The mechanisms driving long-term consequences following acute kidney injury (AKI) were unknown. Vessel instability, an early reaction to endothelial damage, might represent a common mechanism and early trigger for chronic kidney disease (CKD) and heart failure. For a study, researchers sought to see if plasma angiopoietins, which are markers of vessel homeostasis, were associated with CKD progression and heart failure admissions after hospitalization in patients with and without AKI, they, therefore, conducted a prospective cohort study to look at the balance between angiopoietin-1 (Angpt-1) and angiopoietin-2 (Angpt-2). They studied the relationships between angiopoietins and the development of the major outcomes of CKD progression and heart failure, as well as the secondary outcome of all-cause death three months after discharge or later. 

The median age of the 1,503 patients was 65.8, with 746 (50%) having AKI. The highest quartile of the Angpt-1:Angpt-2 ratio was associated with a 72% lower risk of CKD progression (aHR, 0.28; 95% CI, 0.15 to 0.51), a 94% lower risk of heart failure (aHR, 0.06; 95% CI, 0.02 to 0.15), and an 82% lower risk of mortality (aHR, 0.18; 95% CI, 0.09 to 0.35) for those with AKI. The highest quartile of the Angpt-1:Angpt-2 ratio was linked with a 71% reduced risk of heart failure (aHR, 0.29; 95% CI, 0.12 to 0.69) and a 68% lower risk of death among individuals without AKI (aHR, 0.32; 95% CI, 0.15 to 0.68). There were no links to CKD progression. In the context of AKI, a larger Angpt-1:Angpt-2 ratio was substantially related to reduced CKD development, heart failure, and death.

Reference:jasn.asnjournals.org/content/33/3/613