ReviewAmerican journal of kidney diseases : the official journal of the National Kidney Foundation2011
Aldosterone-induced fibrosis in the kidney: questions and controversies.
Review in American journal of kidney diseases : the official journal of the National Kidney Foundation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Biochemical and clinical remission after adrenalectomy in patients with primary aldosteronism: a retrospective two-center study.Gland surgery · 2026Article
- Aldosterone in Chronic Kidney Disease.Biomedicines · 2025Review
- Progressive 11β-Hydroxysteroid Dehydrogenase Type 2 Insufficiency as Kidney Function Declines.The Journal of clinical endocrinology and metabolism · 2025Article
- A Narrative Review of Signaling Pathway and Treatment Options for Diabetic Nephropathy.Current molecular medicine · 2025Review
- Anti-Hypertensive Effect of Solanum muricatum Aiton Leaf Extract In Vivo and In Vitro.Plant foods for human nutrition (Dordrecht, Netherlands) · 2024Article
- The role of a novel mineralocorticoid receptor antagonist, finerenone, in chronic kidney disease: mechanisms and clinical advances.Clinical and experimental nephrology · 2024Review
- Kidney function predicts new-onset cardiorenal events and mortality in primary aldosteronism: approach of the 2021 race-free eGFR equation.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Observational
- Parallelism and non-parallelism in diabetic nephropathy and diabetic retinopathy.Frontiers in endocrinology · 2024Review
- Genetic inhibition of serum glucocorticoid kinase 1 prevents obesity-related atrial fibrillation.JCI insight · 2022Article
- The role of mineralocorticoid receptor activation in kidney inflammation and fibrosis.Kidney international supplements · 2022Review
- Cortisol excess in chronic kidney disease - A review of changes and impact on mortality.Frontiers in endocrinology · 2022Review
- Renal Injuries in Primary Aldosteronism: Quantitative Histopathological Analysis of 19 Patients With Primary Adosteronism.Hypertension (Dallas, Tex. : 1979) · 2021Article
- Regulation of Monocytes/Macrophages by the Renin-Angiotensin System in Diabetic Nephropathy: State of the Art and Results of a Pilot Study.International journal of molecular sciences · 2021Review
- Diabetic Nephropathy: Challenges in Pathogenesis, Diagnosis, and Treatment.BioMed research international · 2021Review
- Extracellular matrix induced by steroids and aging through a G-protein-coupled receptor in aDisease models & mechanisms · 2020Article
- Treatment of diabetic kidney disease: current and future targets.The Korean journal of internal medicine · 2017Review
- Aldosterone Induces Renal Fibrosis and Inflammatory M1-Macrophage Subtype via Mineralocorticoid Receptor in Rats.PloS one · 2016Article
- Combination use of medicines from two classes of renin-angiotensin system blocking agents: risk of hyperkalemia, hypotension, and impaired renal function.Therapeutic advances in drug safety · 2015Review
- Horizon 2020 in Diabetic Kidney Disease: The Clinical Trial Pipeline for Add-On Therapies on Top of Renin Angiotensin System Blockade.Journal of clinical medicine · 2015Review
- Therapeutic approaches to diabetic nephropathy--beyond the RAS.Nature reviews. Nephrology · 2014Review
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Over the years, aldosterone has been a favorite topic of renal physiologists given its role in the maintenance of body fluids. Investigators only recently are coming to appreciate a second proinflammatory and profibrotic role for this hormone. Mineralocorticoids such as aldosterone trigger a profibrotic process that in many respects mimics the early phase of wound healing. Depending on the type of cell involved, aldosterone may activate the profibrotic process through classic mineralocorticoid receptors, nonclassic membrane-associated mineralocorticoid receptors, and/or glucocorticoid receptors. In the kidney, the actions of aldosterone can be attenuated by 11-dehydro metabolites of endogenous glucocorticoids generated by isoforms of the enzyme 11β-hydroxysteroid dehydrogenase (11β-HSD-1 and 11β-HSD-2). Thus, the renal 11β-HSD isoforms may have 2 functions: to block the improper activation of mineralocorticoid receptors by binding endogenous glucocorticoids and to synthesize agents that limit the actions of aldosterone. Although sodium in the diet has been implicated in aggravating aldosterone-induced renal fibrotic processes, preliminary findings are consistent with the view that aldosterone alone can initiate matrix production in renal tissue even in the absence of active sodium transport. Thus, there is a growing body of laboratory and clinical evidence supporting the use of inhibitors of aldosterone action in patients with both glomerular and tubular diseases.
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