title: Inotropes for the management of acute heart failure patients with renal dysfunction. Still an option?
abstract: BACKGROUND
  Renal dysfunction is highly prevalent in patients with acute heart failure (AHF). These patients are more vulnerable in worsening of kidney function and have also higher mortality rates.
  
  
  METHODS
  Recent developments in the understanding of bidirectional interaction between heart and kidney are reviewed in the context of the potential impact of inotropes on renal function. Key clinical trials reporting the use of inotropes in AHF patients with renal dysfunction are discussed in this review.
  
  
  CONCLUSIONS
  Inotropes may be indicated on a short-term basis and under close monitoring in AHF with renal dysfunction mostly in cases of low output heart failure that can provoke renal hypoperfusion. Dopamine administration with low dose of i.v. furosemide has been recently compared with high dose of i.v. furosemide alone, demonstrating lower rates of worsening renal function and electrolyte disturbances. Moreover, small clinical trials have shown that the novel inodilator levosimendan seems to be superior to dobutamine or placebo in improving renal function in patients with acutely decompensated heart failure. The impact of novel inotropes on kidney function is still unclear. Randomized clinical trials are required in order to identify the role of inotropes in the management and/or prevention of acute cardiorenal syndrome.
authors.affiliation: Attikon University Hospital, Heart Failure Clinic, Rimini 1, Haidari, 124 62, Athens, Greece. penelopestergiou@yahoo.com
authors.forename: Pinelopi
authors.initials: P
authors.lastname: Rafouli-Stergiou
authors.forename: John T
authors.initials: JT
authors.lastname: Parissis
authors.forename: Maria
authors.initials: M
authors.lastname: Anastasiou-Nana
mesh_terms: D000318:Adrenergic beta-Agonists / Q000009:adverse effects / Q000627:therapeutic use; D000818:Animals; D002316:Cardiotonic Agents / Q000009:adverse effects / Q000627:therapeutic use*; D019317:Evidence-Based Medicine; D006321:Heart / Q000187:drug effects* / Q000503:physiopathology; D006333:Heart Failure / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D010726:Phosphodiesterase Inhibitors / Q000009:adverse effects / Q000627:therapeutic use; D051437:Renal Insufficiency / Q000139:chemically induced / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology
chemical_list: D000318:Adrenergic beta-Agonists; D002316:Cardiotonic Agents; D010726:Phosphodiesterase Inhibitors