Idiopathic hypercalciuria

Idiopathic hypercalciuria (IH) is a metabolic condition characterized by excessive excretion of calcium in the urine without an identifiable underlying cause such as hyperparathyroidism, vitamin D excess, or other systemic diseases. It is one of the most common metabolic abnormalities associated with kidney stone formation (nephrolithiasis) and can also contribute to reduced bone mineral density (osteopenia or osteoporosis). The condition primarily affects the urinary and skeletal systems. Patients with idiopathic hypercalciuria may present with recurrent calcium-containing kidney stones, flank pain (renal colic), blood in the urine (hematuria), frequent urinary tract infections, and in some cases, bone pain or fractures related to decreased bone density. In children, the condition may manifest as microscopic or gross hematuria, urinary frequency, urgency, or abdominal pain. Many affected individuals may remain asymptomatic and are only identified through routine urine testing or during evaluation for kidney stones. The pathophysiology involves one or more mechanisms including increased intestinal calcium absorption (absorptive hypercalciuria), impaired renal tubular calcium reabsorption (renal leak hypercalciuria), or enhanced bone resorption. Management typically includes dietary modifications such as adequate fluid intake, moderate sodium and protein restriction, and ensuring appropriate (not excessive) calcium intake. Thiazide diuretics are commonly used as pharmacological treatment, as they reduce urinary calcium excretion by enhancing calcium reabsorption in the distal renal tubule. Potassium citrate may also be prescribed to reduce stone formation risk. The condition has a strong familial component, and family members of affected individuals may benefit from screening.

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