Seen in 30 – 60 % adult stone formers.
Some strict definitions to define hypercalcaemia (>200 mg/day calcium in urine after adherence to 400 mg calcium diet; or > 4 mL/kg/day calcium in urine), but really is a continuous variable.
Recall calcium is regulated in three ways:
- Bone
- Gut absorption (via 1,25-dihydroxycholecalciferol)
- Renal reabsorption
Typically characterised as:
Absorptive – increased intestinal absorption
Normal serum calcium, but transiently elevated serum levels after absorption -> hypercalciuria
Type 1 – dietary independent
Type 2 – dietary dependent (normalises with dietary Ca restriction)
Type 3 – phosphate renal leak (low PO4)
Renal – impaired tubular reabsorption
Directly leads to increased urinary excretion – normal serum Ca, but may have 2’ high PTH
Resorptive – excessive bone resorption
Usually primary hyperparathyroidism or PTH adenoma. High PTH also causes increased gut absorption
Conditions associated with hypercalciuria:
- Idiopathic
- Granulomatous disorders (sarcoidosis)
- Hyperparathyroidism
- Pregnancy
- Metabolic acidosis (RTA, urinary diversion, topiramate)
- Vitamin D excess
- Malignancy causing hypercalcaemia
Treatment of hypercalciuria:
- General measures – fluid intake, dietary measures (do not restrict dietary Ca), lifestyle and weight loss
- Low salt diet – Na and Ca share transporter in tubules, high salt increases calcium in urine
- Hydrochlorothiazide – most useful for renal hypercalciuria, don’t affect the underlying cause if absorptive hypercalciuria (need to watch for hypokalaemia and subsequent hypocitraturia)
- Treat any PTH abnormalities
- Alkaline citrates (potassium citrate) can prevent calcium oxalate stone formation
- Sodium cellulose phosphate and orthophosphate – poor evidence