Abstract
Potassium is the main cation in the intracellular space and its content in healthy adults is around 3700 mmol. Its retention is one of the dangers that accompanies chronic renal failure, especially when glomerular filtration rate (GFR) falls toward 20% of normal. There exist different mechanisms by which hyperkalemia is avoided in patients with renal failure. These include spontaneous restriction of dietary potassium intake to 40-60 mmol/day and aldosterone induced increase in potassium excretion in renal distal tubules and colonic epithelium. Although renal and intestinal adaptation are important in maintaining overall potassium balance during CKD, movement of potassium into the cells is extremely important in the body's acute defense against hyperkalemia, and occurs daily during postprandial potassium overload, through shift of this cation into hepatic cells mediated by insulin and thus avoiding post-prandial hyperkalemia. The above described mechanisms contribute to maintenance of normal serum potassium in patients with CKD.
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