Table 4.
Hepatic and systemic RAS components in liver tissue samples and plasma samples of 5 ACLD patients (#1–5).
| #1 | #2 | #3 | #4 | #5 | |
|---|---|---|---|---|---|
| Patient characteristics | |||||
| Age, years | 69 | 67 | 62 | 64 | 52 |
| Body mass index, kg m−2 | 26.1 | 24.6 | 23.1 | 33.9 | 19.3 |
| Etiology | NASH | VIRAL | ALD | NASH | ALD |
| cACLD/dACLD | cACLD | cACLD | cACLD | dACLD | dACLD |
| HVPG, mmHg | 15 | 3 | 8 | 10 | 18 |
| MAP, mmHg | 112 | 94 | 106 | 119 | 123 |
| CTP score | 5 | 5 | 5 | 6 | 8 |
| MELD | 11 | 12 | 9 | 8 | 19 |
| Liver tissue | |||||
| ACE activity | 286.0 | 292.0 | 119.0 | 116.0 | 185.0 |
| Chymase activity | 6971.0 | 302.0 | 359.0 | 731.0 | 2237.0 |
| NEP activity | 59.0 | 669.0 | 304.0 | 403.0 | 86.0 |
| ACE2 activity | 186.0 | 80.0 | 54.0 | 130.0 | 110.0 |
| Plasma | |||||
| PRA-S | 28.6 | 137.4 | 37.2 | 147.2 | 446.7 |
| Ang I (1–10) | 12.4 | 18.2 | 7.9 | 49.2 | 151.8 |
| Ang II (1–8) | 16.1 | 119.2 | 29.3 | 98.0 | 295.0 |
| Ang 1–7 | 3.0 | 3.0 | 3.0 | 6.0 | 23.9 |
| Ang 1–5 | 2.0 | 7.4 | 6.6 | 27.9 | 114.0 |
| Ang III (2–8) | 7.6 | 22.1 | 3.0 | 5.1 | 23.3 |
| Ang IV (3–8) | 2.0 | 5.7 | 2.0 | 2.9 | 12.0 |
| Aldosterone | 43.3 | 158.7 | 66.9 | 383.6 | 1339.9 |
In the liver tissue, activity of ACE and chymase as enzymes of the classical RAS and ACE2 and NEP as enzymes of the non-classical RAS were assessed. In plasma, levels of classical (PRA-S, Ang I, Ang II, aldosterone) and non-classical RAS (Ang 1–7, Ang III, Ang IV, Ang 1–5) were quantified.
ACE angiotensin converting enzyme, Ang angiotensin, cACLD compensated advanced chronic liver disease, CTP Child–Turcotte–Pugh, dACLD decompensated advanced chronic liver disease, HVPG hepatic venous pressure gradient, MAP mean arterial pressure, MELD model for end-stage liver disease, NEP neprilysin, PRA-S plasma renin activity surrogate, RAS renin–angiotensin system.