ReviewLife (Basel, Switzerland)2024
Primary Role of the Kidney in Pathogenesis of Hypertension.
Review in Life (Basel, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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
9 citing papers in PubMed, 16 citations in OpenAlex.
- Phenotyping Kidney Function in Young Adults With High Blood Pressure: The African-PREDICT Study.Journal of clinical hypertension (Greenwich, Conn.) · 2024Trial
- Salt and chronic kidney disease.Nature reviews. Nephrology · 2026Review
- Neuraminidase1 Activity Contributes to Vasopressin Receptor-mediated Augmentation of Water and Electrolyte Retention by the Kidney inbioRxiv : the preprint server for biology · 2026Article
- Rare variant optimized GWAS with functional validation identifies causal architecture of kidney function in East Asian population.Scientific reports · 2026Article
- Review
- Cardio-Renal-Metabolic Syndrome with Emphasis on Chronic Kidney Disease: Educational Attainment and Progression-A Retrospective Cohort Study.Healthcare (Basel, Switzerland) · 2025Article
- Silent Effects of High Salt: Risks Beyond Hypertension and Body's Adaptation to High Salt.Biomedicines · 2025Review
- Chronic kidney disease.Nature reviews. Disease primers · 2025Review
- Hypertension: A Continuing Public Healthcare Issue.International journal of molecular sciences · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous transplantation studies and the concept of 'nephron underdosing' support the idea that the kidney plays a crucial role in the development of essential hypertension. This suggests that there are genetic factors in the kidney that can either elevate or decrease blood pressure. The kidney normally maintains arterial pressure within a narrow range by employing the mechanism of pressure-natriuresis. Hypertension is induced when the pressure-natriuresis mechanism fails due to both subtle and overt kidney abnormalities. The inheritance of hypertension is believed to be polygenic, and essential hypertension may result from a combination of genetic variants that code for renal tubular sodium transporters or proteins involved in regulatory pathways. The renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system (SNS) are the major regulators of renal sodium reabsorption. Hyperactivity of either the RAAS or SNS leads to a rightward shift in the pressure-natriuresis curve. In other words, hypertension is induced when the activity of RAAS and SNS is not suppressed despite increased salt intake. Sodium overload, caused by increased intake and/or reduced renal excretion, not only leads to an expansion of plasma volume but also to an increase in systemic vascular resistance. Endothelial dysfunction is caused by an increased intracellular Na
Indexed as
Identifiers
What Socratic 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 Socratic graph.