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Chapter 12B: Renal potassium excretion

Burton D Rose, MD
Theodore W Post, MD
Section Editor
Burton D Rose, MD
Deputy Editor
John P Forman, MD, MSc


Although small amounts of K+ are lost each day in stool (5 to 10 meq) and sweat (0 to 10 meq), the kidney plays the major role in the maintenance of K+ balance, appropriately varying K+ secretion with changes in dietary intake (normal range is 40 to 120 meq/day). The primary event in urinary K+ excretion is the secretion of K+ from the tubular cell into the lumen in the distal nephron, particularly in the principal cells in the cortical collecting tubule and in the cells in the adjacent connecting segment and outer medullary collecting tubule [1-3].


The sequential handling of filtered K+ by the different nephron segments is depicted in the micropuncture experiments in Figure 1 (figure 1) [3,4]. The clearance of K+ is compared to that of inulin, which is filtered and then is neither reabsorbed nor secreted. As a result, a fall in the CK+/Cin ratio indicates that K+ has been removed from the tubular fluid (or reabsorbed), and an elevation in the ratio indicates that K+ has been added to the tubular fluid (or secreted). Almost all of the filtered K+ is reabsorbed in the proximal tubule and the loop of Henle, so that less than 10 percent of the filtered load is delivered to the early distal tubule (CK+/Cin <0.1). Proximal K+ transport appears to passively follow that of Na+ and water [5], whereas reabsorption in the thick ascending limb of the loop of Henle is mediated by the Na+-K+-2Cl- carrier in the luminal membrane (figure 2) [2].

In comparison to these reabsorptive processes, K+ is secreted by the connecting segment, the principal cells in the cortical and outer medullary collecting tubule (figure 3), and the papillary (or inner medullary) collecting duct (as shown by the rising CK+/Cin ratio in figure 1) [1,3,6]. Secretion in these segments can be varied according to physiologic needs and is generally responsible for most of urinary K+ excretion.

Distal secretion can be partially counteracted by K+ reabsorption by the intercalated cells in the cortical and outer medullary collecting tubules [7,8]. This process may be mediated by an active H+-K+-ATPase pump in the luminal membrane, which results in both H+ secretion and K+ reabsorption (figure 4) [9-11]. The activity of this pump is increased with K+ depletion [9,11,12] and is reduced with K+ loading [13]. The former adaptation is probably responsible for the observation that net K+ reabsorption, not secretion, appropriately occurs in the distal nephron with K+ depletion [4,7,10]. Selective inhibition of the H+-K+-ATPase pump in the setting of K+ depletion abolishes distal K+ reabsorption [12].

Medullary recycling — The K+ reabsorbed in the thick ascending limb initially enters the medullary interstitium. Some of this K+ is then secreted into either the S3 segment of the late proximal tubule or the thin descending limb of the loop of Henle; this extra K+ can be reabsorbed again when it enters the outer medulla [14]. Thus, K+ is recycled within the medulla, resulting in the attainment of a relatively high concentration in the interstitium†. The physiologic function of this phenomenon is uncertain. It is possible, for example, that K+ accumulation in the interstitium promotes K+ excretion by minimizing the degree of passive backleak out of the collecting tubular lumen (where the highest urine K+ concentrations are attained). The high interstitial K+ concentration also may contribute to K+ excretion by a second mechanism, by diminishing the gradient for passive K+ reabsorption via the Na+-K+-2Cl- carrier in the loop of Henle [15].


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Literature review current through: Feb 2015. | This topic last updated: Sep 15, 2000.
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