Urinary kallikrein excretion in Bartter's syndrome

Urinary excretion of kallikrein has been studied in a patient with hypokalemic alkalosis, hyperplasia of the renal juxtaglomerular apparatus and hyperreninemia, secondary aldosteronism and resistance to the pressor effect of angiotensin II (Bartter's syndrome). Urinary kallikrein was found exceedingly high in several determination, whereas it was low in patients with essential hypertension and high in patients with primary aldosteronism. Urinary kallikrein decreased after spironolactone therapy. The rise of kallikrein excretion (which is not related to plasma renin) in this case is probably caused by a direct action of the chronic excess of plasma aldosterone; it could not be accounted for as secondary to natriuresis.