Preascitic cirrhosis is characterized by subtle renal sodium retention. Calcium inhibits Na+- K+-2Cl- cotransport in the Henle's loop and could potentially correct sodium handling abnormalities at that site. We investigated the effects of calcium infusion on sodium handling in ten pre- ascitic cirrhotics and nine healthy controls after one week of sodium loading of 200 mmol sodium/day. All subjects underwent a 3-hour supine determination of inulin, para-aminohippurate, lithium and free-water clearances, absolute and fractional excretions of sodium, potassium and calcium, and plasma concentrations of renin, aldosterone, norepinephrine and vasopressin. The same were repeated over a further 3-hour supine period including 60 min i.v. infusion of 33 mg/min calcium gluconate. After sodium loading, the 24-hour urinary sodium excretion in the cirrhotics was lower than that in controls (P<0.03). Calcium infusion significantly decreased plasma norepinephrine levels (p<0.03), and induced greater increases in fractional delivery of sodium to the Henle's loop (p<0.5) in the cirrhotics compared to controls, associated with a decreased fractional reabsorption of sodium beyond the proximal tubule (P<0.03), resulting in greater urinary volume, sodium excretion and free-water clearance in the cirrhotics compared to controls (all P<0.05). Since the aldosterone-driven potassium secretion, as assessed by the computation of tubular- capillary gradient of [K+] in the collecting duct, was similar in the two groups, and unaffected by calcium, sodium retention must have occurred in the Henle's loop in the cirrhotics. In conclusion, calcium is natriuretic in pre-ascitic cirrhosis. It also decreases norepinephrine release which may be responsible for decreased sodium reabsorption in the Henle's loop.
- Liver cirrhosis
- Loop of Henle
- Sodium metabolism
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