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Frontiers in Nephrology
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Renin-Angiotensin-Aldosterone System and Progression of Renal Disease

Christiane Rüster and Gunter Wolf
JASN November 2006, 17 (11) 2985-2991; DOI: https://doi.org/10.1681/ASN.2006040356
Christiane Rüster
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Gunter Wolf
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    Figure 1.

    Overview of the renin-angiotensin-aldosterone system (RAAS). The system has become increasingly complex with alternative ways of angiotensin II (AngII) formation besides angiotensin-converting enzyme (ACE; (Chymase, chymostatin-sensitive AngII-generating enzyme [CAGE]), a second form of ACE (ACE2), and novel peptides such as AngIV, angiotensin 1-9, and angiotensin 1-7. Clinically important could be that AngII can bind to AngII type 2 (AT2) receptors and AngIV to AT4 receptors that are not antagonized by sartanes, inducing proinflammatory and profibrotic effects (e.g., induction of chemokines, stimulation of plasminogen activator inhibitor-1).

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    Figure 2.

    Proximal tubular cells as an example of a local RAAS. Tubular cells could generate AngII in nanomolar concentrations and secrete into the tubular fluid as well as the interstitial space. Furthermore, tubular cells secrete intact angiotensinogen into the tubular fluid. Cells also could take renin and angiotensinogen up from the circulation, indicating a close interaction with the systemic RAAS. Although proximal tubular cells have ACE in their brush border membranes, it is controversial whether intracellular ACE contributes to AngII formation.

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    Figure 3.

    AngII is a cytokine with many effects on the kidney, clearly beyond the classical function as a hemodynamic mediator.

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Journal of the American Society of Nephrology: 17 (11)
Journal of the American Society of Nephrology
Vol. 17, Issue 11
November 2006
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Renin-Angiotensin-Aldosterone System and Progression of Renal Disease
Christiane Rüster, Gunter Wolf
JASN Nov 2006, 17 (11) 2985-2991; DOI: 10.1681/ASN.2006040356

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Renin-Angiotensin-Aldosterone System and Progression of Renal Disease
Christiane Rüster, Gunter Wolf
JASN Nov 2006, 17 (11) 2985-2991; DOI: 10.1681/ASN.2006040356
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  • Article
    • Abstract
    • How the RAAS Was Seen in the Past
    • Generation of AngII and Other Peptides
    • AngII Receptors
    • Local RAAS
    • Proteinuria
    • Inflammation
    • Growth Effects and Apoptosis
    • Fibrosis
    • ACE Inhibitor and AT1 Receptor Effects Independent of the RAAS
    • What about Aldosterone?
    • Conclusion
    • Acknowledgments
    • Footnotes
    • References
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More in this TOC Section

  • Polycystic Kidney Disease
  • Genotype–Phenotype Correlations in Autosomal Dominant and Autosomal Recessive Polycystic Kidney Disease
  • Role of Primary Cilia in the Pathogenesis of Polycystic Kidney Disease
Show more Frontiers in Nephrology

Cited By...

  • Mechanisms of Metabolic Acidosis-Induced Kidney Injury in Chronic Kidney Disease
  • Association of B-Type Natriuretic Peptide Level With Residual Kidney Function in Incident Peritoneal Dialysis Patients
  • Alterations of Hepatic Metabolism in Chronic Kidney Disease via D-box-binding Protein Aggravate the Renal Dysfunction
  • Angiotensin II down-regulates nephrin-Akt signaling and induces podocyte injury: role of c-Abl
  • Smad7 inhibits AngII-mediated hypertensive nephropathy in a mouse model of hypertension
  • RETRACTION: Angiotensin II and Canonical Transient Receptor Potential-6 Activation Stimulate Release of a Signal Transducer and Activator of Transcription 3-Activating Factor from Mouse Podocytes
  • High urinary ACE2 concentrations are associated with severity of glucose intolerance and microalbuminuria
  • Silencing of Hypoxia-Inducible Factor-1{alpha} Gene Attenuated Angiotensin II-Induced Renal Injury in Sprague-Dawley Rats
  • Angiotensin II as a Morphogenic Cytokine Stimulating Renal Fibrogenesis
  • ACE Inhibition Is Renoprotective among Obese Patients with Proteinuria
  • Mechanisms of Tubulointerstitial Fibrosis
  • Angiotensin II revisited: new roles in inflammation, immunology and aging
  • Renin-Angiotensin-Aldosterone System Blockade Effects on the Kidney in the Elderly: Benefits and Limitations
  • Calcineurin Inhibitor Nephrotoxicity
  • Renin-Angiotensin System Blockade Is Renoprotective in Immune Complex-Mediated Glomerulonephritis
  • Angiotensin II Induced Reactive Oxygen Species and the Kidney
  • Obesity and Obesity-Initiated Metabolic Syndrome: Mechanistic Links to Chronic Kidney Disease
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