Monotherapy of RAAS blockers and mobilization of aldosterone: A mechanistic perspective study in kidney disease

Gupta G 1 , Dahiya R 2 , Singh Y 3 , Mishra A 4 , Verma A 5 , Gothwal SK 6 Show all authors , Aljabali AAA 7 , Dureja H 8 , Prasher P 9 , Negi P 10 , Kapoor DN 10 , Goyal R 10 , Tambuwala MM 11 , Chellappan DK 12 , Dua K 13

Affiliations 

  • 1 School of Pharmacy, Suresh Gyan Vihar University, Mahal Road, Jagatpura, Jaipur, India. Electronic address: [email protected]
  • 2 Laboratory of Peptide Research and Development, School of Pharmacy, Faculty of Medical Sciences, The University of the West Indies, St. Augustine, Trinidad & Tobago, West Indies
  • 3 Mahatma Gandhi College of Pharmaceutical Sciences, Sitapura, Jaipur, India. Electronic address: [email protected]
  • 4 School of Pharmacy, Suresh Gyan Vihar University, Mahal Road, Jagatpura, Jaipur, India
  • 5 Mahatma Gandhi College of Pharmaceutical Sciences, Sitapura, Jaipur, India
  • 6 Department of Medicine, JLN Medical College, Ajmer, India
  • 7 Faculty of Pharmacy, Department of Pharmaceutical Sciences, Yarmouk University, Irbid, 21163, Jordan
  • 8 Department of Pharmaceutical Sciences, Maharishi Dayanand University, Rohtak, Haryana, 124001, India
  • 9 Department of Chemistry, University of Petroleum & Energy Studies, Dehradun, 248007, India
  • 10 School of Pharmaceutical Sciences, Shoolini University of Biotechnology and Management Sciences, Solan, 173229, India
  • 11 School of Pharmacy and Pharmaceutical Sciences, Ulster University, Coleraine, County, Londonderry, BT52 1SA, Northern Ireland, United Kingdom
  • 12 Department of Life Sciences, School of Pharmacy, International Medical University, Bukit Jalil, Kuala Lumpur, 57000, Malaysia
  • 13 Centre for Inflammation, Centenary Institute, Sydney, NSW, 2050, Australia; Priority Research Centre for Healthy Lungs, Hunter Medical Research Institute (HMRI) & School of Biomedical Sciences and Pharmacy, The University of Newcastle (UoN), Callaghan, NSW, 2308, Australia; Discipline of Pharmacy, Graduate School of Health, University of Technology Sydney (UTS), Ultimo, NSW, 2007, Australia
Chem Biol Interact, 2020 Feb 01;317:108975.
PMID: 32032593 DOI: 10.1016/j.cbi.2020.108975

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.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.

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