Urea absorption in the inner medullary collecting duct provides a mechanism to elevate the concentration of urea in the papillary interstitial fluid and thereby permit the excretion of urea with as little water as possible. Urea reabsorption may have another important effect – to aid in the excretion of potassium (K). K excretion depends on two processes: first, factors such as aldosterone which cause the concentration of K in the luminal fluid of the cortical distal nephron to be high and, second, factors which augment the flow rate through those nephron segments. Since the osmolality of the luminal fluid in the cortical collecting duct (CCD) and plasma are equal when antidiuretic hormone acts, the flow rate in the CCD is dependent on solute delivery. Urea is a major solute in the lumen of the CCD and thereby plays an important role in maintaining the CCD flow rate. Since urea and K are often found in the same foods, having urea help the excretion of K is potentially advantageous. If the excretion of urea was low, the flow rate in the terminal CCD would decline. In this circumstance, the luminal K concentration would have to rise in proportion to the fall in flow rate or there would be a diminished rate of excretion of K and, possibly, hyperkalemia.