ArticlePediatric nephrology (Berlin, Germany)2022
Monogenic forms of low-renin hypertension: clinical and molecular insights.
Article in Pediatric nephrology (Berlin, Germany), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- A frameshift mutation in theMolecular medicine reports · 2024Pooled it
- Adrenal causes of endocrine hypertension in childhood or adolescence.Journal of endocrinological investigation · 2025Review
- Diagnosing apparent mineralocorticoid excess in a child with hypertension and nephrocalcinosis: from symptoms to genetics.CEN case reports · 2025Article
- Genetic background of neonatal hypokalemia.Pediatric nephrology (Berlin, Germany) · 2025Review
- Monogenic Hypertension Linked to the Renin-Angiotensin-Aldosterone System.Anatolian journal of cardiology · 2024Article
- Genetics of Hypertension: From Monogenic Analysis to GETomics.Journal of cardiovascular development and disease · 2024Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Monogenic disorders of hypertension are a distinct group of diseases causing dysregulation of the renin-angiotensin-aldosterone system and are characterized by low plasma renin activity. These can chiefly be classified as causing (i) excessive aldosterone synthesis (familial hyperaldosteronism), (ii) dysregulated adrenal steroid metabolism and action (apparent mineralocorticoid excess, congenital adrenal hyperplasia, activating mineralocorticoid receptor mutation, primary glucocorticoid resistance), and (iii) hyperactivity of sodium and chloride transporters in the distal tubule (Liddle syndrome and pseudohypoaldosteronism type 2). The final common pathway is plasma volume expansion and catecholamine/sympathetic excess that causes urinary potassium wasting; hypokalemia and early-onset refractory hypertension are characteristic. However, several single gene defects may show phenotypic heterogeneity, presenting with mild hypertension with normal electrolytes. Evaluation is based on careful attention to family history, physical examination, and measurement of blood levels of potassium, renin, and aldosterone. Genetic sequencing is essential for precise diagnosis and individualized therapy. Early recognition and specific management improves prognosis and prevents long-term sequelae of severe hypertension.
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