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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

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. AIM: 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. CONCLUSION: 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.[1]

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