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This editorial refers to ‘Changes in renal function during hospitalization and soon after discharge in patients admitted for worsening heart failure in the placebo group of the EVEREST trial’, by J.E.A. Blair et al. doi:10.1093/eurheartj/ehr238. In a post-hoc analysis of the Efficacy of Vasopressin Antagonism in Heart Failure Outcome Study with Tolvaptan (EVEREST), Blair and co-workers found that worsening kidney function shortly after hospitalization and in the early post-discharge period independently predicted cardiovascular mortality and re-hospitalizations because of heart failure (HF).1 These findings confirmed previous evidence that worsening kidney function following hospitalization for decompensated HF is a strong independent predictor of long-term adverse outcomes. An intriguing finding of the above study, however, was that worsening kidney function was also associated with a decrease in body weight and circulating levels of the B-type natriuretic peptide (BNP), changes that reflected an amelioration of fluid congestion and that per se were expected to predict improved outcomes in the long term. To explain this apparent paradox, we have to go back to the old days of Arthur J. Merril who in 1946 measured renal plasma flow and the glomerular filtration rate (GFR) by using the sodium para -amino hippurate and inulin renal clearance techniques, in 37 subjects admitted because of HF from different aetiologies.2 In these patients, the renal plasma flow was reduced to one-third to one-fifth of normal, whereas the cardiac output was rarely reduced below half the resting value. On the basis of these findings, he suggested that in HF there is a specific diversion of blood away from the kidneys, organs which normally receive ∼20% of the cardiac output. Despite the large reduction in …