Renal effects

Hypokalemia may produce a state resembling diabetes insipidus as a result of reduced medullary solute concentrations. There is an association between potassium depletion and metabolic alkalosis, particularly in the hypovolemic patient. This may be partly due to shifts of hydrogen ions into cells but probably also reflects increased renal retention of sodium and bicarbonate.

Chronic potassium depletion produces morphological changes in the kidney with the development of cytoplasmic vacuoles in proximal and distal cortical tubular cells. Metabolic effects

These include reduced protein synthesis, a negative nitrogen balance, glucose intolerance, a metabolic alkalosis, and reduced carbohydrate synthesis. Treatment of hypokalemia

Underlying abnormalities and causes should be corrected where possible. Potassium should be replaced in conjunction with correction of other metabolic and electrolyte abnormalities. If there are symptoms or ECG signs, or [K+] is below 2 mmol/l, this should be replaced rapidly (up to 40 mmol/h). At higher potassium levels and in asymptomatic patients, intravenous correction at rates of 10 to 20 mmol/h are usually adequate. Potassium replacement is usually performed using potassium chloride, although potassium phosphate can be used if there is concomitant phosphate deficiency. In extremis (lethal arrhythmias in the presence of severe hypokalemia), potassium can be given by rapid infusion of 50 to 100 ml of 40 mmol/l KCl over 2 to 5 min. In patients with coexistent metabolic acidosis and hypokalemia, potassium should be replaced before correction of the acidosis in order to prevent further severe falls in serum potassium.

After the extracellular deficit has been corrected, there will usually also be a whole-body intracellular deficit to correct. There is no single satisfactory way of judging the adequacy of potassium repletion, but looking for an increase in urinary potassium, a tendency for plasma potassium to stay elevated after potassium infusion, or the correction of a metabolic alkalosis may all give useful clues. Continuing replacement of magnesium should accompany potassium replacement. Extracellular fluid potassium may be restored in the magnesium-deficient patient, but magnesium is needed for potassium to enter cells and prevent continuing renal potassium wasting

(Solomon 1987). Hypokalemia in hyperaldosteronism may be minimized by reducing sodium intake. Spironolactone may also be useful for reducing renal potassium wasting.

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