Tubular handling of sodium and phosphate in non-ascitic liver cirrhosis.
The renal response to a maximal water load was evaluated in eight cirrhotic patients free of ascites and without previous evidence of ascites and in seven controls. Fractional sodium reabsorption in the proximal and diluting segment was estimated by clearance methods during hypotonic diuresis. Since phosphate excretion has been proposed as a proximal marker in liver cirrhosis, sodium reabsorption in the proximal tubule was compared with phosphate fractional excretion. In spite of a normal sodium balance during the pre-study period, non-ascitic cirrhotics showed a blunted proximal natriuretic response to maximal water load. In fact sodium excretion during hypotonic diuresis was reduced (p less than 0.05) and proximal sodium reabsorption increased (p less than 0.005) in cirrhotics. Fractional phosphate excretion was not impaired in our patients, and no correlation was found between phosphate excretion and proximal sodium reabsorption, as evaluated by clearance methods. This study demonstrates that an increased reabsorption of sodium in the proximal tubule is responsible for the impaired response to maximal water load in non-ascitic cirrhotics. Abnormalities in tubular handling of phosphate may account for the dissociation between proximal sodium reabsorption and phosphate excretion during hypotonic diuresis in these patients.
D000328:Adult; D000368:Aged; D001201:Ascites / Q000175:diagnosis; D005260:Female; D006801:Humans; D007687:Kidney Tubules, Proximal / Q000378:metabolism*; D008103:Liver Cirrhosis / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D010710:Phosphates / Q000378:metabolism*; D012079:Renal Circulation; D012964:Sodium / Q000378:metabolism*; D014882:Water-Electrolyte Balance
D010710:Phosphates; D012964:Sodium