title: Abnormal red-cell calcium pump in patients with idiopathic hypercalciuria.
abstract: Idiopathic hypercalciuria is a common disorder whose inheritance suggests an enzyme abnormality in calcium transport. We measured calcium-magnesium-ATPase activity in erythrocytes from 38 patients (mean age [+/- SEM], 40 +/- 2.1 years) with idiopathic hypercalciuria (24-hour urinary calcium excretion greater than or equal to 0.1 mmol per kilogram of body weight) and a history of multiple calcium oxalate kidney stones. As compared with 41 healthy controls, the patients with hypercalciuria had increased erythrocyte-membrane calcium-magnesium-ATPase activity (64.2 +/- 2.19 vs. 51.6 +/- 1.91 nmol of ATP split per milligram per minute; P less than 0.01) and increased sodium-potassium pump activity (6866 +/- 233 vs. 6096 +/- 228 mumol of sodium per liter of red cells per hour; P less than 0.05). No significant difference between the two groups was found in erythrocyte sodium-potassium cotransport, sodium-lithium countertransport, or potassium content. In 66 patients with kidney stones (38 with hypercalciuria and 28 with normal calcium excretion), 24-hour urinary calcium excretion correlated with calcium-magnesium-ATPase activity (r = 0.46, P less than 0.001). Erythrocyte calcium-magnesium-ATPase activity remained unchanged in eight subjects studied after four months on a low-calcium diet. A study of 30 healthy families found significant correlations between mean values in parents and those in offspring for calcium-magnesium-ATPase (r = 0.68, P less than 0.001) and urinary calcium excretion (r = 0.45, P less than 0.02), with no significant correlations between parents with respect to these measures (r = 0.27 and r = 0.08, respectively). We conclude that abnormalities in erythrocyte calcium-magnesium-ATPase activity may represent an inherited defect in calcium transport related to the cause of idiopathic hypercalciuria.
authors.affiliation: Institute of Medical Sciences, Postgraduate School of Nephrology, University of Milan, Italy.
authors.forename: G
authors.initials: G
authors.lastname: Bianchi
authors.forename: G
authors.initials: G
authors.lastname: Vezzoli
authors.forename: D
authors.initials: D
authors.lastname: Cusi
authors.forename: T
authors.initials: T
authors.lastname: Cova
authors.forename: A
authors.initials: A
authors.lastname: Elli
authors.forename: L
authors.initials: L
authors.lastname: Soldati
authors.forename: G
authors.initials: G
authors.lastname: Tripodi
authors.forename: M
authors.initials: M
authors.lastname: Surian
authors.forename: E
authors.initials: E
authors.lastname: Ottaviano
authors.forename: P
authors.initials: P
authors.lastname: Rigatti
mesh_terms: D000328:Adult; D001692:Biological Transport; D017301:Ca(2+) Mg(2+)-ATPase / Q000097:blood*; D002118:Calcium / Q000097:blood / Q000652:urine*; D000252:Calcium-Transporting ATPases / Q000097:blood*; D002648:Child; D004910:Erythrocyte Membrane / Q000201:enzymology*; D005260:Female; D006801:Humans; D007669:Kidney Calculi / Q000209:etiology / Q000378:metabolism; D007700:Kinetics; D008297:Male; D011188:Potassium / Q000097:blood; D012964:Sodium / Q000097:blood
chemical_list: D012964:Sodium; D017301:Ca(2+) Mg(2+)-ATPase; D000252:Calcium-Transporting ATPases; D011188:Potassium; D002118:Calcium