Abstract
In this review, recent advances in the epidemiology, genetics, clinical associations and management of idiopathic hypercalciuria will be discussed. A significant genetic contribution exists in the pathophysiology of hypercalciuria. Although several candidate genes and genetic alterations have been proposed, identification of precise gene(s) responsible remains elusive. Decreased bone density has been increasingly associated with hypercalciuria. Recent publications have suggested that bisphosphonates may play a role in the management in patients in whom both hypercalciuria and decreased bone density are present. Idiopathic hypercalciuria is a common disorder in children and can present with a range of clinical presentations such as hematuria, voiding dysfunction, flank pain, abdominal pain, nephrolithiasis, urinary tract infection and decreased bone mineral density. Dietary modifications are often sufficient in the management of hypercalciuria. If the symptoms persist or a rare monogenic disorder is present, consideration should be given to medical treatment with a thiazide diuretic and/or citrate therapy.
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