Contents

Disclaimer

Oxford University Press makes no representation, express or implied, that the drug dosages in this book are correct. Readers must therefore always check the product information and clinical procedures with the most up to date published product information and data sheets provided by the manufacturers and the most recent codes of conduct and safety regulations. The authors and the publishers do not accept responsibility or legal liability for any errors in the text or for the misuse or misapplication of material in this work. Except where otherwise stated, drug dosages and recommendations are for the non-pregnant adult who is not breastfeeding.

Show Summary Details
Page of

Primary aldosteronism and other steroid-related causes of endocrine hypertension 

Primary aldosteronism and other steroid-related causes of endocrine hypertension
Chapter:
Primary aldosteronism and other steroid-related causes of endocrine hypertension
Author(s):

John M.C. Connell

and E. Marie Freel

DOI:
10.1093/med/9780199235292.003.0570
Page of

PRINTED FROM OXFORD MEDICINE ONLINE (www.oxfordmedicine.com). © Oxford University Press, 2016. All Rights Reserved. Under the terms of the licence agreement, an individual user may print out a PDF of a single chapter of a title in Oxford Medicine Online for personal use (for details see Privacy Policy and Legal Notice).

date: 17 November 2019

Mineralocorticoid hypertension is characterized by increased distal renal tubular sodium reabsorption, raised body sodium content, plasma volume expansion, markedly reduced body potassium content, with a metabolic alkalosis and suppression of renin production by the juxtaglomerular cells of the kidney (and correspondingly low levels of angiotensin II). Primary aldosteronism is the most common cause of mineralocorticoid hypertension (1); less frequent causes include the rare inborn errors of adrenal steroid synthesis (11β‎-hydroxylase and 17α‎-hydroxylase deficiency), alterations in corticosteroid metabolism (syndrome of apparent mineralocorticoid excess), and constitutive activation of the epithelial sodium channel (Liddle’s syndrome).

Access to the complete content on Oxford Medicine Online requires a subscription or purchase. Public users are able to search the site and view the abstracts for each book and chapter without a subscription.

Please subscribe or login to access full text content.

If you have purchased a print title that contains an access token, please see the token for information about how to register your code.

For questions on access or troubleshooting, please check our FAQs, and if you can't find the answer there, please contact us.