Abstract
The form of renal tubular acidosis associated with hyperkalemia is usually attributable to real or apparent hypoaldosteronism. It is therefore a common feature in diabetes and a number of other conditions associated with underproduction of renin or aldosterone. In addition, the close relationship between potassium levels and ammonia production dictates that hyperkalemia per se can lead to acidosis. Here I describe the modern relationship between molecular function of the distal portion of the nephron, pathways of ammoniagenesis, and hyperkalemia.
- Copyright © 2009 by the American Society of Nephrology
In this issue
Mechanisms in Hyperkalemic Renal Tubular Acidosis
Jump to section
More in this TOC Section
UP FRONT MATTERS
Cited By...
- Mechanisms of Metabolic Acidosis-Induced Kidney Injury in Chronic Kidney Disease
- Reply to Farfel et al.: Is enhanced chloride reabsorption in proximal tubule a possible mechanism of metabolic acidosis in PHAII?
- Fatal cardiac arrest in a calf with uroperitoneum
- Mechanism of Hyperkalemia-Induced Metabolic Acidosis
- Renal Tubular Acidosis
- Review of the Diagnostic Evaluation of Renal Tubular Acidosis
- Daptomycin-induced hyperkalemia in a patient with normal renal function
- Distal Renal Tubular Acidosis Associated with Concurrent Leptospirosis in a Dog
- Activation of mTORC1 in Collecting Ducts Causes Hyperkalemia
- A clinical approach to paediatric acid-base disorders
- Aldosterone Requires Vasopressin V1a Receptors on Intercalated Cells to Mediate Acid-Base Homeostasis
- Renal Tubular Acidosis