Autosomal Dominant Pseudohypoaldosteronism Type 1: Mechanisms, Evidence for Neonatal Lethality, and Phenotypic Expression in Adults-Reference-Cited by-同舟云学术

Autosomal Dominant Pseudohypoaldosteronism Type 1: Mechanisms, Evidence for Neonatal Lethality, and Phenotypic Expression in Adults

Published:2006-04-12 Issue:5 Volume:17 Page:1429-1436
ISSN:1046-6673
Container-title:Journal of the American Society of Nephrology
language:en
Short-container-title:JASN

Author:

Geller David S.,Zhang Junhui,Zennaro Maria-Christina,Vallo-Boado Alberto,Rodriguez-Soriano Juan,Furu Laszlo,Haws Robert,Metzger Daniel,Botelho Barbara,Karaviti Lefkothea,Haqq Andrea M.,Corey Howard,Janssens Sandra,Corvol Pierre,Lifton Richard P.

Publisher

American Society of Nephrology (ASN)

Subject

Nephrology,General Medicine

Reference25 articles.

1. Type I Pseudohypoaldosteronism Includes Two Clinically and Genetically Distinct Entities with either Renal or Multiple Target Organ Defects

2. Mutations in subunits of the epithelial sodium channel cause salt wasting with hyperkalaemic acidosis, pseudohypoaldosteronism type 1

3. Localisation of Pseudohypoaldosteronism Genes to Chromosome 16p12.2–13.11 and 12p13.1-Pter by Homozygosity Mapping

4. Pseudohypoaldosteronism due to renal and multisystem resistance to mineralocorticoids respond differently to carbenoxolone

5. Mutations in the mineralocorticoid receptor gene cause autosomal dominant pseudohypoaldosteronism type I

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