We investigated active and inactive (acid-activatable) plasma renin in anephric and in normal persons. In anephric patients (n = 15) plasma concentration of active and inactive renin was 1.15 +/-- 0.2 and 40.7 +/- 7.1 microunits ml, respectively; angiotensin II (n = 13) was 14.5 +/- 1.9 pg/ml. Furosemide (n = 10), 40 mg i.v., and upright posture (n = 8) did not change active or inactive renin in the anephric state. In normal men, furosemide (n = 9) within 15 min increased active renin from 29.9 +/- 5.8 to 82.4 +/- 14.8 microunits/ml (P less than 0.001), while inactive renin slightly but not significantly decreased from 136.3 +/- 29.9 to 121.1 +/- 19.2 microunits/ml; orthostasis (n = 15) within 4 h stimulated active renin (P less than 0.001) and slightly raised inactive renin (P less than 0.05). Both furosemide and orthostasis increased (P less than 0.001 each) the proportion of active renin in normal persons. Studies in one patient within 24 h after bilateral nephrectomy indicated half-life to be 30-60 min for active and 2-4 h for inactive renin. Thus, we detected low levels of active renin and considerable amounts of inactive renin and angiotensin II in anephric patients. Our data suggest that about 30% of inactive renin in normal plasma is of extrarenal origin. The stimulation of active renin by furosemide and orthostasis is bound to the presence of the kidney. Our studies provide indirect evidence that both manoeuvres may stimulate the conversion of inactive to active renin within the human kidney.

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Active renin was detected in 6 of 7 anephric patients (mean value: 0.72 +/- 0.27 microU/ml, n = 7; normals: 19.7 +/- 2.4 microU/ml, n = 10), using an assay method without intrinsic acid- or cryoactivation. Prorenin, measured as the difference between plasma renin concentration (PRC) before and after acid-activation in vitro, was present in considerable amounts in all patients (32.4 +/- 3.5 microU/ml; normals: 80.7 +/- 9.7 microU/ml). PRC after cryoactivation at--5 degrees C during 1 week was insignificantly lower than after acid-activation in the patients. There was a linear correlation between PRC after either activation procedure (p less than 0.01). Supine or upright posture did not influence active or inactive renin in the anephric subjects. Our studies show that low but significant levels of active renin and a considerable amount of prorenin are detectable in anephric patients. The data suggest that prorenin in normal subjects in a significant proportion is of extrarenal origin. Orthostasis has no effect on extrarenal active or inactive renin.