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Related Experiment Video

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A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis

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Renoprotection by statins is linked to a decrease in renal oxidative stress, TGF-beta, and fibronectin with

Ming-Sheng Zhou¹, Ivonne Hernandez Schuman, Edgar A Jaimes

¹Nephrology-Hypertension Section, Veterans Affairs Medical Center, Vascular Biology Institute, University of Miami Miller School of Medicine, Miami, FL 33125, USA. mzhou2@med.miami.edu

American Journal of Physiology. Renal Physiology

|May 9, 2008

Summary

Statins like atorvastatin protect kidneys from high salt-induced injury by reducing oxidative stress and inflammation. They help restore nitric oxide (NO) balance, improving kidney function in hypertensive models.

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Assessment of Vascular Function in Patients With Chronic Kidney Disease

Assessment of Vascular Function in Patients With Chronic Kidney Disease

Published on: June 16, 2014

Area of Science:

Nephrology
Cardiovascular Research
Pharmacology

Background:

Hypertension and high salt intake induce renal injury via oxidative stress and reduced nitric oxide (NO) bioavailability.
Dahl salt-sensitive (DS) rats model this injury, showing increased angiotensin II-dependent NADPH oxidase activation.
Statins are known to have potential renoprotective effects, but mechanisms require elucidation.

Purpose of the Study:

Investigate the renoprotective mechanisms of statins in a hypertensive rat model.
Determine how atorvastatin affects oxidative stress, inflammation, and NO pathways in the kidney.
Clarify the role of statins in mitigating salt-induced renal damage.

Main Methods:

Utilized hypertensive Dahl salt-sensitive (DS) rats fed a high-salt diet (4% NaCl) for 10 weeks.
Administered atorvastatin (30 mg/kg/day) and assessed systolic blood pressure (SBP), proteinuria, glomerulosclerosis, and renal biomarkers.
Measured urinary 8-F(2alpha)-isoprostane, NADPH oxidase activity, TGF-beta, fibronectin, MCP-1, LOX-1, and eNOS activity/expression.

Main Results:

High salt diet induced significant hypertension (SBP ~200 mmHg), proteinuria, glomerulosclerosis, oxidative stress, inflammation (MCP-1, LOX-1), and reduced eNOS activity.
Atorvastatin attenuated proteinuria, glomerulosclerosis, normalized oxidative stress, TGF-beta, fibronectin, MCP-1, LOX-1, and improved eNOS activity/expression.
Atorvastatin alone had a modest effect on SBP; combined with salt removal, it normalized SBP and proteinuria.

Conclusions:

Statins, exemplified by atorvastatin, mitigate hypertensive renal injury by restoring balance between NO, TGF-beta1, and oxidative stress.
These findings support the renoprotective role of statins in clinical settings, potentially explaining benefits alongside renin-angiotensin system inhibitors.
Atorvastatin effectively combats key molecular pathways contributing to salt-induced kidney damage.