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The paradox of the renin-angiotensin system in chronic renal disease
M E Rosenberg1, L J Smith, R Correa-Rotter
1Department of Medicine, University of Minnesota, Minneapolis.
Abstract:
Despite normal to suppressed levels of renin activity in chronic renal disease, multiple lines of evidence suggest a role for the RAS, especially its intrarenal expression, in several critical aspects of this condition. Alterations in the distribution and control of components of the renal RAS could account for localized areas of activation of this system. Renal scarring may be particularly important as a major stimulus to renin synthesis in the diseased kidney. While both intrarenal and systemic hypertension may depend in part upon actions of the RAS, other non-hemodynamic actions of the RAS may also contribute to the adaptation of residual nephrons as well as their progressive injury.
Insights
The renin-angiotensin system (RAS) plays a key role in chronic kidney disease (CKD) progression, even with normal or low renin activity. Intrarenal RAS activation, particularly due to renal scarring, contributes to hypertension and kidney injury.
Area of Science:
- Nephrology
- Renal Physiology
- Cardiovascular Research
Background:
- Chronic renal disease (CKD) often presents with normal to suppressed systemic renin activity.
- Evidence suggests the renin-angiotensin system (RAS), particularly its intrarenal components, is implicated in CKD pathogenesis.
- Dysregulation of the renal RAS may lead to localized activation and contribute to disease progression.
Purpose of the Study:
- To investigate the role of the intrarenal renin-angiotensin system (RAS) in chronic renal disease.
- To explore how alterations in RAS components contribute to renal adaptation and injury in CKD.
- To understand the link between renal scarring and RAS activation in diseased kidneys.
Main Methods:
- Analysis of evidence regarding intrarenal RAS expression and control in CKD.
- Review of studies on the impact of renal scarring on renin synthesis.
- Examination of the hemodynamic and non-hemodynamic actions of the RAS in CKD models.
Main Results:
- Despite suppressed systemic renin activity, intrarenal RAS activation is evident in CKD.
- Altered distribution and control of renal RAS components facilitate localized activation.
- Renal scarring emerges as a significant stimulus for renin synthesis in diseased kidneys.
- Both hemodynamic and non-hemodynamic RAS actions contribute to nephron adaptation and injury.
Conclusions:
- The intrarenal RAS is critically involved in the pathophysiology of chronic renal disease.
- Localized RAS activation, driven by factors like renal scarring, contributes to hypertension and progressive kidney damage.
- Non-hemodynamic effects of the RAS are important in the adaptation and injury of residual nephrons in CKD.