Chapter 046. Sodium and Water (Part 11) pdf

Chapter 046. Sodium and Water (Part 11) Potassium: Introduction Potassium Balance Potassium is the major intracellular cation. The normal plasma K + concentration is 3.5–5.0 mmol/L, whereas that inside cells is about 150 mmol/L. Therefore, the amount of K + in the ECF (30–70 mmol) constitutes <2% of the total body K + content (2500–4500 mmol). The ratio of ICF to ECF K + concentration (normally 38:1) is the principal result of the resting membrane potential and is crucial for normal neuromuscular function. The basolateral Na + , K + -ATPase pump actively transports K + in and Na + out of the cell in a 2:3 ratio, and the passive outward diffusion of K + is quantitatively the most important factor that generates the resting membrane potential. The activity of the electrogenic Na + , K + -ATPase pump may be stimulated as a result of an increased intracellular Na + concentration and inhibited in the setting of digoxin toxicity or chronic illness such as heart failure or renal failure. The K + intake of individuals on an average western diet is 40–120 mmol/d, or approximately 1 mmol/kg per day, 90% of which is absorbed by the gastrointestinal tract. Maintenance of the steady state necessitates matching K + ingestion with excretion. Initially, extrarenal adaptive mechanisms, followed later by urinary excretion, prevent a doubling of the plasma K + concentration that would occur if the dietary K + load remained in the ECF compartment. Immediately following a meal, most of the absorbed K + enters cells as a result of the initial elevation in the plasma K + concentration and facilitated by insulin release and basal catecholamine levels. Eventually, however, the excess K + is excreted in the urine (see below). The regulation of gastrointestinal K + handling is not well understood. The amount of K + lost in the stool can increase from 10 to 50% or 60% (of dietary intake) in chronic renal insufficiency. In addition, colonic secretion of K + is stimulated in patients with large volumes of diarrhea, resulting in potentially severe K + depletion. Potassium Excretion (See also Chap. 272) Renal excretion is the major route of elimination of dietary and other sources of excess K + . The filtered load of K + (GFR x plasma K + concentration = 180 L/d x 4 mmol/L = 720 mmol/d) is ten- to twentyfold greater than the ECF K + content. Some 90% of filtered K + is reabsorbed by the proximal convoluted tubule and loop of Henle. Proximally, K + is reabsorbed passively with Na + and water, whereas the luminal Na + -K + -2Cl – co-transporter mediates K + uptake in the thick ascending limb of the loop of Henle. Therefore, K + delivery to the distal nephron [distal convoluted tubule and cortical collecting duct (CCD)] approximates dietary intake. Net distal K + secretion or reabsorption occurs in the setting of K + excess or depletion, respectively. The cell responsible for K + secretion in the late distal convoluted tubule (or connecting tubule) and CCD is the principal cell. Virtually all regulation of renal K + excretion and total body K + balance occurs in the distal nephron. Potassium secretion is regulated by two physiologic stimuli—aldosterone and hyperkalemia. Aldosterone is secreted by the zona glomerulosa cells of the adrenal cortex in response to high renin and angiotensin II or hyperkalemia. The plasma K + concentration, independent of aldosterone, can directly affect K + secretion. In addition to the K + concentration in the lumen of the CCD, renal K + loss depends on the urine flow rate, a function of daily solute excretion (see above). Since excretion is equal to the product of concentration and volume, increased distal flow rate can significantly enhance urinary K + output. Finally, in severe K + depletion, secretion of K + is reduced and reabsorption in the cortical and medullary collecting ducts is upregulated. Hypokalemia Etiology (Table 46-3) Hypokalemia, defined as a plasma K + concentration <3.5 mmol/L, may result from one (or more) of the following: decreased net intake, shift into cells, increased net loss. Diminished intake is seldom the sole cause of K + depletion since urinary excretion can be effectively decreased to <15 mmol/d as a result of net K + reabsorption in the distal nephron. With the exception of the urban poor and certain cultural groups, the amount of K + in the diet almost always exceeds that excreted in the urine. However, dietary K + restriction may exacerbate the hypokalemia secondary to increased gastrointestinal or renal loss. An unusual cause of decreased K + intake is ingestion of clay (geophagia), which binds dietary K + and iron. This custom was previously common among African Americans in the American South. . Chapter 046. Sodium and Water (Part 11) Potassium: Introduction Potassium Balance Potassium is the major intracellular. membrane potential and is crucial for normal neuromuscular function. The basolateral Na + , K + -ATPase pump actively transports K + in and Na + out of the cell in a 2:3 ratio, and the passive. concentration and facilitated by insulin release and basal catecholamine levels. Eventually, however, the excess K + is excreted in the urine (see below). The regulation of gastrointestinal K + handling