Chronic kidney disease: metabolic acidosis and hyperkalemia
Under normal physiological situations, hydrogen ions are secreted in the distal tubule under exchange of sodium ions. Hydrogen ions are generated by the dissociation of carbonic acid and secreted into the tubular fluid by counter transport in exchange for sodium ions. In CKD, there is loss of tubular cells and thus of the function of all transport mechanisms. In this view, the distal tubular cells are no longer able to secrete enough hydrogen ions. This results in a decrease of the pH in the blood.
Renal metabolic acidosis in renal failure requires treatment because:
- bones can buffer the excess hydrogen ions, but this will result in calcium and phosphate release of the bones causing osteodystrophy
- acidosis stimulates breakdown of skeletal muscle and decrease of albumin synthesis, resulting in muscle weakness
- acidosis can contribute to hyperkalemia
Alkalic therapy with sodium bicarbonate helps to increase plasma bicarbonate levels.
Hyperkalemia: Excretion of potassium is usually maintained in CKD patients until the creatinine clearance drops below 15ml/min. Oliguria and a potassium-rich diet are the main causes of hyperkalemia in these patients. However, several drugs can contribute to hyperkalemia as well:
- ACE inhibitors and AT-II receptor antagonists
- non-selective β-blockers
Rational drug use and dietary potassium restriction are usually sufficient to control hyperkalemia.
In metabolic acidosis, the blood results will show:
Extra info: In acidosis, the pH is below 7.35. The excess of protons (H+) will form H2CO3 which will dissociate to water and CO2. The latter is lost through the lungs.