L’hypercalciurieHypercalciuria.

Hypercalciuria is a biological syndrome defined as excretion in the urine of more than 0.1 mmol/kg/24 hours of calcium in the absence of dietary restrictions. A number of endocrine, renal, and bone diseases can cause hypercalciuria. Urinary calcium excretion is substantially influenced by the intakes of calcium, sodium, protein, carbohydrates, alcohol, and potassium, so that a poorly balanced diet can result in hypercalciuria. Recently, there has been a burst of interest in molecular studies of rare lithiasis syndromes, all of which are due to mutations in the ClCN5 chlorine channel gene. Mutations affecting the calcium-sensitive receptor (CaSR) have been identified in other forms of hypercalciuria. Idiopathic hypercalciuria is defined as hypercalciuria that persists after correction of dietary imbalances and has no detectable cause. The classification suggested by Pak (class I, class II, class III, and “renal” hypercalciuria) is controversial and of little assistance in clinical practice. Three mechanisms can be incriminated in idiopathic hypercalciuria: increased intestinal absorption of calcium, defective reabsorption of calcium by the renal tubule, and increased bone resorption. Overexpression of the vitamin D receptor and a deficiency in renal tubule enzymes may be involved also. Bone mineral density is moderately decreased in idiopathic hypercalciuria, particularly of the renal type. The risk of vertebral fracture seems increased, however. Overproduction of calcitriol and of cytokines that stimulate bone resorption have been incriminated in the bone loss. Treatment of the cause is essential in secondary hypercalciuria (dietary advice, treatment of an underlying disease…). A diet low in sodium and meat and containing no more than 800 mg of calcium per day has been advocated in idiopathic hypercalciuria. Hydrochlorothiaide therapy is warranted in patients with osteopenia and an inadequate response to dietary therapy.