Why the study?
How is proximal tubular sodium reabsorption altered in patients with liver cirrhosis and ascites?
How is proximal tubular sodium reabsorption altered in patients with liver cirrhosis and ascites?
Patients with liver cirrhosis and ascites have enhanced proximal fractional sodium reabsorption, which impairs maximal urine osmolality and can be partially reversed by mannitol but not dextran.
Answers are grounded in this paper and cite their sources.
May underlie diuretic resistance in cirrhosis; hypothesis-generating and should not yet change practice.
Proximal tubular reabsorption was examined in patients with liver cirrhosis and ascites by a variety of indirect methods. Maximal diluting ability, urine flow rate, and free water clearance were reduced. During frusemide administration V/GFR was lower than in normal control subjects, indicating that proximal fractional reabsorption is enhanced in liver cirrhosis. This, by reducing Na delivery to the loop of Henle, impairs maximal urine osmolality. Mannitol, by reducing proximal reabsorption, restores availability of Na to the loop and urine concentrating ability during osmotic diuresis, whereas volume expansion with dextran was ineffective. This could be due to a persistent increase in renal vascular resistance preventing the rise in interstitial pressure responsible for driving fluid back into the proximal tubular lumen.
No takes yet. Share an insight, caveat, or question.
Chiandussi et al. (1978) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: