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

The renal tubular acidoses 

The renal tubular acidoses
Chapter:
The renal tubular acidoses
Author(s):

John A. Sayer

, and Fiona E. Karet

DOI:
10.1093/med/9780198746690.003.0505
Page of

PRINTED FROM OXFORD MEDICINE ONLINE (www.oxfordmedicine.com). © Oxford University Press, 2021. 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: 25 February 2021

Renal tubular acidosis (RTA) arises when the kidneys either fail to excrete sufficient acid, or are unable to conserve bicarbonate, with both circumstances leading to metabolic acidosis of varying severity with altered serum potassium. Proximal and distal types of RTA can be differentiated according to which nephron segment is malfunctioning. Proximal RTA: aetiology and diagnosis—the condition may be (1) secondary to generalized proximal tubular dysfunction (part of the renal Fanconi’s syndrome), or rarely (2) due to an inherited mutation of a single transporter (NBC1) located at the basolateral surface of the proximal tubular epithelium. The combination of normal anion gap acidosis with other features of proximal tubular dysfunction such as renal phosphate wasting (and hypophosphataemia), renal glycosuria, hypouricaemia (due to uricosuria), aminoaciduria, microalbuminuria, and other low molecular weight proteinuria suggests the diagnosis. Management—this requires large quantities of oral alkali with (in most cases) potassium supplements to prevent severe hypokalaemia. Distal RTA: aetiology/diagnosis—two main classes are differentiated by whether (1) the acid-handling cells in the collecting ducts are themselves functioning inadequately, in which case there is associated hypokalaemia (this is ‘classic’ distal RTA); or (2) the main abnormality is of the salt-handling principal cells in the same nephron segment, in which case hyperkalaemia occurs and the acidosis is a secondary phenomenon—this is hyperkalaemic distal RTA. The combination of normal anion gap acidosis with a urine pH higher than 5.5 suggests classic distal RTA. Management—(1) classic distal RTA—1 to 3 mg/kg per day of oral alkali; (2) hyperkalaemic distal RTA—treatment is with sodium bicarbonate, but fludrocortisone and/or potassium-lowering measures may also be necessary. Precipitating drugs should be stopped.

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.