Hyponatremia predicts the acute (type 1) cardio-renal syndrome

Background: The acute (type 1) cardio-renal syndrome (CRS) refers to an acute worsening of heart function leading to acute kidney injury (AKI), and frequently complicates acute decompensated heart failure (ADHF) and acute myocardial infarction (AMI). The aim of this study was to investigate whether hyponatremia, a surrogate of profound neurohormonal activation, could identify patients (pts) at risk for AKI. Methods: We studied the association between hyponatremia and AKI (defined as an increase of >0.3 mg/dl in creatinine above baseline) in 2 separate cohorts: 1) pts with ADHF (n=525) and 2) pts with AMI (n=1184 STEMI pts). Hyponatremia was defined as sodium <136 mmol/L. The association between hyponatremia and AKI was determined using logistic regression, adjusting for age, gender, baseline renal function, diabetes, hypertension, hemoglobin, BNP levels in the ADHF cohort, Killip class in the AMI cohort, and ejection fraction. Results: Hyponatremia was present on admission in 156 pts (19.7%) with ADHF and in 244 pts in AMI (21%). In ADHF, AKI occurred in 82 (22%) pts without hyponatremia and 54 (35%) with hyponatremia (P=0.0003). In AMI, AKI occurred in 135 (17%) pts without and 109 (27%) pts with hyponatremia (P<0.001). In a multivariable logistic regression model, the adjusted odds ratio for AKI was 1.90 among ADHF pts with hyponatremia (95% CI 1.25-2.88; P=0.003), and 2.06 among AMI pts with hyponatremia (95% CI 1.48-2.87; P<0.0001). When sodium was used as a continuous variable, the risk for AKI was inversely related to sodium levels (Figure). ![Figure][1] Probability of AKI Conclusion: Hyponatremia predicts the development of AKI in two clinical scenarios that frequently lead to the type I CRS. These data suggest that neurohormonal activation contribute to the development of acute CRS. [1]: pending:yes