Abundance and activity of Ca2+-ATPase in hypercalciuric children

I. Kocsis, B. Vásárhelyi, E. Héninger, A. Szabó, G. Reusz, T. Tulassay

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

The plasma membrane Ca2+-ATPase (PMCA) is one of the main regulators of cell Ca2+ homeostasis. The aim of our study was to determine whether the abundance and activity of PMCA are altered in erythrocytes of children with idiopathic hypercalciuria. Twenty-four children with idiopathic hypercalciuria (13 girls and 11 boys, mean age 10.6±4.8 years; mean urinary calcium concentration 0.85±0.20 mmol/mmol creatinine) and 30 healthy age-matched children were enrolled. PMCA protein abundance was determined by Western blot analysis. Enzyme activity was determined spectrophotometrically. The abundance of PMCA did not differ in hypercalciuric patients from that of control subjects (98±22% vs 100±18%). Moreover, the activity was not different between the studied groups (3141±1494 vs 2953±780 nmol ATP/mg protein/h). The extent of hypercalciuria did not correlate with enzyme abundance or activity. Assuming that erythrocytes may reflect the renal tubular transporting processes, our data suggest that other Ca2+-transport mechanisms than PMCA might be involved in the development of idiopathic hypercalciuria in children.

Original languageEnglish
Pages (from-to)739-741
Number of pages3
JournalPediatric Nephrology
Volume16
Issue number9
DOIs
Publication statusPublished - 2001

Fingerprint

Calcium-Transporting ATPases
Hypercalciuria
Cell Membrane
Erythrocytes
Enzymes
Creatinine
Proteins
Homeostasis
Adenosine Triphosphate
Western Blotting
Calcium
Kidney

Keywords

  • Ca-ATPase
  • Erythrocyte
  • Hypercalciuria
  • Plasma membrane

ASJC Scopus subject areas

  • Nephrology
  • Pediatrics, Perinatology, and Child Health

Cite this

Abundance and activity of Ca2+-ATPase in hypercalciuric children. / Kocsis, I.; Vásárhelyi, B.; Héninger, E.; Szabó, A.; Reusz, G.; Tulassay, T.

In: Pediatric Nephrology, Vol. 16, No. 9, 2001, p. 739-741.

Research output: Contribution to journalArticle

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AU - Tulassay, T.

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