Hypokalemia (low potassium) has been
found in >90% of hypertensive patients with primary aldosteronism
(Conn syndrome). This uncommon entity is a curable cause of
hypertension. Low potassium occurs with endogenous or exogenous increase
in other corticosteroids, including that in Cushing syndrome as well as
with dietary or parenteral deprivation of potassium (eg, parenteral
therapy without adequate potassium replacement). Hypokalemia occurs with
vomiting, diarrhea, fistulas, laxatives, diuretics, burns, excessive
perspiration, Bartter syndrome, some cases of alcoholism and folic acid
deficiency, in alkalosis and in renal tubular acidosis as well as in
other entities.
Low potassium is much more significant with a low
pH than with a high pH. When pH increases by 0.1, potassium decreases
approximately 0.6 mmol/L. With low pH, as in ketoacidosis, as
therapeutic adjustment towards normal is made, plasma/serum K+
levels will decrease. Phosphorus levels tend to follow potassium levels
downwards during therapy of diabetic ketoacidosis; both are largely
intracellular. With insulin therapy (and increased utilization of
carbohydrate), potassium moves into cells and serum/plasma level falls.
Hyperalimentation may have a similar effect. Hypokalemia has been
reported in slightly over one-half of a series of 32 patients with acute
myelogenous leukemia,1 but thrombocytosis can increase serum potassium levels, vide supra.
Thiazide/chlorthalidone therapy may cause hyperuricemia and hypercalcemia as well as hypokalemia.
The watery diarrhea-hypokalemia-achlorhydria (WDHA) syndrome most often is related to vasoactive intestinal polypeptide (VIP).
Hyperkalemia (high potassium)
reflects generally inadequate renal excretion, mobilization of
potassium from the tissues, or excessive intake or administration.
Hyperkalemia occurs with hemolysis, trauma, with administration of
potassium salts of some drugs, Addison disease, acidosis, insulin lack,
with increased osmolality (eg, glucose, mannitol), and in other entities
as well as with renal diseases. Increased potassium can occur with
potassium sparing diuretics, nonsteroidal anti-inflammatory drugs,
especially in the presence of renal disease. Systemic heparin therapy
can suppress aldosterone release and increase potassium, especially in
the presence of other factors.
A discussion of the relation
between lactic acidosis and ketoacidosis and elevated serum potassium
levels is provided in a paper by Fulop.2
Drug effects are summarized.3
