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Imbalanced Plasma ACE and ACE2 ratio in the Uremic Patients with Cardiovascular Diseases and Its Change during a Single Hemodialysis Session
Author(s) -
Cho ChingChang,
Lu LiChe,
Chang ChiaChu,
Lin ChungI,
Wang GuanHua,
Yang ChungWei,
Lin ChihSheng
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.1028.2
Subject(s) - hemodialysis , medicine , renin–angiotensin system , kidney disease , endocrinology , angiotensin ii , disease , angiotensin converting enzyme , kidney , gastroenterology , blood pressure
Background The renin‐angiotensin system (RAS) has significant influences on heart and renal disease progression. Angiotensin converting enzyme (ACE) and angiotensin converting enzyme II (ACE2) are major peptidases of RAS components and play counteracting functions through classical angiotensin II (Ang II)/ATIR and non‐classical angiotensin‐(1–7) (Ang‐(1–7))/Mas axis, respectively. Based on crucial roles of RAS in the pathogenic development of chronic kidney disease (CKD), we tested the hypothesis whether plasma ACE and ACE2 levels might be significantly changed in the patients with end‐stage CKD (ESRK), i.e., uremic patients or HD patients. Methods This study included 372 uremic patients (aged 66.0 ± 13.4; 184 women; the mean hemodialysis (HD) therapy time was 7.5 years) who were on regular HD treatment and 50 healthy controls. The HD patients were grouped by the clinical symptoms or previous history of CVD ( n = 122) and without CVD ( n = 250). Hematological and biochemical parameters were determined by routine procedures. The plasma ACE and ACE2 levels were detected using fluorogenic substrates assay, and plasma Ang II and Ang‐(1–7) concentrations were determined by ELISA assay. Results The clinical characteristics of the HD patients with CVD ( n = 122) and without CVD ( n = 250) were shown that few of the clinical determinants detected differs significantly between the HD patient subgroups. However, we compared pre‐HD levels of plasma ACE, ACE2, Ang II and Ang‐(1–7) in the HD patients with and without cardiovascular disease (CVD) to those of the controls. The HD patients, particularly those with CVD, showed a significant increase in the levels of plasma ACE and Ang II, whereas ACE2 and Ang‐(1–7) levels were lower than those in the healthy controls. Therefore, markedly loss of ACE and ACE2 correlation, i.e., imbalanced ACE/ACE2, was observed in the HD patients with CVD. In the course of a single HD session, the plasma ACE, ACE/ACE2 and Ang II levels in the HD patients with CVD were increased from pre‐HD to post‐HD. On the contrary, plasma ACE2 level were decreased after the HD session. These changes were not detected in the HD patients without CVD. Conclusion Pathogenically imbalanced circulating ACE/ACE2 was detected in the HD patients, particularly those with CVD. HD session could increase ACE/Ang II/AT1R axis and decrease ACE2/Ang‐(1–7)/Mas axis activity in the circulation of HD patients with CVD. The imbalanced ACE/ACE2 due to a single HD session in the HD patients with CVD is required to further validate on its mechanism.