Endocrine Abstracts

Distribution of K+ contrasts with Na+: Na+ is predominantly extracellular (EC) and K+ is intracellular (IC ~98% = ~3,500 mmoles). High IC K+ is needed for regulation of cell volume, pH, enzyme function, DNA/protein synthesis, and growth. Low EC K+ (plasma K+; PK), and the associated steep transmembrane K+ gradient, is largely responsible for the membrane potential difference (p.d.) of excitable and non-excitable cells; any change in the gradient (doubling or halving PK) will disturb cell excitation and contraction. Chronic K+ depletion impairs urinary concentrating ability, causes metabolic alkalosis and increases NH4+ excretion.

Normal K+ homeostasis depends on extrarenal balance - intake (80-120 mmole/day) versus excretion (kidney ~95%; colon ~5%) and intrarenal balance: distribution of K+ between IC (most in skeletal muscle cells) and EC compartments. A shift of ~1% of K+ between IC and EC will cause a ~50% change in PK - a good steak meal could do it, if there were no 'buffering' mechanisms. The important ones are hormonal (insulin, b-adrenergic agonists-adrenaline-and aldosterone) and promote the rapid transfer of K+ from EC to IC via the 'sodium' pump.

Renal K+ handling: proximal nephron (including loop of Henle) - almost all the filtered K+ (~90%) is reabsorbed; distal nephron - K+ is (predominantly) secreted and this segment determines the final urine K+ content. With normal or high K+ intake, distal K+ secretion accounts for most of the urinary K+; factors affecting K+ excretion are flow rate, lumen negative transepithelial p.d., and aldosterone.

In K+ dyskalaemias consider: (1) altered Na+ delivery to the K+ secreting site; (2) altered mineralocorticoid status; (3) altered (damaged) distal site (collecting duct) function. In the ITU, the cause is probably a cell shift in K+, or acute renal failure; in Outpatients, it is probably a mineralocorticoid or collecting duct defect.