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Hyponatraemia predicts the acute (type 1) cardio‐renal syndrome
Author(s) -
Aronson Doron,
Darawsha Wisam,
Promyslovsky Marina,
Kaplan Marielle,
Abassi Zaid,
Makhoul Badira F.,
Goldberg Alexander,
Azzam Zaher S.
Publication year - 2014
Publication title -
european journal of heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.149
H-Index - 133
eISSN - 1879-0844
pISSN - 1388-9842
DOI - 10.1093/eurjhf/hft123
Subject(s) - medicine , cardiorenal syndrome , cardiology , heart failure , acute decompensated heart failure , acute kidney injury , intensive care medicine
Aims The acute (type 1) cardio‐renal syndrome (CRS) refers to an acute worsening of heart function leading to worsening renal function (WRF), and frequently complicates acute decompensated heart failure (ADHF) and acute myocardial infarction (AMI). The aim of this study was to investigate whether hyponatraemia, a surrogate marker of congestion and haemodilution and of neurohormonal activation, could identify patients at risk for WRF. Methods and results We studied the association between hyponatraemia (sodium <136 mmol/L) and WRF (defined as an increase of >0.3 mg/dL in creatinine above baseline) in two separate cohorts: patients with ADHF ( n = 525) and patients with AMI ( n = 2576). Hyponatraemia on admission was present in 156 patients (19.7%) with ADHF and 461 patients (17.7%) with AMI. Hyponatraemia was more frequent in patients who subsequently developed WRF as compared with patients who did not, in both the ADHF (34.6% vs. 22.2%, P = 0.0003) and AMI (29.7% vs. 21.8%, P <0.01) cohorts. In a multivariable logistic regression model, the multivariable adjusted odds ratio for WRF was 1.90 [95% confidence interval (CI) 1.25–2.88; P = 0.003] and 1.56 (95% CI 1.13–2.16; P = 0.002) in the ADHF and AMI cohorts, respectively. The mortality risk associated with hyponatraemia was attenuated in the absence of WRF. Conclusion Hyponatraemia predicts the development of WRF in two clinical scenarios that frequently lead to the type I CRS. These data are consistent with the concept that congestion and neurohormonal activation play a pivotal role in the pathophysiology of acute cardio‐renal failure.