ReviewInternational journal of molecular sciences2022
Primary Aldosteronism and Resistant Hypertension: A Pathophysiological Insight.
Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 2 syntheses or guidelines pooled it, 40 citations in OpenAlex.
- Efficacy and Safety of Lorundrostat in Uncontrolled Hypertension: A Systematic Review and Meta-Analysis.Journal of clinical hypertension (Greenwich, Conn.) · 2025Pooled it
- Risk factors for persistent hypertension in primary aldosteronism after surgery: a systematic review and meta-analysis.Frontiers in physiology · 2025Pooled it
- Neurohumoral Biomarker Profile Associated With Blood Pressure Response After Renal Denervation.Journal of clinical hypertension (Greenwich, Conn.) · 2026Article
- Severe Hypokalemia With Rhabdomyolysis-A Case Report.Clinical case reports · 2026Article
- Resistant hypertension, hyperaldosteronism, and the emerging understanding of hypercortisolism.Current opinion in cardiology · 2026Review
- The amount of sodium intake may affect the susceptibility to treatment with mineralocorticoid receptor antagonists in patients with primary aldosteronism.Clinical and experimental nephrology · 2026Article
- Familial Hyperaldosteronism Type IV (FH-IV)-Clinical Phenotypes, Genetics and Management ofJournal of clinical medicine · 2026Review
- Multiparametric diffusion-weighted MRI for renal microstructural assessment in patients with primary aldosteronism at varying direct renin concentrations.Abdominal radiology (New York) · 2026Article
- Metabolomics and Precision Medicine in Resistant Hypertension: Pathophysiological Insights, Biomarker Discovery, and Translational Strategies.International journal of hypertension · 2026Review
- Resistant hypertension: Epidemiology, mechanisms and contemporary therapeutic strategies.Heart international · 2026Review
- Multidimensional Mechanisms of Hypertension and Advances in Diagnosis and Integrated TCM-Based Treatment: A Review.International journal of general medicine · 2026Review
- Structural and Computational Insights into the Angiotensin II Type 1 Receptor: Advances in Antagonist Design and Implications for Hypertension Therapy (2020-2024).Biomolecules · 2025Review
- Exploring the Plasma Fatty Acid Signature of Primary Aldosteronism: Comparison with Essential Hypertension and Longitudinal Therapy Effects.Diagnostics (Basel, Switzerland) · 2025Article
- The relationship between aldosterone-induced retinal ganglion cell loss, blood pressure, and intraocular pressure.Japanese journal of ophthalmology · 2025Article
- Prevalence of Metabolic-Associated Steatotic Liver Disease in Patients With Primary Aldosteronism.Clinical endocrinology · 2025Article
- Associations of Blood Pressure Variability, Heart Rate, and Target Organ Damage in Resistant Hypertension Patients.Journal of clinical hypertension (Greenwich, Conn.) · 2025Article
- Primary aldosteronism diagnosis in the intensive care unit: resistant alkalosis and hypokalemia during severe sepsis with hyperlactatemia: a case report.Journal of medical case reports · 2025Article
- Occurrence of Metabolic Disorders in Bilateral Primary Aldosteronism Compared to Unilateral Primary Aldosteronism.Diseases (Basel, Switzerland) · 2025Article
- Approach to Endocrine Hypertension: A Case-Based Discussion.Current hypertension reports · 2025Review
- Mineralocorticoid Receptor and Aldosterone: Interaction Between NR3C2 Genetic Variants, Sex, and Age in a Mixed Cohort.The Journal of clinical endocrinology and metabolism · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary aldosteronism (PA) is a pathological condition characterized by an excessive aldosterone secretion; once thought to be rare, PA is now recognized as the most common cause of secondary hypertension. Its prevalence increases with the severity of hypertension, reaching up to 29.1% in patients with resistant hypertension (RH). Both PA and RH are "high-risk phenotypes", associated with increased cardiovascular morbidity and mortality compared to non-PA and non-RH patients. Aldosterone excess, as occurs in PA, can contribute to the development of a RH phenotype through several mechanisms. First, inappropriate aldosterone levels with respect to the hydro-electrolytic status of the individual can cause salt retention and volume expansion by inducing sodium and water reabsorption in the kidney. Moreover, a growing body of evidence has highlighted the detrimental consequences of "non-classical" effects of aldosterone in several target tissues. Aldosterone-induced vascular remodeling, sympathetic overactivity, insulin resistance, and adipose tissue dysfunction can further contribute to the worsening of arterial hypertension and to the development of drug-resistance. In addition, the pro-oxidative, pro-fibrotic, and pro-inflammatory effects of aldosterone may aggravate end-organ damage, thereby perpetuating a vicious cycle that eventually leads to a more severe hypertensive phenotype. Finally, neither the pathophysiological mechanisms mediating aldosterone-driven blood pressure rise, nor those mediating aldosterone-driven end-organ damage, are specifically blocked by standard first-line anti-hypertensive drugs, which might further account for the drug-resistant phenotype that frequently characterizes PA patients.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.