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[Pathological aspects of water transport in the collecting ducts].
Nephrologie. 1996; 17(7):417-22.N

Abstract

In a normal adult subject, 12 liters of tubular urine with an osmolality of 100 mmol/kg exit per 24 hours from the loop of Henle. The antidiuretic hormone arginine-vasopressin increases the water permeability of the renal collecting ducts and induces the reabsorption of 11 liters of water: the final urinary osmolality is 1200 mmol/kg for a urinary flow rate of 1 litre per 24 hours. In nephrogenic diabetes insipidus the urine cannot be concentrated maximally. Congenital nephrogenic diabetes insipidus is secondary to either mutations in the AVPR2 gene (Xq28) that codes for the vasopressin antidiuretic (V2) receptor or to mutations in the AQP2 gene (12q13) that codes for the vasopressin dependent water channel. AVPR2 mutations are numerous and diverse: 72 different putative disease causing mutations in the AVPR2 gene have been reported in 102 unrelated families with X-linked nephrogenic diabetes insipidus. AQP2 mutations are rare. Nephrogenic diabetes insipidus could also be secondary to lithium or demeclocycline administration and to hypokaliemia. Some of these conditions are inducing, experimentally, a downregulation of aquaporin II. We encourage physicians who follow families with hereditary nephrogenic diabetes insipidus to recommend molecular genetic analysis because early diagnosis and treatment of infants can avert the physical and mental retardation associated with episodes of dehydration.

Authors+Show Affiliations

Unité de recherches cliniques, Hôpital du Sacré-Coeur, Montréal.

Pub Type(s)

English Abstract
Journal Article
Review

Language

fre

PubMed ID

9019668

Citation

Bichet, D G.. "[Pathological Aspects of Water Transport in the Collecting Ducts]." Nephrologie, vol. 17, no. 7, 1996, pp. 417-22.
Bichet DG. [Pathological aspects of water transport in the collecting ducts]. Nephrologie. 1996;17(7):417-22.
Bichet, D. G. (1996). [Pathological aspects of water transport in the collecting ducts]. Nephrologie, 17(7), 417-22.
Bichet DG. [Pathological Aspects of Water Transport in the Collecting Ducts]. Nephrologie. 1996;17(7):417-22. PubMed PMID: 9019668.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Pathological aspects of water transport in the collecting ducts]. A1 - Bichet,D G, PY - 1996/1/1/pubmed PY - 1996/1/1/medline PY - 1996/1/1/entrez SP - 417 EP - 22 JF - Nephrologie JO - Nephrologie VL - 17 IS - 7 N2 - In a normal adult subject, 12 liters of tubular urine with an osmolality of 100 mmol/kg exit per 24 hours from the loop of Henle. The antidiuretic hormone arginine-vasopressin increases the water permeability of the renal collecting ducts and induces the reabsorption of 11 liters of water: the final urinary osmolality is 1200 mmol/kg for a urinary flow rate of 1 litre per 24 hours. In nephrogenic diabetes insipidus the urine cannot be concentrated maximally. Congenital nephrogenic diabetes insipidus is secondary to either mutations in the AVPR2 gene (Xq28) that codes for the vasopressin antidiuretic (V2) receptor or to mutations in the AQP2 gene (12q13) that codes for the vasopressin dependent water channel. AVPR2 mutations are numerous and diverse: 72 different putative disease causing mutations in the AVPR2 gene have been reported in 102 unrelated families with X-linked nephrogenic diabetes insipidus. AQP2 mutations are rare. Nephrogenic diabetes insipidus could also be secondary to lithium or demeclocycline administration and to hypokaliemia. Some of these conditions are inducing, experimentally, a downregulation of aquaporin II. We encourage physicians who follow families with hereditary nephrogenic diabetes insipidus to recommend molecular genetic analysis because early diagnosis and treatment of infants can avert the physical and mental retardation associated with episodes of dehydration. SN - 0250-4960 UR - https://www.unboundmedicine.com/medline/citation/9019668/[Pathological_aspects_of_water_transport_in_the_collecting_ducts]_ DB - PRIME DP - Unbound Medicine ER -