Hypercalciuria

Hypercalciuria is by far the most common metabolic abnormality detected in calcium stone-formers.

Approximately 8% of men excrete in excess of 7.5 mmol of calcium in 24 hours. Calcium stone formation is more common in this group, but as the majority of even these individuals do not form stones the definition of 'pathological' hypercalciuria is arbitrary. A reasonable definition is 24-hour calcium excretion of more than 7.5 mmol in male stone-formers and more than 6.25 mmol in female stone-formers.

The kidney is the major site for plasma calcium regulation. Approximately 90% of the ionized calcium filtered by the kidney is reabsorbed. Renal tubular reabsorption is controlled largely by parathyroid hormone (PTH).

Approximately 65% of the filtered calcium is absorbed in the proximal convoluted tubule, 20% by the thick ascending limb of the loop of Henle, and 15% by the distal convoluted tubule and collecting ducts. The cells of the thick ascending limb express Ca 2+ -sensing receptors. A high luminal calcium concentration is 'sensed' by these receptors and this triggers a series of events leading to reduced calcium reabsorption; conversely a low luminal concentration leads to avid calcium reabsorption and hypocalciuria.

Causes of hypercalciuria are:

• hypercalcaemia
• an excessive dietary intake of calcium
• excessive resorption of calcium from the skeleton, such as occurs with prolonged immobilization or weightlessness
• idiopathic hypercalciuria.

There are two main mechanisms of idiopathic hypercalciuria. The majority of patients with idiopathic hypercalciuria can be shown to have increased absorption of calcium from the gut. Dietary calcium restriction in this group markedly reduces urinary calcium excretion. A proportion of patients appear to have a renal tubular calcium leak with secondary compensatory hyperabsorption of calcium from the gut. Calcium restriction has less effect on urinary calcium excretion in this group.