Potassium Binding for Conservative and Preservative Management of Chronic Kidney Disease

Deborah J. Clegg; Biff F. Palmer


Curr Opin Nephrol Hypertens. 2020;29(1):29-38. 

In This Article

Normal Potassium Homeostasis

The normal kidney has a large capacity to excrete K+. Accumulation of K+ in the interstitium following increased intake exerts an inhibitory effect on the thick ascending limb and to a lesser extent proximal tubular NaCl reabsorption resulting in increased flow and Na+ delivery to the distal nephron.[2] High K+ intake modulates flow and Na+ delivery through direct effects in the distal convoluted tubule (DCT1). Elevations in plasma K+ are registered by cells in the initial portion of the DCT1 decreasing activity of the thiazide-sensitive Na+-Cl co-transporter.[3] In consequence, flow and Na+ are delivered increasingly to the adjacent aldosterone-sensitive distal nephron (DCT2 and collecting duct) where electrogenic and flow-mediated K+ secretion is enhanced. There is also a gastric-kidney reflex, providing an inhibitory effect on the Na+-Cl co-transporter, which is initiated upon K+ entry into the stomach.[4] Lastly, K+ secretion is influenced by a circadian rhythm facilitating K+ homeostasis during the day when K+ intake is highest (Figure 1). For further review of the mechanisms of normal kidney K+ handling the reader is guided to several recent reviews.[2,5,6]

Figure 1.

A summary of the mechanisms that underlie the prodigious capacity of the kidney to excrete K+. CD, collecting duct; DCT1, initial portion of the distal convoluted tubule; DCT2, second portion of the distal convoluted tubule; ENaC, epithelial Na+ channel; NCC, thiazide sensitive Na+-Cl cotransporter; ROMK, renal outer medullary K+ channel.