Format

Send to

Choose Destination
See comment in PubMed Commons below
J Nephrol. 2003 Mar-Apr;16(2):260-6.

Bone mass loss in calcium stone disease: focus on hypercalciuria and metabolic factors.

Author information

1
Department of Nephrology, Dialysis and Kidney Transplant, Unit of Mineral Metabolism, University of Bologna, Via Massarenti 9, 40138 Bologna, Italy. renataca@med.unibo.it

Abstract

BACKGROUND:

Several authors have observed that idiopathic calcium stone formers show a bone mass reduction, which is more evident in those with idiopathic hypercalciuria. The aim of this work was the evaluation of osteopenia and osteoporosis rate in a group of idiopathic calcium stone formers. The influence of hypercalciuria, nutritional factors and anthropometric parameters on bone mass was evaluated in these patients as well.

METHODS:

We enrolled 196 idiopathic calcium stone formers; 102 males, and 94 females. All subjects underwent a metabolic study. BMC and BMD were evaluated as well as QUS.

RESULTS:

Males showed greater weight, height, BMI, densitometric values and plasma creatinine, uric acid, urea, sodium, magnesium, GFR and urinary osmolarity than females. Moreover males excreted more uric acid, urea, creatinine, sulphate, phosphate, oxalate and citrate than females. The prevalence of osteopenia and osteoporosis, according to T-score, was 54% and 14% respectively. Hypercalciuria was demonstrated in 21.7% of the patients. Hypercalciuric men showed a higher excretion of urea, phosphate, sulphate and magnesium.

CONCLUSIONS:

Our results confirm the importance of QUS in the evaluation of stone formers' bone mass. Anthropometric characteristics and dietary habits seem to play a role in bone loss. We did not demonstrate any influence of hypercalciuria on bone mass. Although the pathogenesis of bone loss in stone formers still remains unclear, it can be hypothesized that a slight degree of metabolic acidosis, probably of alimentary origin, may be involved in the reduction of bone mass.

PMID:
12768074
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Loading ...
    Support Center