Abstract
Acute kidney injury (AKI) is an independent risk factor for ensuing chronic kidney disease (CKD). Animal studies have demonstrated that renin-angiotensin system (RAS) inhibitor can reduce ensuing CKD after functional recovery from AKI. Here we study the association between ensuing CKD and use of RAS inhibitor including angiotensin converting enzyme inhibitor or angiotensin II type 1a receptor blocker starting after renal functional recovery in our prospectively collected observational AKI cohort. Adult patients who had cardiac surgery–associated AKI (CSA-AKI) are studied. Patients with CKD, unrecovered AKI, and use of RAS inhibitor before surgery are excluded. Among 587 eligible patients, 94 patients are users of RAS inhibitor which is started and continued after complete renal recovery during median follow-up period of 2.99 years. The users of RAS inhibitor show significantly lower rate of ensuing CKD (users vs. non-users, 26.6% vs. 42.2%) and longer median CKD-free survival time (users vs. non-users, 1079 days vs. 520 days). Multivariate Cox regression analyses further demonstrate that use of RAS inhibitor is independently associated with lower risk of ensuing CKD (hazard ratio = 0.46, P < 0.001). We conclude that use of RAS inhibitor in CSA-AKI patients after renal functional recovery is associated with lower risk of ensuing CKD development.
Highlights
The mechanisms underlying Acute kidney injury (AKI)-chronic kidney disease (CKD) transition are incompletely understood in humans, animal studies have shown a number of pathogenetic mechanisms such as maladaptive repair[14], profibrogenic cytokine production by G2/M cell-cycle arrested epithelia[15], pericyte-myofibroblast transition[16,17], and microvascular rarefaction[18,19]
Animal studies have demonstrated that activation of intrarenal renin–angiotensin system (RAS) after AKI underlies the possible mechanism for development and progression of ensuing CKD20–22
To get insight into the clinical application of RAS inhibitor and its impact on development of ensuing CKD in AKI survivors with complete renal recovery, we studied the outcomes and relevant risk factors of cardiac surgery–associated AKI (CSA-AKI) patients who did not have CKD history before surgery in our prospectively collected observational cohort
Summary
The mechanisms underlying AKI-CKD transition are incompletely understood in humans, animal studies have shown a number of pathogenetic mechanisms such as maladaptive repair[14], profibrogenic cytokine production by G2/M cell-cycle arrested epithelia[15], pericyte-myofibroblast transition[16,17], and microvascular rarefaction[18,19]. These mechanisms open up opportunities to innovate therapeutic strategies for prevention of AKI-CKD transition. To get insight into the clinical application of RAS inhibitor and its impact on development of ensuing CKD in AKI survivors with complete renal recovery, we studied the outcomes and relevant risk factors of cardiac surgery–associated AKI (CSA-AKI) patients who did not have CKD history before surgery in our prospectively collected observational cohort
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