Pediatric Hypercalciuria 

Hypercalciuria is defined by a 24-hour urinary calcium excretion more than 150 mg in an adult female, more than 200 mg in an adult male, or more than 4 mg/kg/d in a child who weighs less than 60 kg. In infants younger than 3 months, 5 mg/kg/d is considered the upper limit of normal for calcium excretion.

Hypercalciuria can be classified as idiopathic or secondary. Idiopathic hypercalciuria can be diagnosed when clinical, laboratory, and radiographic investigations fail to delineate an underlying cause. Secondary hypercalciuria occurs when a known process produces excessive urinary calcium. Elevated urinary calcium occurs by 3 primary mechanisms, as follows: (1) the filtered load of calcium is abnormally increased without an adequate compensatory increase in tubular calcium reabsorption, (2) the filtered calcium load is normal but tubular calcium reabsorption is reduced, or (3) the filtered load is increased and the reabsorbed load is reduced. A good screening test for hypercalciuria compares the ratio of urinary calcium to creatinine. To validate the screening test, an accurately timed urinalysis should be used to confirm any positive screens.

Urinary excretion of calcium is the result of the complex interplay of the GI tract, bone, and the kidney, which is regulated by multiple hormones. Hypercalciuria is believed to be a polygenic trait and is significantly influenced by diet.

Idiopathic hypercalciuria is the most common metabolic abnormality in patients with calcium kidney stones. Subjects with idiopathic hypercalciuria have a generalized increase in calcium turnover, which includes increased gut calcium absorption, decreased renal calcium reabsorption, and a tendency to lose calcium from bone. Despite the increase in intestinal calcium absorption, a negative calcium balance is commonly seen in balance studies, especially in patients on a low-calcium diet. The mediator of decreased renal calcium reabsorption is unclear; it is not associated with either an increase in filtered renal calcium or altered parathyroid hormone (PTH) levels.

An increased incidence of hypercalciuria is observed in first-degree relatives of individuals with idiopathic hypercalciuria, but it appears to be a complex polygenic trait with a large contribution from diet to expression of increased calcium excretion. Increased tissue vitamin D response may be responsible for manifestations of idiopathic hypercalciuria in at least some patients.^{[1, 2]}

The association between obesity and kidney stones has been well documented in the adult literature.^[3] In children, an increased percentage of body fat was associated with an increased occurrence of kidney stones in patients with idiopathic hypercalciuria.^[4]

Frequency

United States

Hypercalciuria occurs in as many as 10% of children.

International

Incidence varies, with rates of 3-7% in Eastern Europe. Incidence and prevalence data from nonindustrialized countries are lacking; however, calcium-containing urinary stones occur in children from all parts of the world.

Race

Idiopathic hypercalciuria has no ethnic, racial, or gender predominance among children in the United States. Secondary hypercalciuria occurs in a distribution consistent with the underlying etiology.

Sex

Idiopathic hypercalciuria occurs with equal frequency in boys and girls.

Age

Hypercalciuria can occur at any age, including newborns. The peak incidence of idiopathic hypercalciuria is in children aged 4-8 years. The age distribution of children with secondary hypercalciuria reflects that observed in the underlying etiology.