Chloride Shunt

Here is a quick review of how the “chloride shunt” first described by Batlle et al in 1981 occurs. This can cause a voltage-dependent type of hyperkalemic distal renal tubular acidosis.

In the cortical collecting duct, Na+

enters from the tubular lumen into the

principal cell through the epithelial Na+ channel, ENaC. This electrogenic transport step creates a favorable electrical driving force for apical K+ and H+ secretion from the principal cell and the α-intercalated cell, respectively, and paracellular Cl− reabsorption. Abnormal increases in Cl− reabsorption across the tight junction (TJ) ( ala the chloride shunt) can increase salt reabsorption and intravascular volume, while at the same time dissipate the electrical gradient for K+ and H+ secretion with consequent hyperkalemia and metabolic acidosis.

Chloride Shunt in the CD

K+ and H+ excretion in cortical collecting duct. Luminal Na+ entry into the principal cell through the epithelial Na+ channel (ENaC) creates a favorable electrical driving force for apical K+ and H+ secretion from the principal cell and the α-intercalated cell, respectively, and Cl− reabsorption across the TJ, through the paracellular conduit. An abnormal increase in Cl− reabsorption (“chloride shunt”) would be expected to reduce the normal lumen-negative potential and, thereby, reduce K+ and H+ secretion.

And hence the mechanism for why these patients end up with high potassium, and a non-anion gap acidosis.

-Adrian

Source: AJP Renal | Tight Junction Biology and Kidney Dysfunction Dr. D.N.B Lee et al.

JASN | Renal Tubular Acidosis: The Clinical Entity Dr. J.R Soriano



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