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Abstract
Sodium and water retention, frequently associated with hyponatraemia, occur commonly in liver cirrhosis because of central hypovolaemia, nephron hypoperfusion, excess fractional reabsorption in the proximal tubule and reduced fluid delivery to the distal nephron. Under these circumstances, whilst solute free water formation is curbed by the reduced delivery of fluid, antidiuretic hormone (ADH)-independent water abstraction can be unaltered, thus reclaiming a larger fraction of the inflow to the distal nephron. This leads to the excretion of a reduced volume of Na-free, concentrated urine, even in the absence of ADH, causing water retention and reduced diluting power. Enhanced ADH secretion further contributes to excessive water retention. Hyponatraemia develops either as a consequence of excessive water retention or solute depletion, or a combination of both. As the normal kidney is capable of excreting any water excess, hyponatraemia requires an important defect in renal diluting ability. Thus, the cause of hyponatraemia is the same as that leading to oedema. Na retention, being due to central hypovolaemia, can be corrected by centrally redistributing the volume trapped in the splanchnic district. New somatostatin and octreotide analogues proved quite effective in correcting this uneven blood distribution. Whilst formerly the treatment of excess solvent retention required techniques of excreting large volumes of hypotonic fluids with the aid of loop diuretics, the discovery of aquaporins brought about the development of specific water channel blockers, which may be more effective than anti-ADH receptors, the old aquaretics. The new aquaretics capable of blocking aquaporins represent the major advancement in the treatment of oedema.