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Updated: Jul 6, 2026
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Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion
Published on: May 26, 2022
Autonomic renal denervation ameliorates experimental glomerulonephritis
Roland Veelken1, Eva-Maria Vogel, Karl Hilgers
1Department of Nephrology and Hypertension, University of Erlangen-Nuremberg, Erlangen, Germany.
Journal of the American Society of Nephrology : JASN
|April 11, 2008
Summary
Autonomic nerves influence kidney inflammation. Denerving the kidney reduced inflammation and damage in a rat model of glomerulonephritis, suggesting nerve targets for treatment.
Area of Science:
- Neuroscience
- Immunology
- Nephrology
Background:
- Visceral organ inflammation is modulated by the autonomic nervous system.
- Neuroimmune interactions in the kidney remain understudied.
- Kidneys are innervated by sympathetic and sensory nerve fibers near immune cells.
Purpose of the Study:
- To investigate the role of autonomic renal innervation in acute kidney inflammation.
- To determine if renal denervation affects the development of glomerulonephritis.
Main Methods:
- Surgical bilateral renal denervation in rats 2 days before inducing glomerulonephritis with anti-Thy-1.1 antibody (OX-7).
- Assessment of kidney injury markers (albuminuria, mesangiolysis, microaneurysms, collagen IV deposition).
- Evaluation of inflammatory markers (macrophage accumulation, TNF-alpha, TGF-beta) and mesangial cell proliferation.
Main Results:
- Renal denervation significantly reduced albuminuria, mesangiolysis, microaneurysms, and glomerular collagen IV deposition.
- Denervation decreased TGF-beta expression, interstitial macrophage accumulation, and TNF-alpha levels.
- Mesangial cell proliferation was also significantly reduced following denervation.
Conclusions:
- Autonomic renal denervation ameliorates acute glomerulonephritis in rats.
- Kidney innervation appears to exacerbate acute kidney inflammation.
- Neurotransmitters and their receptors are potential therapeutic targets for acute glomerulonephritis.
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