Related Experiment Video
Updated: Feb 6, 2026

Development of Human Renal Tubular Epithelial Cell Primary Cultures in Monolayers and Three-Dimensional Conditions
Published on: June 13, 2025
Pendred, pendrin, pseudohypoaldosteronism type II, and renal tubular acidosis
Friedrich C Luft1, Carsten A Wagner2
1Experimental and Clinical Research Center, Max-Delbrück Center and Charité Medical Faculty, Berlin, Germany.
Abstract:
The sodium chloride cotransporter is regulated by the with-no-lysine kinases 1 and 4. Mutations in these genes are responsible for Mendelian hypertension, increased sodium chloride cotransporter activity, metabolic acidosis, and hyperkalemia. Explaining metabolic acidosis and hyperkalemia has been difficult. We now learn that the versatile bicarbonate-chloride exchanger, pendrin, is important in the process. As a result, we are confronted with still another mechanism causing renal tubular acidosis.
Related Concept Videos
Renal Drug Excretion: Tubular Reabsorption
Renal Drug Excretion: Tubular Secretion
Drug Elimination by Renal Route: Tubular Secretion
Drug Elimination by Renal Route: Tubular Reabsorption
Diagnosing Acidosis and Alkalosis
First, the pH level is assessed to determine whether the blood pH is normal (7.35–7.45), low (acidosis), or high (alkalosis).
Next, the PCO2 and...
Vesicular Tubular Clusters
With the help of motor proteins such...

