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Updated: Apr 11, 2026

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
Published on: September 26, 2018
The renal effects of mineralocorticoid receptor antagonists
Stefano Bianchi1, Valentina Batini2, Roberto Bigazzi2
1Unità Operativa di Nefrologia e Dialisi II, Livorno, Italy.
Abstract:
Beyond its well known classic effects on renal water and electrolytes metabolism, an increasing amount of experimental and clinical evidence suggests that aldosterone contributes to the pathogenesis and progression of kidney disease. The binding of aldosterone on epithelial and non-epithelial cells of the kidney induces many deleterious effects, such as podocyte apoptosis and injury, mesangial cell proliferation and deformability and tubulointerstitial inflammation, finally resulting in glomerular fibrosis and sclerosis. Moreover, aldosterone acting by fast non-genomic mechanisms, may induce other potential deleterious effects on kidney function and structure. Indeed, many experimental studies have shown that aldosterone participates to the progression of kidney disease through hemodynamic and direct cellular actions and that antagonists of aldosterone may retard the progression of kidney disease, independently of effects on blood pressure. Therefore, blockade of the aldosterone pathway may prove to be a beneficial therapy for kidney disease. In this brief review we summarize the reported data that support an independent role of aldosterone in inducing kidney damage both in human and experimental models, and interventional studies that highlight how strategies aimed to antagonize its action may favorably modify the progressive decline of renal function in patient with kidney disease and in patients with extrarenal disease frequently associated with kidney function impairment.
Insights
Aldosterone significantly contributes to kidney disease progression through direct cellular damage and hemodynamic changes. Blocking aldosterone pathways offers a promising therapeutic strategy for slowing kidney function decline.
Area of Science:
- Nephrology
- Endocrinology
- Pathophysiology
Background:
- Aldosterone classically regulates renal water and electrolyte balance.
- Emerging evidence implicates aldosterone in kidney disease pathogenesis and progression.
- Aldosterone exerts deleterious effects on various kidney cell types, including podocytes and mesangial cells.
Purpose of the Study:
- To review evidence supporting aldosterone's independent role in kidney damage.
- To summarize interventional studies on aldosterone antagonism in kidney disease.
- To highlight the therapeutic potential of blocking aldosterone pathways.
Main Methods:
- Review of experimental and clinical studies on aldosterone's renal effects.
- Analysis of data on aldosterone's impact on podocyte injury, mesangial cell proliferation, and tubulointerstitial inflammation.
- Evaluation of interventional studies using aldosterone antagonists.
Main Results:
- Aldosterone binding induces podocyte apoptosis, mesangial cell changes, and tubulointerstitial inflammation.
- Aldosterone contributes to glomerular fibrosis and sclerosis.
- Aldosterone antagonists show potential in retarding kidney disease progression, independent of blood pressure effects.
Conclusions:
- Aldosterone plays an independent role in inducing kidney damage in human and experimental models.
- Blockade of the aldosterone pathway represents a potentially beneficial therapeutic strategy for kidney disease.
- Targeting aldosterone may favorably modify the decline of renal function in patients with kidney and associated extrarenal diseases.
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