Abstract
Introduction:
Heart failure (HF) patients are prone to postoperative hemodynamic instability after cardiac surgery, possibly due to upregulated renin-angiotensin-aldosterone system (RAAS) activity. We evaluated perioperative RAAS activity in control and HF patients and its impact on acute kidney injury (AKI) incidence.
Materials and Methods:
Pre-specified analysis of a prospective observational cohort study (VASOR). Plasma renin, angiotensinogen and aldosterone were measured perioperatively in 18 control and 18 HF patients.
Results:
RAAS blocker use was identical in both groups. HF patients displayed a diminished preoperative renal function. AKI occurred in 1 control and 8 HF patients. Preoperatively, HF patients exhibited 5-fold higher renin and aldosterone levels, identical aldosterone/renin ratios, and modestly lower angiotensinogen levels than controls. During surgery, renin rose 10-fold higher in HF patients. Aldosterone increased proportionally, but was blunted when normalized for renin (aldosterone/renin ratio). This was not due to angiotensinogen depletion. Postoperatively, angiotensinogen increased 50% in both groups, allowing aldosterone to increase, despite a modest postoperative renin decline. Preoperative renin levels and the surgery-induced renin rise predicted postoperative AKI.
Conclusions:
HF patients exhibit dysregulated RAAS responses to surgery may reflect impaired angiotensin I-angiotensin II conversion. Elevated renin signals RAAS dysregulation, identifying patients who might benefit from angiotensin II infusion. The Netherlands Trial Register (NTR5647); http://www.trialregister.nl/trialreg/admin/rctview.asp?TC=5647.
| Original language | English |
|---|---|
| Journal | JRAAS - Journal of the Renin-Angiotensin-Aldosterone System |
| Volume | 27 |
| DOIs | |
| Publication status | E-pub ahead of print - 19 Jan 2026 |
Bibliographical note
Publisher Copyright:© The Author(s) 2026. This article is distributed under the terms of the Creative Commons Attribution 4.0 License (https://creativecommons.org/licenses/by/4.0/) which permits any use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page (https://us.sagepub.com/en-us/nam/open-access-at-sage).
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