Abnormal red-cell calcium pump in patients with idiopathic hypercalciuria

G. Bianchi, G. Vezzoli, D. Cusi, T. Cova, A. Elli, L. Soldati, G. Tripodi, M. Surian, E. Ottaviano, P. Rigatti, S. Ortolani

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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 ≥0.1 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 <0.01) and increased sodium-potassium pump acitivity (6866 ± 233 vs. 6096 ± 228 μmol of sodium per liter of red cells per hour; P <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 <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 <0.001) and urinary calcium excretion (r = 0.45, P <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 idopathic hypercalciuria.

Original languageEnglish
Pages (from-to)897-901
Number of pages5
JournalNew England Journal of Medicine
Volume319
Issue number14
Publication statusPublished - 1988

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Hypercalciuria
Ca(2+) Mg(2+)-ATPase
Calcium
Erythrocytes
Kidney Calculi
Sodium
Potassium
Parents
Sodium-Potassium-Exchanging ATPase
Calcium Oxalate
Erythrocyte Membrane
Lithium
Adenosine Triphosphate
Body Weight
Diet
Enzymes

ASJC Scopus subject areas

  • Medicine(all)

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Abnormal red-cell calcium pump in patients with idiopathic hypercalciuria. / Bianchi, G.; Vezzoli, G.; Cusi, D.; Cova, T.; Elli, A.; Soldati, L.; Tripodi, G.; Surian, M.; Ottaviano, E.; Rigatti, P.; Ortolani, S.

In: New England Journal of Medicine, Vol. 319, No. 14, 1988, p. 897-901.

Research output: Contribution to journalArticle

Bianchi, G, Vezzoli, G, Cusi, D, Cova, T, Elli, A, Soldati, L, Tripodi, G, Surian, M, Ottaviano, E, Rigatti, P & Ortolani, S 1988, 'Abnormal red-cell calcium pump in patients with idiopathic hypercalciuria', New England Journal of Medicine, vol. 319, no. 14, pp. 897-901.
Bianchi G, Vezzoli G, Cusi D, Cova T, Elli A, Soldati L et al. Abnormal red-cell calcium pump in patients with idiopathic hypercalciuria. New England Journal of Medicine. 1988;319(14):897-901.
Bianchi, G. ; Vezzoli, G. ; Cusi, D. ; Cova, T. ; Elli, A. ; Soldati, L. ; Tripodi, G. ; Surian, M. ; Ottaviano, E. ; Rigatti, P. ; Ortolani, S. / Abnormal red-cell calcium pump in patients with idiopathic hypercalciuria. In: New England Journal of Medicine. 1988 ; Vol. 319, No. 14. pp. 897-901.
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AU - Vezzoli, G.

AU - Cusi, D.

AU - Cova, T.

AU - Elli, A.

AU - Soldati, L.

AU - Tripodi, G.

AU - Surian, M.

AU - Ottaviano, E.

AU - Rigatti, P.

AU - Ortolani, S.

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N2 - 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 ≥0.1 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 <0.01) and increased sodium-potassium pump acitivity (6866 ± 233 vs. 6096 ± 228 μmol of sodium per liter of red cells per hour; P <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 <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 <0.001) and urinary calcium excretion (r = 0.45, P <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 idopathic hypercalciuria.

AB - 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 ≥0.1 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 <0.01) and increased sodium-potassium pump acitivity (6866 ± 233 vs. 6096 ± 228 μmol of sodium per liter of red cells per hour; P <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 <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 <0.001) and urinary calcium excretion (r = 0.45, P <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 idopathic hypercalciuria.

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