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Updated: Aug 30, 2026

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay
Published on: September 9, 2012
Plasma active renin, inactive renin and kallikrein in patients with disseminated intravascular coagulation
1Department of Internal Medicine, Provincial Taoyuan General Hospital, Taiwan R.O.C.
Insights
Plasma kallikrein
Area of Science:
- Biochemistry
- Physiology
Background:
- Inactive renin activation is crucial for blood pressure regulation.
- The role of plasma kallikrein in this process remains unclear.
Purpose of the Study:
- To investigate the potential role of plasma kallikrein in the in vivo activation of inactive renin.
Main Methods:
- Measured plasma active renin, inactive renin, kallikrein, and prekallikrein levels in 10 disseminated intravascular coagulation (DIC) patients and 16 controls.
- Assayed kallikrein activity using synthetic substrate S-2302.
- Activated plasma inactive renin with trypsin.
Main Results:
- DIC patients showed significantly lower plasma prekallikrein levels compared to controls (p < 0.01).
- No significant differences in plasma kallikrein or inactive renin levels were observed.
- Active renin levels were higher in DIC patients, but the proportion of active renin did not differ significantly.
Conclusions:
- Results suggest a possible role for plasma kallikrein in inactive renin activation in vivo.
- Further research is needed to confirm this association.
Abstract:
To investigate the role plasma kallikrein plays in the in vivo activation of inactive renin, we measured plasma active renin, inactive renin, kallikrein and prekallikrein levels in 10 patients with disseminated intravascular coagulation (DIC), with 16 normal persons as controls. The plasma active renin concentration was expressed by the angiotensin I generation rate after the addition of sheep renin substrate. Plasma inactive renin was activated by trypsin. The plasma total kallikrein level was measured by an assay of kallikrein activity on synthetic substrate S-2302 after the addition of a prekallikrein activator. Plasma kallikrein was assayed by its activity on S-2302 without addition of the activator. The prekallikrein level was obtained by subtracting the kallikrein activity from the total kallikrein activity. A significant decrease in the plasma prekallikrein concentration was observed in DIC patients, as compared to that of controls (p less than 0.01). There was no significant difference in plasma levels of kallikrein, inactive renin, and the proportion of active renin between DIC patients and normal controls, but the active renin level was higher in DIC patients. There was no significant correlation between the level of plasma kallikrein and the proportion of active renin in either normal controls or DIC patients. These results are compatible with, but do not prove, the theory that plasma kallikrein plays a role in the in vivo activation of inactive renin.
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