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The renin-angiotensin-aldosterone system and the kidney: effects on kidney disease
Ursula C Brewster1, Mark A Perazella
1Section of Nephrology, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520-8029, USA.
Abstract:
The renin-angiotensin-aldosterone system regulates renal vasomotor activity, maintains optimal salt and water homeostasis, and controls tissue growth in the kidney. However, pathologic consequences can result from overactivity of this cascade, involving it in the pathophysiology of kidney disease. An activated renin-angiotensin-aldosterone system promotes both systemic and glomerular capillary hypertension, which can induce hemodynamic injury to the vascular endothelium and glomerulus. In addition, direct profibrotic and proinflammatory actions of angiotensin II and aldosterone may also promote kidney damage. The majority of the untoward effects associated with angiotensin II appear to be mediated through its binding to the angiotensin II type 1 receptor. Aldosterone can also induce renal injury by binding to its receptor in the kidney. An understanding of this system is important to appreciate that inhibitors of this cascade can reduce the progression of chronic kidney disease in proteinuric disease states. Pharmacologic agents that can interfere with this cascade include angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and aldosterone receptor antagonists. This paper will provide an overview of the renin-angiotensin system, review its role in kidney disease, examine the renal effects of inhibition of this cascade in experimental animal models, and review clinical studies utilizing renin-angiotensin-aldosterone inhibitors in patients with diabetic and nondiabetic nephropathies.
Insights
The renin-angiotensin-aldosterone system contributes to kidney disease progression. Inhibiting this system, using agents like ACE inhibitors, can slow chronic kidney disease advancement in proteinuric conditions.
Area of Science:
- Nephrology
- Endocrinology
- Cardiovascular Physiology
Background:
- The renin-angiotensin-aldosterone system (RAAS) is crucial for regulating blood pressure, fluid balance, and kidney growth.
- Overactivation of the RAAS contributes significantly to the pathophysiology of various kidney diseases.
- RAAS overactivity leads to hypertension and direct cellular damage within the kidney.
Purpose of the Study:
- To provide an overview of the renin-angiotensin system.
- To review the role of RAAS in kidney disease.
- To examine the effects of RAAS inhibition in preclinical models and clinical studies.
Main Methods:
- Review of existing literature on the renin-angiotensin-aldosterone system and kidney disease.
- Analysis of experimental animal models demonstrating the renal effects of RAAS inhibition.
- Review of clinical studies evaluating RAAS inhibitors in diabetic and nondiabetic nephropathies.
Main Results:
- Activated RAAS promotes systemic and glomerular hypertension, causing hemodynamic injury.
- Angiotensin II and aldosterone exert direct profibrotic and proinflammatory effects on the kidney.
- Inhibitors of the RAAS cascade have shown potential in reducing chronic kidney disease progression.
Conclusions:
- Understanding the RAAS is key to managing kidney disease.
- Pharmacologic inhibition of the RAAS, including ACE inhibitors, ARBs, and aldosterone antagonists, is a viable strategy to mitigate kidney damage.
- RAAS inhibitors demonstrate efficacy in slowing the progression of proteinuric kidney diseases.
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