ReviewNature reviews. Endocrinology2011
Familial forms of diabetes insipidus: clinical and molecular characteristics.
Review in Nature reviews. Endocrinology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 168 citations in OpenAlex.
- Genetic Insights Into AVP Deficiency: Identification of a Novel AVP Variant and Compilation of a Curated Catalogue of Pathogenic Variants.Clinical genetics · 2026Article
- [Hypophisitis in pregnant women with persistent diabetes insipidus in the outcome].Problemy endokrinologii · 2024Article
- Insights into the role of RNA mGenes & diseases · 2024Review
- New insights on diagnosis and treatment of AVP deficiency.Reviews in endocrine & metabolic disorders · 2024Review
- Approach to the Patient: "Utility of the Copeptin Assay".The Journal of clinical endocrinology and metabolism · 2022Article
- Partial nephrogenic diabetes insipidus with a novel arginine vasopressin receptor 2 gene variant.Clinical pediatric endocrinology : case reports and clinical investigations : official journal of the Japanese Society for Pediatric Endocrinology · 2022Article
- Brain dysfunction in tubular and tubulointerstitial kidney diseases.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2021Review
- Autosomal dominant familial neurohypophyseal diabetes insipidus caused by a novel missense mutation in AVP gene in a large Italian kindred.Endocrine · 2021Article
- Deficiency of WFS1 leads to the impairment of AVP secretion under dehydration in male mice.Pituitary · 2021Article
- Asymptomatic obstructive hydronephrosis associated with diabetes insipidus: a case report and review.Translational pediatrics · 2021Article
- NovelFrontiers in endocrinology · 2021Article
- Molecular Characterization of an Aquaporin-2 Mutation Causing Nephrogenic Diabetes Insipidus.Frontiers in endocrinology · 2021Article
- Case Report: A Case of Congenital Nephrogenic Diabetes Insipidus Caused by Thr273Met Mutation in Arginine Vasopressin Receptor 2.Frontiers in pediatrics · 2021Article
- Degradation of Mutant Protein Aggregates within the Endoplasmic Reticulum of Vasopressin Neurons.iScience · 2020Article
- Central diabetes insipidus unveiled by glucocorticoid therapy in a patient with an empty sella: A case report and literature review.Medicine · 2020Review
- Comparative transcriptomic analysis reveals mechanisms of divergence in osmotic regulation of the turbot Scophthalmus maximus.Fish physiology and biochemistry · 2020Article
- A Self-Assembling Lipidic Peptide and Selective Partial V2 Receptor Agonist Inhibits Urine Production.Scientific reports · 2020Article
- Copeptin in the differential diagnosis of hypotonic polyuria.Journal of endocrinological investigation · 2020Review
- A Case of Congenital Nephrogenic Diabetes Insipidus Caused by Thr108Met Variant of Aquaporin 2.Frontiers in pediatrics · 2020Article
- Copeptin and its role in the diagnosis of diabetes insipidus and the syndrome of inappropriate antidiuresis.Clinical endocrinology · 2019Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Over the past two decades, the genetic and molecular basis of familial forms of diabetes insipidus has been elucidated. Diabetes insipidus is a clinical syndrome characterized by the excretion of abnormally large volumes of diluted urine (polyuria) and increased fluid intake (polydipsia). The most common type of diabetes insipidus is caused by lack of the antidiuretic hormone arginine vasopressin (vasopressin), which is produced in the hypothalamus and secreted by the neurohypophysis. This type of diabetes insipidus is referred to here as neurohypophyseal diabetes insipidus. The syndrome can also result from resistance to the antidiuretic effects of vasopressin on the kidney, either at the level of the vasopressin 2 receptor or the aquaporin 2 water channel (which mediates the re-absorption of water from urine), and is referred to as renal or nephrogenic diabetes insipidus. Differentiation between these two types of diabetes insipidus and primary polydipsia can be difficult owing to the existence of partial as well as complete forms of vasopressin deficiency or resistance. Seven different familial forms of diabetes insipidus are known to exist. The clinical presentation, genetic basis and cellular mechanisms responsible for them vary considerably. This information has led to improved methods of differential diagnosis and could provide the basis of new forms of therapy.
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