Monotherapy of RAAS blockers and mobilization of aldosterone: A mechanistic perspective study in kidney disease.
Gupta, G
Dahiya, R
Singh, Y
Mishra, A
Verma, A
Gothwal, SK
Aljabali, AAA
Dureja, H
Prasher, P
Negi, P
Kapoor, DN
Goyal, R
Tambuwala, MM
Chellappan, DK
Dua, K
- Publisher:
- ELSEVIER IRELAND LTD
- Publication Type:
- Journal Article
- Citation:
- Chemico-biological interactions, 2020, 317
- Issue Date:
- 2020-02-04
Closed Access
Filename | Description | Size | |||
---|---|---|---|---|---|
1-s2.0-S0009279720300041-main.pdf | Published version | 954.34 kB | Adobe PDF |
Copyright Clearance Process
- Recently Added
- In Progress
- Closed Access
This item is closed access and not available.
Full metadata record
Field | Value | Language |
---|---|---|
dc.contributor.author | Gupta, G | |
dc.contributor.author | Dahiya, R | |
dc.contributor.author | Singh, Y | |
dc.contributor.author | Mishra, A | |
dc.contributor.author | Verma, A | |
dc.contributor.author | Gothwal, SK | |
dc.contributor.author | Aljabali, AAA | |
dc.contributor.author | Dureja, H | |
dc.contributor.author | Prasher, P | |
dc.contributor.author | Negi, P | |
dc.contributor.author | Kapoor, DN | |
dc.contributor.author | Goyal, R | |
dc.contributor.author | Tambuwala, MM | |
dc.contributor.author | Chellappan, DK | |
dc.contributor.author |
Dua, K https://orcid.org/0000-0002-7507-1159 |
|
dc.date.accessioned | 2020-08-24T06:09:53Z | |
dc.date.available | 2020-02-03 | |
dc.date.available | 2020-08-24T06:09:53Z | |
dc.date.issued | 2020-02-04 | |
dc.identifier.citation | Chemico-biological interactions, 2020, 317 | |
dc.identifier.issn | 0009-2797 | |
dc.identifier.issn | 1872-7786 | |
dc.identifier.uri | http://hdl.handle.net/10453/142329 | |
dc.description.abstract | In patients with acute kidney injury progressively converting into chronic kidney disease (CKD), proteinuria and high blood pressure predict progression to end-stage renal disease (ESRD). Although, Renin-angiotensin-aldosterone system (RAAS) regulates blood pressure and kidney disease through both direct and indirect mechanisms. RAAS blockers that act at the level of angiotensin or lower in the cascade can cause compensatory increases in the plasma renin and angiotensin II level. Here, in this review article, we are exploring the evidence-based on RAAS blockade action releases of aldosterone and hypothesizing the molecular mechanism for converting the acute kidney injury into chronic kidney disease to end-stage renal disease. | |
dc.format | Print-Electronic | |
dc.language | eng | |
dc.publisher | ELSEVIER IRELAND LTD | |
dc.relation.ispartof | Chemico-biological interactions | |
dc.relation.isbasedon | 10.1016/j.cbi.2020.108975 | |
dc.rights | info:eu-repo/semantics/closedAccess | |
dc.subject | 0601 Biochemistry and Cell Biology | |
dc.subject.classification | Toxicology | |
dc.subject.mesh | Humans | |
dc.subject.mesh | Kidney Diseases | |
dc.subject.mesh | Aldosterone | |
dc.subject.mesh | Adrenal Cortex Hormones | |
dc.subject.mesh | Angiotensin-Converting Enzyme Inhibitors | |
dc.subject.mesh | Renin-Angiotensin System | |
dc.subject.mesh | Angiotensin Receptor Antagonists | |
dc.subject.mesh | Humans | |
dc.subject.mesh | Kidney Diseases | |
dc.subject.mesh | Aldosterone | |
dc.subject.mesh | Adrenal Cortex Hormones | |
dc.subject.mesh | Angiotensin-Converting Enzyme Inhibitors | |
dc.subject.mesh | Renin-Angiotensin System | |
dc.subject.mesh | Angiotensin Receptor Antagonists | |
dc.subject.mesh | Adrenal Cortex Hormones | |
dc.subject.mesh | Aldosterone | |
dc.subject.mesh | Angiotensin Receptor Antagonists | |
dc.subject.mesh | Angiotensin-Converting Enzyme Inhibitors | |
dc.subject.mesh | Humans | |
dc.subject.mesh | Kidney Diseases | |
dc.subject.mesh | Renin-Angiotensin System | |
dc.title | Monotherapy of RAAS blockers and mobilization of aldosterone: A mechanistic perspective study in kidney disease. | |
dc.type | Journal Article | |
utslib.citation.volume | 317 | |
utslib.location.activity | Ireland | |
utslib.for | 0601 Biochemistry and Cell Biology | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Health | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Health/Graduate School of Health/GSH.Pharmacy | |
pubs.organisational-group | /University of Technology Sydney | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Health/Graduate School of Health | |
utslib.copyright.status | closed_access | * |
pubs.consider-herdc | false | |
dc.date.updated | 2020-08-24T06:09:44Z | |
pubs.publication-status | Published | |
pubs.volume | 317 |
Abstract:
In patients with acute kidney injury progressively converting into chronic kidney disease (CKD), proteinuria and high blood pressure predict progression to end-stage renal disease (ESRD). Although, Renin-angiotensin-aldosterone system (RAAS) regulates blood pressure and kidney disease through both direct and indirect mechanisms. RAAS blockers that act at the level of angiotensin or lower in the cascade can cause compensatory increases in the plasma renin and angiotensin II level. Here, in this review article, we are exploring the evidence-based on RAAS blockade action releases of aldosterone and hypothesizing the molecular mechanism for converting the acute kidney injury into chronic kidney disease to end-stage renal disease.
Please use this identifier to cite or link to this item:
Download statistics for the last 12 months
Not enough data to produce graph