical studies consistently demonstrate a positive
correlation between urinary AGT levels and albuminuria
in CKD patients. Elevated urinary AGT levels are
associated with increased albuminuria, independent of
traditional risk factors, suggesting a potential role for
AGT in the pathogenesis of kidney damage and
proteinuria in CKD. Mechanistic insights suggest that
increased intrarenal RAS activity may lead to enhanced
AGT production and secretion, contributing to
glomerular hypertension, inflammation, and fibrosis,
ultimately promoting albuminuria and CKD
progression.
The clinical implications of this correlation are
profound. Elevated urinary AGT levels may serve as a
non-invasive biomarker for assessing intrarenal RAS
activity and predicting CKD progression and adverse
outcomes. Furthermore, interventions targeting the RAS
pathway, such as angiotensin-converting enzyme (ACE)
inhibitors and angiotensin receptor blockers (ARBs),
may help reduce urinary AGT levels and mitigate
albuminuria, offering promising therapeutic
opportunities for improving patient outcomes in CKD.
In conclusion, the correlation between urinary AGT
and albuminuria in CKD represents a complex interplay
between renal physiology, RAS activation, and kidney
damage. By elucidating this correlation, we gain valuable
insights into the pathogenesis of CKD and identify
urinary AGT as a potential biomarker and therapeutic
target for personalized CKD management. Further
research is warranted to validate these findings, explore
the clinical utility of urinary AGT measurement, and
develop targeted interventions aimed at mitigating
albuminuria and slowing CKD progression. Through
continued investigation, we can strive to improve
outcomes and quality of life for patients living with
CKD.
Keywords :
Chronic Kidney Disease, Albuminuria, Angiotensinogen, Urinary Angiotensinogen
Chronic kidney disease (CKD) is a global
health concern associated with significant morbidity and
mortality. Albuminuria, a hallmark of kidney damage, is
a strong predictor of CKD progression and adverse
outcomes. Recent research has focused on understanding
the correlation between urinary angiotensinogen (AGT)
levels, a component of the renin-angiotensin system
(RAS), and albuminuria in CKD patients. This review
article synthesizes evidence from various studies
exploring this correlation and elucidates its mechanistic
insights and clinical implications.
Clinical studies consistently demonstrate a positive
correlation between urinary AGT levels and albuminuria
in CKD patients. Elevated urinary AGT levels are
associated with increased albuminuria, independent of
traditional risk factors, suggesting a potential role for
AGT in the pathogenesis of kidney damage and
proteinuria in CKD. Mechanistic insights suggest that
increased intrarenal RAS activity may lead to enhanced
AGT production and secretion, contributing to
glomerular hypertension, inflammation, and fibrosis,
ultimately promoting albuminuria and CKD
progression.
The clinical implications of this correlation are
profound. Elevated urinary AGT levels may serve as a
non-invasive biomarker for assessing intrarenal RAS
activity and predicting CKD progression and adverse
outcomes. Furthermore, interventions targeting the RAS
pathway, such as angiotensin-converting enzyme (ACE)
inhibitors and angiotensin receptor blockers (ARBs),
may help reduce urinary AGT levels and mitigate
albuminuria, offering promising therapeutic
opportunities for improving patient outcomes in CKD.
In conclusion, the correlation between urinary AGT
and albuminuria in CKD represents a complex interplay
between renal physiology, RAS activation, and kidney
damage. By elucidating this correlation, we gain valuable
insights into the pathogenesis of CKD and identify
urinary AGT as a potential biomarker and therapeutic
target for personalized CKD management. Further
research is warranted to validate these findings, explore
the clinical utility of urinary AGT measurement, and
develop targeted interventions aimed at mitigating
albuminuria and slowing CKD progression. Through
continued investigation, we can strive to improve
outcomes and quality of life for patients living with
CKD.
Keywords :
Chronic Kidney Disease, Albuminuria, Angiotensinogen, Urinary Angiotensinogen
