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A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis
Published on: October 26, 2020
Glomerular hemodynamic changes associated with arteriolar lesions and tubulointerstitial inflammation
Laura G Sánchez-Lozada1, Edilia Tapia, Richard J Johnson
1Department of Nephrology, Instituto Nacional de Cardiología Ignacio Chávez, México City, México.
Kidney International. Supplement
|September 13, 2003
Summary
Tubulointerstitial injury, not glomerular changes, better predicts kidney failure. Therapies targeting inflammation and vascular changes may protect kidneys from progressive renal disease.
Area of Science:
- Nephrology
- Renal Pathophysiology
- Cardiovascular Research
Background:
- Tubulointerstitial (TI) injury, rather than glomerular damage, correlates more strongly with kidney disease progression.
- Tubulointerstitial alterations may influence glomerular hemodynamics in renal disease.
- Inflammatory cell infiltration in the tubulointerstitium contributes to renal damage.
Purpose of the Study:
- To investigate the role of tubulointerstitial alterations in modifying glomerular hemodynamics during renal disease progression.
- To evaluate the renoprotective effects of anti-inflammatory agents in experimental models of progressive renal disease.
- To assess the impact of polysulphate pentosan (PPS) and mycophenolate mofetil (MMF) on glomerular hemodynamics and arteriolopathy in subtotally ablated rats.
Main Methods:
- Utilized experimental models of progressive renal disease, including subtotal renal ablation in rats.
- Administered anti-inflammatory drugs, specifically polysulphate pentosan (PPS) and mycophenolate mofetil (MMF).
- Monitored proteinuria, glomerular hypertension, hyperfiltration, arterial hypertension, afferent resistance, and arteriolopathy.
Main Results:
- PPS and MMF treatment prevented proteinuria, glomerular hypertension, and hyperfiltration in subtotally ablated rats.
- Arterial hypertension persisted, but was associated with increased afferent resistance.
- Mycophenolate mofetil (MMF) significantly attenuated arteriolopathy, suggesting preservation of vascular structure and function.
- Arteriolopathy, glomerular hypertension, and renal lesions are linked in various conditions, including hyperuricemia and aging SHR.
- Arteriolopathy can lead to maladaptive transmission of systemic hypertension to glomerular capillaries, causing mechanical damage and protein filtration.
- Tubular reabsorption of filtered proteins can trigger pro-inflammatory and profibrotic responses, leading to tubulointerstitial inflammation and fibrosis.
- In conditions with renin-angiotensin system (RAS) overactivity, arteriolopathy is linked to increased glomerular pressure, reduced plasma flow, and subsequent tubulointerstitial injury.
Conclusions:
- Tubulointerstitial inflammation and vascular changes (arteriolopathy) play a critical role in the progression of renal disease, potentially by altering glomerular hemodynamics.
- Targeting tubulointerstitial inflammation and preserving vascular integrity are promising strategies for renoprotection.
- Mycophenolate mofetil (MMF) demonstrates potential in mitigating both vascular and hemodynamic derangements in experimental renal injury.
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