Ipercalciurie e calcolosi

A recent NHANES survey in the US indicated that 19 percent of men and 9 percent of women will be diagnosed
with a kidney stone by the age of 70 years, pointing to a frequent diease. Calcium stones (mostly calcium
oxalate and less often, calcium phosphate) represent 75% of the cases. Crystal formation in the urine occurs in
normal subjects, but stone formers more likely show significant crystalluria. Medullary interstitium is the site
of initial stone formation, with calcium phosphate crystals that eventually develop into Randall’s plaque.
Among the several predisposing factors, hypercalciuria is observed in up to one-half of idiopathic calcium stone
formers. Hypercalciuria has been classically defined as calcium excretion >250 mg/day (6.24 mmol/day) in
women and >300 mg/day (7.49 mmol/day) in men. However, recent studies also employ a threshold value > 200
mg/day (4.99 mmol/day) in both sexes. Alternatively, hypercalciuria is defined by the presence of calcium excretion
>4 mg/kg (0.1 mmol/kg) per day. However, in this case body weight changes may allow high but risky
values. Finally, also values as high as >100 mg/day have been identified as risky. Therefore, the term “hypercalciuria”
cannot be considered ideal.
Increased urine calcium is typically due to primary hyperparathyroidism and/or chronic acidemia, but in most
cases no cause is identified (so called idiopathic hypercalciuria). Three pathways are claimed to explain high calcium
excretion in idiopathic hypercalciuria: increased intestinal absorption (“absorptive hypercalciuria”); increased
bone resorption (“resorptive hypercalciuria”); increased renal losses (“renal hypercalciuria”). On practical
ground, most patients exibit more than one of these abnormalities thus reducing the utility of recognizing
this classification in every patient. Serum levels of 1,25(OH)D may be increased in some hypercalciuric patients
and are thus considered to contribute to increase intestinal calcium absorption and/or to increase bone resorption
with eventual negative calcium balance. Long term persistence of this metabolic derangement is responsible
for osteopenia and osteoporosis which is a major complication of chronic hypercalciuria. Higher calcitriol
levels in idiopathic hypercalciuria are sometimes referred to urinary phosphate leak and hypophosphatemia
which is a stimulus to 1alpha hydroxylase activity. Life style, dietary and pharmacologic interventions represent
the possible therapeutic approach to hypercalciuria.

« ARTICOLO PRECEDENTE:
» PROSSIMO ARTICOLO:

Lascia un commento

Il tuo indirizzo email non sarà pubblicato. I campi obbligatori sono contrassegnati *