Renal dysfunction and worsening renal function are common in patients with acute decompensated heart failure (ADHF), and both are strong and independent predictors of outcome [1, 2]. The most important cause of renal impairment in ADHF is reduced renal perfusion as a consequence of deteriorating cardiac output [3]. On the other hand, renal impairment itself may predispose to worsening heart failure, by continuous salt and water retention, diuretic resistance and neurohormonal activation, leading to increased cardiac workload [4]. In this issue of Cardiovascular Drugs and Therapy, Yilmaz and colleagues describe the renal effects of levosimendan infusion compared to dobutamine infusion in 88 patients with ADHF [5]. Both treatment regimens were associated with an increase in urine output, but only the group receiving levosimendan (on top of diuretic treatment), showed a significant improvement in estimated glomerular filtration rate (eGFR). This improvement in eGFR was consistent in those patients receiving levosimendan up to 72 h. Dobutamine had a neutral effect on eGFR. Unfortunately, no follow up data is available for these patients, and no adverse events were reported in the present study. How can we explain the differences observed between these treatment groups? Both dobutamine and levosimendan are inotropic agents, specifically targeted at improvement of cardiac contractility [6]. Nevertheless, although both treatment regimens improved cardiac function and increased urine output, only levosimendan showed an improvement in eGFR. The explanation for this observation may be found in another, perhaps more important mechanism of action of levosimendan. Through activation of ATP-sensitive potassium channels, levosimendan causes both aterial, but preferently venous vasodilation [6]. This additive mechanism of action of levosimendan over dobutamine is crucial in ADHF, since central venous pressure is an important, and independent predictor of eGFR in patients with heart failure [3]. So, in patients with ADHF, renal function is dependent on renal blood flow and central venous pressure. Therefore, venodilation that occurs with levosimendan is probably the main mechanism distinguishing the effects of levosimendan and dobutamine on eGFR observed in the study by Yilmaz et al. [5]. This is not the first report to show that levosimendan improves eGFR in patients with heart failure. In a recent study, Zemljic et al. showed sustained improvement in renal function up to 3 months after infusion, in patients with advanced heart failure eligible for heart transplantation [7]. Also in the randomized controlled LIDO trial, levosimendan showed improvement of serum creatinine levels, compared to dobutamine [8]. The majority of randomised controlled trials with levosimendan showed an improvement in hemodynamic status, together with signs and symptoms of Cardiovasc Drugs Ther (2007) 21:403–404 DOI 10.1007/s10557-007-6070-y