Potassium balance in acid-base disorders
- David B Mount, MD
David B Mount, MD
- Assistant Professor of Medicine
- Harvard Medical School
There are important interactions between potassium and acid-base balance that involve both transcellular cation exchanges and alterations in renal function . These changes are most pronounced with metabolic acidosis but can also occur with metabolic alkalosis and, to a lesser degree, respiratory acid-base disorders.
INTERNAL POTASSIUM BALANCE
Acid-base disturbances cause potassium to shift into and out of cells, a phenomenon called "internal potassium balance" . An often-quoted study found that the plasma potassium concentration will rise by 0.6 meq/L for every 0.1 unit reduction of the extracellular pH . However, this estimate was based upon only five patients with a variety of disturbances, and the range was very broad (0.2 to 1.7 meq/L). This variability in the rise or fall of the plasma potassium in response to changes in extracellular pH was confirmed in subsequent studies [2,4].
Metabolic acidosis — In metabolic acidosis, more than one-half of the excess hydrogen ions are buffered in the cells. In this setting, electroneutrality is maintained in part by the movement of intracellular potassium into the extracellular fluid (figure 1). Thus, metabolic acidosis results in a plasma potassium concentration that is elevated in relation to total body stores. The net effect in some cases is overt hyperkalemia; in other patients who are potassium depleted due to urinary or gastrointestinal losses, the plasma potassium concentration is normal or even reduced [5,6]. There is still a relative increase in the plasma potassium concentration, however, as evidenced by a further fall in the plasma potassium concentration if the acidemia is corrected.
A fall in pH is much less likely to raise the plasma potassium concentration in patients with lactic acidosis or ketoacidosis [3,7]. The hyperkalemia that is commonly seen in diabetic ketoacidosis, for example, is more closely related to the insulin deficiency and hyperosmolality than to the degree of acidemia. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis".)
Why this occurs is not well understood. Two factors that may contribute are the ability of the organic anion to accompany the hydrogen ion into the cell, perhaps as the lipid-soluble, intact acid , and differential effects on insulin and glucagon secretion [4,9].
Subscribers log in hereLiterature review current through: Jul 2017. | This topic last updated: Oct 30, 2015.References
- Aronson PS, Giebisch G. Effects of pH on potassium: new explanations for old observations. J Am Soc Nephrol 2011; 22:1981.
- Sterns RH, Cox M, Feig PU, Singer I. Internal potassium balance and the control of the plasma potassium concentration. Medicine (Baltimore) 1981; 60:339.
- Adrogué HJ, Madias NE. Changes in plasma potassium concentration during acute acid-base disturbances. Am J Med 1981; 71:456.
- Adrogué HJ, Madias NE. PCO2 and [K+]p in metabolic acidosis: certainty for the first and uncertainty for the other. J Am Soc Nephrol 2004; 15:1667.
- Magner PO, Robinson L, Halperin RM, et al. The plasma potassium concentration in metabolic acidosis: a re-evaluation. Am J Kidney Dis 1988; 11:220.
- Wiederseiner JM, Muser J, Lutz T, et al. Acute metabolic acidosis: characterization and diagnosis of the disorder and the plasma potassium response. J Am Soc Nephrol 2004; 15:1589.
- Fulop M. Serum potassium in lactic acidosis and ketoacidosis. N Engl J Med 1979; 300:1087.
- Graber M. A model of the hyperkalemia produced by metabolic acidosis. Am J Kidney Dis 1993; 22:436.
- Adrogué HJ, Chap Z, Ishida T, Field JB. Role of the endocrine pancreas in the kalemic response to acute metabolic acidosis in conscious dogs. J Clin Invest 1985; 75:798.
- Szylman P, Better OS, Chaimowitz C, Rosler A. Role of hyperkalemia in the metabolic acidosis of isolated hypoaldosteronism. N Engl J Med 1976; 294:361.
- Altenberg GA, Aristimuño PC, Amorena CE, Taquini AC. Amiloride prevents the metabolic acidosis of a KCl load in nephrectomized rats. Clin Sci (Lond) 1989; 76:649.
- Rose BD, Post TW. Clinical Physiology of Acid-Base and Electrolyte Disorders, 5th ed, McGraw-Hill, New York 2001. p.347.
- DuBose TD Jr, Good DW. Effects of chronic hyperkalemia on renal production and proximal tubule transport of ammonium in rats. Am J Physiol 1991; 260:F680.
- DuBose TD Jr, Good DW. Chronic hyperkalemia impairs ammonium transport and accumulation in the inner medulla of the rat. J Clin Invest 1992; 90:1443.
- Good DW. Ammonium transport by the thick ascending limb of Henle's loop. Annu Rev Physiol 1994; 56:623.
- Attmane-Elakeb A, Mount DB, Sibella V, et al. Stimulation by in vivo and in vitro metabolic acidosis of expression of rBSC-1, the Na+-K+(NH4+)-2Cl- cotransporter of the rat medullary thick ascending limb. J Biol Chem 1998; 273:33681.
- Bourgeois S, Meer LV, Wootla B, et al. NHE4 is critical for the renal handling of ammonia in rodents. J Clin Invest 2010; 120:1895.
- Sabatini S, Kurtzman NA. The maintenance of metabolic alkalosis: factors which decrease bicarbonate excretion. Kidney Int 1984; 25:357.
- COOKE RE, SEGAR WE, CHEEK DB, et al. The extrarenal correction of alkalosis associated with potassium deficiency. J Clin Invest 1952; 31:798.
- Carlisle EJ, Donnelly SM, Vasuvattakul S, et al. Glue-sniffing and distal renal tubular acidosis: sticking to the facts. J Am Soc Nephrol 1991; 1:1019.