Phenotype specific amplification of acute kidney injury mortality risk in cardiogenic shock complicating heart failure: a contemporary national analysis

Background Acute kidney injury frequently complicates cardiogenic shock; however, whether its mortality impact differs by shock phenotype remains unclear. Objectives To evaluate the association between AKI severity and in-hospital mortality in heart failure–related cardiogenic shock and to determine whether this association differs between AMI-related and non-AMI shock. Methods We analyzed the 2023 National Inpatient Sample to identify adult hospitalizations with heart failure (I50) and cardiogenic shock (R57.0). AKI was defined using N17 codes and stratified by dialysis requirement (5A1D procedure codes). AMI-related shock was identified using I21–I22 codes. Survey-weighted multivariable logistic regression adjusted for age, sex, payer status, income quartile, hospital teaching status, and bed size. Interaction testing assessed effect modification by shock phenotype. Results An estimated 174,784 HF-CS hospitalizations were identified nationally; 36.7 percent were women. AKI occurred in 31.3 percent of hospitalizations, and 13.2 percent required dialysis. In-hospital mortality increased stepwise across AKI severity: No AKI: 22.4 percent AKI without dialysis: 28.1 percent AKI with dialysis: 45.8 percent After multivariable adjustment: AKI without dialysis: OR 1.30, 95 percent CI 1.23–1.37 AKI with dialysis: OR 3.10, 95 percent CI 2.84–3.39 A significant interaction was observed between AKI severity and AMI-related shock (p for interaction = 0.0018). In AMI-CS: AKI without dialysis: OR 1.44, 95 percent CI 1.32–1.57 AKI with dialysis: OR 3.34, 95 percent CI 2.91–3.84 In non-AMI CS: AKI without dialysis: OR 1.23, 95 percent CI 1.14–1.32 AKI with dialysis: OR 2.98, 95 percent CI 2.67–3.32 Conclusions AKI confers substantial mortality risk in cardiogenic shock; however, its impact is phenotype-specific. Non-dialysis AKI is associated with significantly amplified mortality in AMI-related shock compared with non-ischemic shock. These findings highlight differential cardiorenal vulnerability in ischemic cardiogenic shock and underscore the importance of early renal preservation strategies in AMI-CS.