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Several segments of the nephron are involved in the management of potassium (K⁺).  However, most handle K⁺ at a relatively fixed rate that is independent of potassium load and do not play a significant role in the regulation of K⁺ excretion in the urine.  These segments include the following:

• Bowman's capsule:  Because K⁺ is freely filtered across the glomerular membrane, the amount of K⁺ within Bowman's space is equal to that in the glomerular capillaries (ie, 100%) (Choice C).

• The proximal tubule: Approximately 65% of the filtered K⁺ load is reabsorbed in the proximal tubule, leaving ~35% of the total filtered load.

• The thick ascending limb of the loop of Henle:  Further resorbs about 25%-30% of the filtered K⁺ load through the action of the Na⁺/K⁺/2Cl^- cotransporter, resulting in only 5-10% of K⁺ remaining in the tubular fluid after this segment (Choices B and D).

Because this is a stable process, even in hyperkalemic states, patients will reabsorb the majority of filtered K⁺ in the proximal tubule and loop of Henle.

Potassium regulation is therefore primarily mediated by the principal and α-intercalated cells of the late distal and cortical collecting tubules.  Hypokalemia stimulates reabsorption of K⁺ via apically located H⁺/K⁺-ATPases on α-intercalated cells and can cause the amount of K⁺ in the collecting tubule to approach 1% of the filtered load.  Conversely, an increased K⁺ load stimulates principal cells to secrete K⁺ through apical K⁺ channels.  High dietary K⁺ intake can cause the amount of K⁺ in the collecting tubules to actually exceed the filtered load (ie, >100%).

Excessive K⁺ intake increases K⁺ excretion through the following mechanisms:

• High extracellular K⁺ levels directly stimulate basolateral Na⁺/K⁺ pumps on principal cells, increasing K⁺ secretion into the tubular fluid.

• Elevated K⁺ levels also increase aldosterone secretion, which further enhances activity of principal cell Na⁺/K⁺ pumps and also increases their apical permeability to Na⁺ and K⁺ (leading to K⁺ loss in the tubular fluid).

Educational objective:
K⁺ is freely filtered by the glomeruli and is mostly reabsorbed in the proximal tubule and loop of Henle.  As such, the late distal and cortical collecting tubules are the primary sites for regulation of K⁺ excretion in the urine.  K⁺ depletion stimulates α-intercalated cells to reabsorb extra potassium; principal cells secrete K⁺ under conditions of increased K⁺ load.