Editor,—We read with interest the commentary by Clària and Rodés ((1999) Gut 45:639–639; OpenUrlAbstract/FREE Full Text) on our paper published inGut which re-examined the mechanisms of renal sodium retention in patients with preascitic cirrhosis.1 In summary, in our patients we observed indirect evidence of expanded central vascular fluid volume compared with healthy controls and thought this physiopathological alteration was due to slightly reduced values of glomerular filtration rate (measured as creatinine clearance) and, mainly, to increased distal tubular retention of sodium when expressed as a fraction of the filtered sodium load that is reabsorbed by the distal nephron (26.9 (6.7)% v 12.5 (3.4)%, respectively; p<0.05).1

Clària and Rodés advanced two criticisms and affirmed that our results, obtained by means of the lithium clearance and fractional excretion technique, may be influenced by two fundamental flaws. Firstly, the reliability of lithium clearance as a marker of distal fluid delivery in clinical conditions characterised by low fractional sodium excretion (below 0.40%) has not been proved due to possible lithium reabsorption in the distal nephron.2 Secondly, in …

Professor J Rodés, Liver Unit, Hospital Clinic, Villarroel 170, 08036 Barcelona, Spain.rodes{at}medicina.ub.es