The hypertensive patient with hypokalaemia: the search for hyperaldosteronism.

Introduction Factitious normokalaemia The physical chemical determination of plasma potassium concentration is very precise. However, the matrix where potassium is determined, the plasma, is a notoriously unreliable partner. This fact is generally recognized when patients with hyperkalaemia are considered. Because potassium concentrations are 20-fold higher within the cell than outside, the potassium concentration is facticiously high whenever potassium shifts from the intra-to the extracellular compartment during or after venipuncture. As a corollary, in a subject with hypokalaemia in vivo one might measurènormal' potassium concentrations when such a facti-tious potassium shift has occurred. Patients like this may in reality be hypokalaemic. Thus, in clinical practice we have to ascertain that normokalaemia is not an artifact in patients with hypertension. The mechanisms accounting for factitious normalkalaemia are: (i) repeated ®st clenching with or without tour-niquet; (ii) traumata venipuncture with a small gauge needle; (iii) delayed centrifugation or placing the sample on ice; (iv) thrombocytosis or myeloprolifer-ative disorders; (v) blood clotting; (vi) acute hyper-ventilation due to fear of venipuncture; and (vii) abnormal leak of potassium through red blood cell membranes at lower temperature as a consequence of hereditary stomatocytosis (rare) w1±9x. In view of all these caveats it is completely unknown how often we miss the diagnosis of hypokalaemia. Hypokalaemia has arbitrarily been de®ned as plasma potassium level less than 3.5 mmolul. In the distal nephron, mineralocorticoids increase reabsorption of sodium and secretion of potassium. Therefore, three indirect markers of renal mineralo-corticoid activity have been utilized in the past based on the urinary excretion of sodium and potassium. The fractional excretion of potassium (i.e. the fraction of the ®ltered potassium load excreted into the urine), is probably a poor re¯ection of aldosterone action because ®ltered potassium is almost completely reab-sorbed and the amount of potassium detected in urine is almost exclusively the result of distal secretion. Under steady-state conditions urinary potassium excretion must equal dietary potassium intake w10x. The urinary potassiumusodium ratio depends on dietary sodium and potassium intake as well. For the same reasons it is not a reliable indicator of mineralocorti-coid activity w11x. The transtubular potassium gradient (TTKG) derived from the urineuplasma potassium ratio divided by the urineuplasma osmolality ratio has been popularized w12,13x. This index provides a semi-quantitative assessment of the apparent transtubular potassium concentration gradient in the major distal nephron segment, where potassium is secreted. This index can be applied to situations where the urine is not hypotonic and …