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Updated: Aug 9, 2026

Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
[State of the kallikrein-kinin system in chronic circulatory insufficiency]
Insights
Chronic circulatory insufficiency activates the kinin system, indicated by reduced plasma prekallikrein. Cardiac glycoside treatment normalized kinin system indices alongside clinical improvement.
Area of Science:
- Biochemistry
- Cardiology
- Pharmacology
Background:
- The kallikrein-kinin system plays a role in cardiovascular function.
- Chronic circulatory insufficiency is a complex condition affecting hemodynamics.
- Understanding the kallikrein-kinin system's involvement may reveal therapeutic targets.
Purpose of the Study:
- To investigate the kallikrein-kinin system's status in patients with chronic circulatory insufficiency.
- To evaluate the impact of cardiac glycosides on the kallikrein-kinin system in these patients.
Main Methods:
- Studied 93 patients with chronic circulatory insufficiency.
- Assessed plasma prekallikrein and kallikrein inhibitor levels.
- Analyzed changes in 25 patients before and after cardiac glycoside treatment, monitoring central hemodynamics.
Main Results:
- All patients exhibited significant activation of the kinin system, evidenced by decreased plasma prekallikrein and altered kallikrein inhibitor levels.
- Clinical improvement and enhanced central hemodynamics correlated with normalization of kinin system indices.
- Patients intolerant to cardiac glycosides did not show restoration of kinin system components.
Conclusions:
- The kallikrein-kinin system is activated in chronic circulatory insufficiency.
- Cardiac glycoside therapy can normalize kinin system function in conjunction with clinical improvement.
- Kinin system normalization may be a marker of successful cardiac glycoside treatment.
Abstract:
The condition of the kallikrein-kinin system was studied in 93 patients with chronic circulatory insufficiency. In 25 of them it was studied in dynamics--before and after treatment with cardiac glycosides. Marked activation of the kinin system was found in all patients; this was manifested by a decreased level of plasma prekallikrein and phase changes in the content of the kallikrein inhibitor. Improvement in the clinical picture and values of central hemodynamics during treatment was attended by normalization of the main indices of the kinin system. In tolerance of patients to treatment with cardiac glycosides, restoration of the content of the main components of the kinin system was not encountered.
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