Serum Potassium Concentration in Acidemic States

Abstract

It has been generally accepted that acidosis results in hyperkalemia because of shifts of potassium from the intracellular to the extracellular compartment. There is ample clinical and experimental evidence, however, to support the conclusion that uncomplicated organic acidemias do not produce hyperkalemia. In acidosis associated with mineral acids (respiratory acidosis, end-stage uremic acidosis, NH₄CI- or CaCl₂-induced acidosis), acidemia per se, results in predictable increases in serum potassium concentration. In acidosis associated with nonmineral organic acids (diabetic and alcoholic acidosis, lactic acidosis, methanol and the less common forms of organic acidemias secondary to methylmalonic and isovaleric acids, and ethylene glycol, paraldehyde and salicylate intoxications), serum potassium concentration usually remains within the normal range in uncomplicated cases. A number of factors, however, may be responsible for hyperkalemia in some of these patients other than the acidemia per se. These include dehydration and renal hypoperfusion, preexisting renal disease, hypercatabolism, diabetes mellitus, hypoaldosteronism, the status of potassium balance, and therapy. The mechanism(s) of this differing effect of mineral and organic acidemias on transmembrane movement of potassium remains undefined. The prevalent hypothesis, however, favors the free penetrance of the organic anion into cells without creating a gradient for the hydrogen ions and, thus, obviating the efflux of intracellular potassium. The importance of the presence of hyperkalemia in clinical states of organic acidemias is obvious. A search for the complicating factors reviewed above should be undertaken since organic acidemias per se, should not be expected to be accompanied by elevations of serum potassium concentration. Moreover, the classical teaching that the absence of hyperkalemia during severe acidosis is indicative of severe potassium deficiency, may not be universally valid in patients with uncomplicated organic acidemias.

Antinephrolithiatic and antioxidative efficacy ofDolichos biflorusseeds in a lithiasic rat model

“…The increase in serum potassium level could be due to the fact that EG leads to the acidosis which results in hyperkalemia because of shift of potassium from the intracellular to the extracellular compartment. Similar hyperkalemia due to EG administration has also been reported in an earlier report (Perez et al, 1981).…”

Antioxidative mechanism involved in the preventive efficacy ofBergenia ciliatarhizomes against experimental nephrolithiasis in rats

“…In the present investigation, increase in serum potassium level could be due to the fact that EG caused acidosis followed by hyperkalemia because of shift of potassium from the intracellular to the extracellular compartment. Similar hyperkalemia due to EG administration has been reported earlier (Perez et al, 1981). However, these changes were significantly restored in extract treated rats, probably due to the presence of polyphenolic compounds such as gallic acid.…”

Role of the endocrine pancreas in the kalemic response to acute metabolic acidosis in conscious dogs.

“…Fluxes of potassium among the fluid compartments were previously thought to be solely determined by changes in acidity. Other factors, however, have been identified as modulators of the plasma potassium response (5); prominent among them is the nature of the anion escorting the protons responsible for acidemia (6)(7)(8)(9). In sharp contrast with mineral acid acidosis that consistently leads to hyperkalemia, acute organic acid acidosis is not associated with a significant increase in plasma potassium (10).…”