Renal dysfunction is one of the most important comorbidities in patients with chronic heart failure (HF) and frequently accentuated in the setting of acute HF (AHF).1 In either context, renal dysfunction has important clinical implications that deserve to be highlighted: (A) the added increase in risk of adverse clinical outcomes2 and (B) at greater degrees of renal failure, well evidenced therapies are lacking and current management remains mostly empirical.1

The pathophysiology of renal dysfunction in AHF is complex, multifactorial and not completely understood, which may potentially explain why patients with worsening renal function (WRF) show mixed clinical response and outcomes.1 An imbalance between abnormal haemodynamic (arterial hypoperfusion and/or venous congestion), neurohormonal activation, inflammatory responses, intrinsic tubular damage and heterogeneous response to therapeutic interventions have been proposed as the most common pathogenic pathways.1

Serum creatinine and blood urea nitrogen (BUN) have been classically used as proxies for renal function assessment; nevertheless, there are several concerns regarding their performance.1 Serum is influenced by important extrarenal factors such as muscle mass, gender, age, nutrition and race. It is well established that serum creatinine underestimates renal function in highly prevalent subgroups of patients with HF such as the elderly, women and low-weight individuals. In contrast, creatinine overestimates renal damage when renal dysfunction is already present.1 Other additional shortcomings are: (A) creatinine is known to be a slow-release marker after acute …