Compared to acute heart failure without cardiorenal syndrome, both de novo CRS and CRS on CKD were associated with nearly three times higher in-hospital mortality (aOR 2.82 and 2.91; p<0.001).
Observational (n=1,137,509)
Yes
Does the presence of cardiorenal syndrome (de novo or superimposed on CKD) increase mortality and resource utilization in patients hospitalized with acute heart failure?
Cardiorenal syndrome, particularly when superimposed on chronic kidney disease, significantly increases in-hospital mortality, length of stay, and the need for advanced organ support in patients with acute heart failure.
Effect estimate: aOR 2.82 (de novo CRS) and 2.91 (CRS on CKD)
p-value: p=<0.001
Abstract Background Acute heart failure (HF) often leads to renal dysfunction, resulting in a cardiorenal syndrome (CRS) that worsens patient outcomes. Although de novo CRS and CRS in CKD are relatively common in ICU acute Heart failure hospitalizations, their distinct effects on mortality and ICU resource utilization are not well established at the national level. Existing data are limited to small studies. Understanding these subtypes could improve risk stratification and help develop targeted reno-protective strategies in acute HF. Methods Using the 2022 National Inpatient Sample, we identified adult hospitalizations with acute HF and AKI. CRS was classified as de novo CRS (acute HF with AKI but without CKD) and CRS on CKD (acute HF with both AKI and CKD). Multivariable logistic and linear regressions analyzed the relationships between CRS subtypes and various outcomes, including in-hospital mortality, non-home discharge, length of stay (LOS), total hospital charges, invasive mechanical ventilation (IMV), continuous renal replacement therapy (CRRT), and ECMO use. Models were adjusted for age, sex, diabetes, obesity, COPD, CAD, CLD, IMV use, and hospital status. Results Among 1, 137, 509 acute HF hospitalizations, 30. 5% had CRS—20. 5% de novo CRS and 10. 0% CRS on CKD. The mean age was 71 ± 13 years, and 47% were female. Compared to the HF group without CRS, both CRS-de novo and CRS-on-CKD were linked to nearly three times higher mortality (aOR 2. 82 and 2. 91; p 0. 001), longer length of stay (+3. 3 and +3. 9 days; p 0. 001), and increased hospital charges (+41-46K; p 0. 001). Non-home discharges occurred more often (52% vs 44%; aOR ≈ 1. 4; p 0. 001). CRRT use increased 21-fold in CRS-de novo and 142-fold in CRS-on-CKD, while ECMO utilization rose from 0. 07% in HF-only to 0. 22% in CRS-on-CKD and 0. 44% in CRS-de novo (p 0. 001). Within CRS, pre-existing CKD further elevated mortality (aOR 1. 52; p 0. 001) and resource use. Conclusion Our study demonstrated that cardiorenal syndrome significantly increases the clinical and economic burden of acute HF, particularly when superimposed on CKD. These patients face notably higher mortality rates, longer hospital stays, and increased costs. Early renal surveillance, hemodynamic optimization, and a multidisciplinary approach are essential to prevent irreversible end-organ damage. Future research should focus on reno-protective and system-level strategies to reduce downstream morbidity and costs. This abstract is funded by: None
Khan et al. (Fri,) conducted a observational in Acute heart failure with cardiorenal syndrome (n=1,137,509). Cardiorenal syndrome (de novo CRS and CRS on CKD) vs. Acute heart failure without cardiorenal syndrome was evaluated on In-hospital mortality (aOR 2.82 (de novo CRS) and 2.91 (CRS on CKD), p=<0.001). Compared to acute heart failure without cardiorenal syndrome, both de novo CRS and CRS on CKD were associated with nearly three times higher in-hospital mortality (aOR 2.82 and 2.91; p<0.001).