Sodium homeostasis with chronic sodium loading in preascitic cirrhosis

Background-Preascitic cirrhotic patients receiving 200 mmol of sodium daily for seven days remain in positive sodium balance. Thereafter, sodium handl ing is unknown. Aim-To assess renal sodium handling in preascitic cirrhosis on a high sodiu m diet for five weeks. Methods-Sixteen biopsy proven preascitic cirrhotics were assessed at weekly intervals for five weeks on a diet of 200 mmol sodium/day using a daily we ight diary and weekly 24 hour urinary sodium estimations. Fasting supine ne urohormone levels were measured at baseline and weekly for five weeks while haemodynamics were measured at baseline and at five weeks. Results-The daily diet of 200 mmol of sodium resulted in weight gain and a positive sodium balance for three weeks, associated with significant suppre ssion of plasma renin activity and aldosterone levels, and a significant ri se in plasma atrial natriuretic peptide levels (p <0.05). Patients' weights plateaued during week 4, associated with complete sodium balance and signi ficant suppression of plasma noradrenaline levels (p <0.05). This was follo wed by a negative sodium balance and weight loss, and finally complete sodi um balance, again despite a mean net gain of 2.3 (0.3) kg, associated with a return of plasma renin activity and aldosterone levels to within normal r anges. The lack of increase in central blood volume in addition to the pers istent increase in plasma atrial natriuretic peptide levels indicated that residual volume expansion, consequent to persistent weight gain, was distri buted on the venous side of the circulation. No free fluid was seen on repe at abdominal ultrasound after five weeks. Conclusion-Preascitic cirrhotics have a natriuretic "escape" after three we eks on high sodium dietary intake, associated with elevated plasma atrial n atriuretic peptide levels and suppression of the renin-angiotensin-aldoster one system. With continued suppressed sympathetic activity, preascitics re- establish complete sodium balance but with a net weight gain and presumed i ncreased intravascular volume, but without ascites. This further elucidates the compensated sodium retaining abnormality that characterises preascitic cirrhosis.