Hepatorenal syndrome: one size does not fit all

(ADQI) VIII consensus statements on the treatment of patients with hepatorenal syndrome (HRS) and acute kidney injury [1]. While we appreciate the authors’ discussion, we question the hemodynamic recommen dations and suggest further areas of study (Section III in [1]). Renal perfusion relies upon cardiac output, renal blood fl ow, and autoregulation. HRS infl uences cardiac output and systemic vascular resistance, and establishing a pressure gradient across the glomerulus ensures renal blood fl ow and glomerular fi ltration rate [2,3]. In fl uid responsive patients, volume resuscitation is a key component of HRS management. Th e traditional target mean arterial pressure (MAP) of 65 mmHg to ensure renal perfusion assumes that ‘one size fi ts all’ in HRS. Th e kidneys are in the abdominal compartment, and intraabdominal pressure varies among individuals. Th e pressure of the compartment during disease states that cause ascites decreases renal perfusion pressure and should be overcome, especially when autoregulation is impaired [4]. In other words, the arbitrary suggestion of increasing the MAP by 10 mmHg (Table 6 in [1]) may not be enough (or may be too much). Titrating norepinephrine to a baseline MAP of 65 mmHg plus the intraabdominal pressure [4] and administering terlipressin or vasopressin (which may constrict the eff erent glomerular arteriole [5]) may be an eff ective hemodynamic strategy to ensure renal perfusion pressure. Although this recommendation may not be based on grade A evidence, it is physiologically sound (establishes a pressure gradient) and may inspire further studies of hemodynamic management in patients with HRS.