Abstract. The present study was attempted to evaluate sodium and water balance in compensated liver cirrhosis. Renal sodium and water handling was studied in six cirrhotic patients without ascites and/or oedema and in six controls before and after saline loading. Fractional sodium reabsorption at the various nephron sites (proximal, diluting and distal) was evaluated by means of clearance techniques during maximal water diuresis and hypotonic saline infusion. Compensated cirrhotic patients showed a normal baseline sodium and water balance but a blunted natriuretic response when saline loaded (urinary sodium excretion after saline load = 338 ± 290 compared to 933 ± 504 μmol min‐1 of controls; P<0±05). The impaired natriuresis was found to be related to an increased reabsorption of sodium in the proximal tubule (proximal fractional sodium reabsorption = 88±4 ± 3±8 compared to 81±7 ± 4±3% of controls; P<0±05). These findings confirm the hypothesis that renal sodium handling abnormalities might precede ascites formation. Additional studies, however, are necessary to further define renal factors mediating the increased reabsorption of sodium in compensated liver cirrhosis. Copyright © 1985, Wiley Blackwell. All rights reserved
Renal water and sodium handling in compensated liver cirrhosis: mechanism of the impaired natriuresis after saline loading.
CAREGARO NEGRIN, LORENZA;LAURO, STEFANO;ANGELI, PAOLO;MERKEL, CARLO;GATTA, ANGELO
1985
Abstract
Abstract. The present study was attempted to evaluate sodium and water balance in compensated liver cirrhosis. Renal sodium and water handling was studied in six cirrhotic patients without ascites and/or oedema and in six controls before and after saline loading. Fractional sodium reabsorption at the various nephron sites (proximal, diluting and distal) was evaluated by means of clearance techniques during maximal water diuresis and hypotonic saline infusion. Compensated cirrhotic patients showed a normal baseline sodium and water balance but a blunted natriuretic response when saline loaded (urinary sodium excretion after saline load = 338 ± 290 compared to 933 ± 504 μmol min‐1 of controls; P<0±05). The impaired natriuresis was found to be related to an increased reabsorption of sodium in the proximal tubule (proximal fractional sodium reabsorption = 88±4 ± 3±8 compared to 81±7 ± 4±3% of controls; P<0±05). These findings confirm the hypothesis that renal sodium handling abnormalities might precede ascites formation. Additional studies, however, are necessary to further define renal factors mediating the increased reabsorption of sodium in compensated liver cirrhosis. Copyright © 1985, Wiley Blackwell. All rights reserved
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