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

Gaurav Gupta, Rajiv Dahiya, Yogendra Singh, Anurag Mishra, Aseem Verma, Sunil Kumar Gothwal, Alaa A.a. Aljabali, Harish Dureja, Parteek Prasher, Poonam Negi, Deepak N. Kapoor, Rohit Goyal, Murtaza M. Tambuwala, Dinesh K. Chellappan, Kamal Dua

Research output: Contribution to journalArticle

5 Citations (Scopus)

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.
Original languageEnglish
Article number108975
JournalChemico-Biological Interactions
Volume317
Early online date4 Feb 2020
DOIs
Publication statusE-pub ahead of print - 4 Feb 2020

Keywords

  • Aldosterone synthase
  • Angiotensin receptor blockers
  • Angiotensin-converting enzyme inhibitors
  • Chronic kidney disease
  • Hyperkalemia
  • Renin-angiotensin-aldosterone system

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