Urinary Kallikrein Excretion

A preliminary report of the data was presented at the Southem Section Meeting of The American Federation for Clinical Research in New Orleans, La. in January 1976. Received for publication 1 May 1978 and in revised form 5 October 1979. tion vs. race and age-matched normal subjects. Stimulation of urinary kallikrein excretion by Florinef was equal in black and white normal subjects vs. hypertensive patients (black normals = 12.3±2.7 [n = 9], NREH = 11.7±1.8 [n = 10], LREH= 10.9+1.5 [n = 12]; white normals = 21.2±2.9 [n = 11], essential hypertension = 20.9±3.2 [10 NREH, 5 LREH]). Stimulation of urinary kallikrein excretion with low sodium diet was decreased (P < 0.05) only in black LREH (black normals = 11.2+2.4 [n = 10], NREH = 10.1±2.7 [n = 10], LREH = 7.4± 1.1 [n = 13]; white normals = 19.1 ±2.7 [n = 13], essential hypertension = 17.5+2.3 [nine NREH, four LREH]). However, during low sodium diet, black patients with LREH had evidence for less sodium depletion as manifested by a decreased rise in urinary aldosterone excretion (16.3+2.7 vs. 33.3±6.4 ,ug/24 h for black normals) and a failure to achieve metabolic balance in 11/13 patients. Thus, the lesser kallikrein stimulation appeared to result from these two factors. Black and white hypertensives with creatinine clearance <80 ml/min had little increase in urinary kallikrein excretion with Florinef or low sodium diet. 5 of 12 patients with primary aldosteronism or 17ahydroxylase deficiency did not have an elevated urinary kallikrein excretion rate. Mild renal insufficiency may have contributed to this finding in two of these five patients. Nevertheless, this finding illustrates a limitation to the use of urinary kallikrein excretion rate as an index of mineralocorticoid activity. However, it appears that the majority of patients with LREH have no evidence for excess production of an unknown mineralocorticoid. The failure to find a decrease in urinary kallikrein excretion in racially matched patients with essential hypertension and normal renal function questions the postulate of a role of the kallikrein-kinin system in the initiation of essential hypertension.