In low renin essential hypertension and hyporeninemic hypoaldosteronism, inactive renin is normal or high despite low active renin, suggesting impaired conversion to active renin rather than decreased synthesis.
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Findings suggest impaired renin activation in low-renin states; hypothesis-generating and should not yet change practice.
Low PRA and active renin (AR) may be accompanied by low inactive renin (IR), indicating impaired renin production, or by normal or elevated IR, suggesting defective conversion to AR. To explore these possibilities, plasma AR and IR (acid activation method) were measured in normal volunteers and in patients with low PRA. All low renin states showed significant low PRA and AR when compared to normals; on the other hand, IR was 11.8 +/- 1.1 ng/ml.h in normals; low in primary aldosteronism (2.1 +/- 0.5 ng/ml.h) and anephric subjects; normal in low renin essential hypertension (7.5 +/- 1.3 ng/ml.h), nondiabetic hyporeninemic hypoaldosteronism (9.4 +/- 1.6 ng/ml.h) and diabetic hyporeninemic hypoaldosteronism (17.3 +/- 2.5 ng/ml.h); and significantly elevated in diabetics with nephropathy (21.0 +/- 1.6 ng/ml.h). The acute iv infusion of 2 liters saline in normal subjects did not decrease IR (11.8 +/- 2.0 vs. 13.0 +/- 1.8 ng/ml.h) despite a reduction in PRA and AR of 50-75%. These data indicate that in cases of primary aldosteronism and in anephric subjects both AR and IR are decreased, suggesting a decrease in total renal synthesis or release, whereas in low renin essential hypertension, nondiabetic hyporeninemic hypoaldosteronism, diabetic hyporeninemic aldosteronism, and diabetics with nephropathy AR is low and IR is normal or high, suggesting the possibility of impaired conversion to AR.
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Antonipillai et al. (1981) studied this question.
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