Role of the Renin-Angiotensin-Aldosterone System in the Regulation of Plasma Potassium in Chronic Renal Disease

Nephron ◽  
1975 ◽  
Vol 15 (1) ◽  
pp. 35-49 ◽  
Author(s):  
P. Weidmann ◽  
M.H. Maxwell ◽  
P. Rowe ◽  
R. Winer ◽  
S.G. Massry
2012 ◽  
Vol 27 (suppl 3) ◽  
pp. iii51-iii57 ◽  
Author(s):  
A. M. van der Graaf ◽  
T. J. Toering ◽  
M. M. Faas ◽  
A. Titia Lely

Circulation ◽  
2015 ◽  
Vol 131 (suppl_1) ◽  
Author(s):  
Tanika N Kelly ◽  
Dominic Raj ◽  
Mahboob Rahman ◽  
Matthias Kretzler ◽  
Radhakrishna R Kallem ◽  
...  

Background: We conducted single-marker, gene-based and pathway-based analyses to examine the association between renin-angiotensin-aldosterone system (RAAS) variants and chronic kidney disease (CKD) progression among Chronic Renal Insufficiency Cohort (CRIC) study participants. Methods: A total of 1,523 white and 1,490 black subjects were genotyped for 490 SNPs in 12 RAAS genes as part of the ITMAT-Broad-CARe array. CKD progression phenotypes included decline in estimated glomerular filtration rate (eGFR) over time and the occurrence of a renal disease event, defined as incident end stage renal disease or halving of eGFR from baseline. Mixed-effects models were used to examine SNP associations with eGFR decline, while Cox proportional hazards models tested SNP associations with renal events. Gene and pathway-based analyses were conducted using the truncated product method. All analyses were stratified by race, and a Bonferroni correction was applied to adjust for multiple testing. Results: Among white and black participants, eGFR declined an average of 1.2 and 2.3 ml/min/1.73m 2 per year, respectively, while renal events occurred in a respective 11.5% and 24.9% of participants. We identified strong gene and pathway-based associations with CKD progression. The AGT and RENBP genes were consistently associated with risk of renal events in separate analyses of white and black participants (all P <1.00х10 -6 ). Driven by the significant gene-based findings, the entire RAAS pathway was also associated with renal events in both groups (both P <1.00х10 -6 ). No single-marker associations with CKD progression were observed. Conclusions: The current study provides strong evidence for a role of the RAAS in CKD progression.


2021 ◽  
Author(s):  
Violeta Capric ◽  
Harshith Priyan Chandrakumar ◽  
Jessica Celenza-Salvatore ◽  
Amgad N. Makaryus

Increased attention has been placed on the activation of the renin-angiotensin-aldosterone system (RAAS) and pathogenetic mechanisms in cardiovascular disease. Multiple studies have presented data to suggest that cardiac and arterial stiffness leading to adverse remodeling of both the heart and vasculature leads to the various pathological changes seen in coronary artery disease, heart failure (with preserved and reduced ejection fractions), hypertension and renal disease. Over-activation of the RAAS is felt to contribute to these structural and endocrinological changes through its control of the Na+/K+ balance, fluid volume, and hemodynamic stability. Subsequently, along these lines, multiple large investigations have shown that RAAS blockade contributes to prevention of both cardiovascular and renal disease. We aim to highlight the known role of the activated RAAS and provide an updated description of the mechanisms by which activation of RAAS promotes and leads to the pathogenesis of cardiovascular disease.


2001 ◽  
Vol 21 (6) ◽  
pp. 580-592 ◽  
Author(s):  
Arnold Boonstra ◽  
Dick de Zeeuw ◽  
Paul E. de Jong ◽  
Gerjan Navis

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