Potassium is readily filtered by the glomerulus with around 7-8% of this filtered potassium load ultimately excreted by the kidney. Of the remainder, the majority (70%) is re-absorbed in the proximal tubule (K+-CL- symport and K+-H+ exchanger) and a smaller amount (20%) in the ascending loop of Henle (Na+-K+-2Cl co-transporter) while the distal tubule and collecting ducts can either reabsorb or secrete potassium and are the main point of control of potassium balance.
Influences over the absorption or secretion of K+ in the distal tubule and collecting duct include:
Aldosterone increases K+ secretion by increasing both numbers and activity of Na+/K+ ATPase in the distal tubule and collecting ducts. These reabsorb Na+ in exchange for pumping out K+ into tubular fluid. Aldosterone secretion from the adrenal cortex is stimulated by rising plasma [K+].
Secretion of K+ is into tubular fluid also occurs by passive diffusion, and is therefore proportional to the flow rate of tubular fluid; increasing flow causes increased K+ secretion.
A rise in serum [H+] (acidaemia) causes an increase in K+ reabsorption. The H+-K+ antiporter in the proximal tubule and H+/K+ ATPase of the intercalating cells of the collecting duct both reciprocally pump H+ out into the tubular fluid in exchange for K+ into the cell for reabsorption. Upregulation of these transporters to secrete more H+ in acid excess will cause a reciprocal increase in K+ reabsorption. This in one of the mechanisms through which metabolic acidosis and hyperkalaemia are linked.
Of the diuretics, the loop and thiazides will increase K+ excretion through increasing distal tubular flow rates (and both have the complication of hypokalaemia), while spironolactone increases potassium reabsorption through its effect as an aldosterone antagonist (hence known as a potassium sparing diuretic). ACE inhibitors suppress the renin-angiotensin-aldosterone system and so reduce aldosterone secretion and lead to greater potassium reabsorption.