Vol. 29 No. 4 (2016), Artykuły
Vol. 29 No. 4 (2016)

The influence of renin angiotensin aldosterone system blockers on asymmetric dimethylarginine levels in patients with chronic glomerulonephritis

Artykuły
Published 2017-01-23
Zbigniew Heleniak
Department of Nephrology, Transplantology and Internal Medicine, Medical University of Gdansk, Debinki 7 80-952 Gdansk, Poland
Zbigniew Zdrojewski
Department of Internal Medicine, Connective Tissue Disease and Geriatrics, Medical University of Gdansk, Debinki 7 80-952 Gdansk, Poland
Piotr Wisniewski
Department of Endocrinology and Internal Medicine, Medical University of Gdansk, Debinki 7 80-952 Gdansk, Poland
Leszek Bieniaszewski
Department of Hypertension and Diabetology, Medical University of Gdansk, Debinki 7 80-952 Gdansk, Poland
Boleslaw Rutkowski
Department of Nephrology, Transplantology and Internal Medicine, Medical University of Gdansk, Debinki 7 80-952 Gdansk, Poland
Alicja Debska-Slizien
Department of Nephrology, Transplantology and Internal Medicine, Medical University of Gdansk, Debinki 7 80-952 Gdansk, Poland
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Keywords

asymmetric dimethylarginine
proteinuria
renin angiotensin aldosterone system

Abstract

Endothelial dysfunction could be related to the limited availability of nitric oxide (NO). NO is synthesized with the participation of an NO synthase whose activity is inhibited by asymmetric dimethylarginine (ADMA). The synthesis of ADMA is exacerbated by oxidative stress, and several studies have shown the efficacy of drugs acting on the renin-angiotensin-aldosterone system (RAAS) (converting enzyme inhibitors and angiotensin II receptor antagonists) in reducing the level of ADMA. The probable mechanism of drug action is a reduction of oxidative stress through a decrease of angiotensin II formation. The aim of this study was to assess the influence of RAAS blockers on the plasma concentration of ADMA in patients with chronic glomerulonephritis (ChGN). The study included 37 patients, placed into group A and group B, depending on the treatment. Both groups were treated with RAAS blockers. In group B, immunosuppressive drugs were additionally administered. The control visits were at the 0, 6 and 12 months of observation. In both the studied groups (A+B), a significant reduction of ADMA (0.77 vs 0.4 μmol/l; p<0.05) was noticed. In patients suffering from ChGN, the use of RAAS blockers resulted in a significant decrease of plasma ADMA concentration, independently of immunosupressive treatment.
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