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Physiopathology and diagnosis of nephrogenic diabetes insipidus


Devuyst, Olivier (2012). Physiopathology and diagnosis of nephrogenic diabetes insipidus. Annales d'endocrinologie, 73(2):128-129.

Abstract

Nephrogenic diabetes insipidus (NDI) is caused by an improper response of the kidney to the antidiuretic hormone arginine vasopressin (AVP), leading to a decreased ability to concentrate urine which results in polyuria and polydipsia. The clinical diagnosis of NDI relies on demonstration of subnormal ability to concentrate urine despite the presence of AVP. NDI is most commonly acquired, secondary to kidney disorders, electrolyte imbalance and various drugs. Congenital forms of NDI are rare, and most commonly inherited in a X-linked manner with mutations of the AVP receptor type 2 (AVPR2). Mutations of the water channel aquaporin-2 (AQP2) can be detected in autosomal recessive or dominant forms of NDI. Management of NDI should focus on free access to drinking water and reduction of polyuria. = Le diabète insipide néphrogénique (DIN) est causé par une réponse inappropriée du rein à l’hormone antidiurétique (ADH), entraînant une diminution de la capacité de concentrer l’urine, se manifestant par l’association polyurie et polydipsie. Le diagnostic clinique de DIN repose sur la démonstration du défaut de concentration de l’urine malgré la présence d’ADH. Le DIN est le plus souvent acquis, suite à diverses maladies rénales, troubles ioniques, ou médicaments. Les formes congénitales de DIN sont rares, le plus souvent liées au chromosome X en relation avec des mutations du récepteur de l’ADH de type 2 (gène AVPR2). Des mutations du gène AQP2 codant pour le canal à eau aquaporine-2 sont retrouvées dans les formes transmises sur un mode dominant ou récessif. Le traitement du DIN vise à maintenir l’accès à l’eau potable et à réduire la polyurie.

Abstract

Nephrogenic diabetes insipidus (NDI) is caused by an improper response of the kidney to the antidiuretic hormone arginine vasopressin (AVP), leading to a decreased ability to concentrate urine which results in polyuria and polydipsia. The clinical diagnosis of NDI relies on demonstration of subnormal ability to concentrate urine despite the presence of AVP. NDI is most commonly acquired, secondary to kidney disorders, electrolyte imbalance and various drugs. Congenital forms of NDI are rare, and most commonly inherited in a X-linked manner with mutations of the AVP receptor type 2 (AVPR2). Mutations of the water channel aquaporin-2 (AQP2) can be detected in autosomal recessive or dominant forms of NDI. Management of NDI should focus on free access to drinking water and reduction of polyuria. = Le diabète insipide néphrogénique (DIN) est causé par une réponse inappropriée du rein à l’hormone antidiurétique (ADH), entraînant une diminution de la capacité de concentrer l’urine, se manifestant par l’association polyurie et polydipsie. Le diagnostic clinique de DIN repose sur la démonstration du défaut de concentration de l’urine malgré la présence d’ADH. Le DIN est le plus souvent acquis, suite à diverses maladies rénales, troubles ioniques, ou médicaments. Les formes congénitales de DIN sont rares, le plus souvent liées au chromosome X en relation avec des mutations du récepteur de l’ADH de type 2 (gène AVPR2). Des mutations du gène AQP2 codant pour le canal à eau aquaporine-2 sont retrouvées dans les formes transmises sur un mode dominant ou récessif. Le traitement du DIN vise à maintenir l’accès à l’eau potable et à réduire la polyurie.

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Additional indexing

Other titles:Physiopathologie et diagnostic du diabète insipide néphrogénique
Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Institute of Physiology
07 Faculty of Science > Institute of Physiology

04 Faculty of Medicine > Center for Integrative Human Physiology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Language:English
Date:2012
Deposited On:24 Jan 2013 13:36
Last Modified:05 Apr 2016 16:19
Publisher:Elsevier
ISSN:0003-4266
Publisher DOI:https://doi.org/10.1016/j.ando.2012.03.032
PubMed ID:22503803

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