Natriuretic and aquaretic effects of intravenously infused calcium in preascitic human cirrhosis: physiopathological and clinical implications.
BACKGROUND
Preascitic cirrhosis is characterised 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.


OBJECTIVE
To investigate the effects of calcium infusion on sodium handling in 10 patients with preascitic cirrhosis and nine healthy controls after 1 week of sodium loading of 200 mmol sodium/day.


METHODS
All patients underwent a 3 h 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 h supine period including 60 min intravenous infusion of 33 mg/min calcium gluconate.


RESULTS
After sodium loading, the 24 h urinary sodium excretion in patients with cirrhosis 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 those with cirrhosis than in controls. This was 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 those with cirrhosis than in controls (all with p<0.05). Because 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 those with cirrhosis.


CONCLUSIONS
Calcium is natriuretic in patients with preascitic cirrhosis; it also decreases norepinephrine release, which could be responsible for decreased reabsorption of sodium in the Henle's loop.
Sansoè
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Division of Gastroenterology, Department of Medicine, Toronto General Hospital, 200 Elizabeth Street, Toronto, Ontario, Canada M5G 2C4.
Wong
F
F
D000042:Absorption; D000316:Adrenergic alpha-Agonists / Q000097:blood; D000450:Aldosterone / Q000097:blood; D002118:Calcium / Q000008:administration & dosage* / Q000097:blood / Q000652:urine; D005260:Female; D006801:Humans; D007262:Infusions, Intravenous; D007687:Kidney Tubules, Proximal / Q000378:metabolism; D008103:Liver Cirrhosis / Q000378:metabolism*; D008138:Loop of Henle / Q000378:metabolism; D008297:Male; D008657:Metabolic Clearance Rate / Q000502:physiology; D008875:Middle Aged; D009638:Norepinephrine / Q000097:blood; D011188:Potassium / Q000378:metabolism; D012083:Renin / Q000097:blood; D012964:Sodium / Q000097:blood / Q000378:metabolism* / Q000652:urine; D016683:Supine Position; D014667:Vasopressins / Q000097:blood
D000316:Adrenergic alpha-Agonists; D014667:Vasopressins; D000450:Aldosterone; D012964:Sodium; D012083:Renin; D011188:Potassium; D002118:Calcium; D009638:Norepinephrine