In order to determine metabolic disorders in children with urolithiasis, 50 patients with urinary calculi were studied. Abdominal pain and/or haematuria were the most predominant symptoms. Surgical procedures were required in 22% of these children and urinary tract infection was observed in 34% of this group. Only 2 children had anatomical malformations of the urinary tract. Absorptive hypercalciuria (32%), renal hypercalciuria (34%) and uric acid hyperexcretion (24%) were the most common metabolic abnormalities in these children. We were unable to find an underlying metabolic abnormality in only 14% of the patients. These data suggest that appropriate metabolic study will allow rational management of children with urinary stones.

Urinary inhibitors are suggested to play a significant role in reducing crystallization in calcium (Ca) stone former and idiopathic hypercalciuria (IH). Urinary inhibitors such as magnesium (Mg), citrate, and glycosaminoglycans (GAGs) were evaluated, as well as urinary Ca and creatinine (Cr), in IH children with nephrolithiasis (LIT) or with hematuria plus IH (HEM) and were compared with a control group. The mean 24-h urinary excretion of Mg was similar in all groups. However, the urine Ca/Mg ratio was significantly increased (P < 0.005) in LIT and HEM groups. A higher mean value for GAGs and citrate was found in the HEM group, but a very low level of GAGs (less than 60% of the normal value) and citrate (less than 30% of the normal value) was found in the LIT group. These data suggest that, despite a high urinary Ca excretion (3.6 +/- 0.1 mg/kg per day) in the HEM group, elevated urinary GAGs (32.0 +/- 1.0 mg/g Cr) and a normal urinary citrate (428.7 +/- 62.3 mg/24 h) excretion may prevent Ca crystallization and thus renal stones. In contrast, in the LIT group low urinary GAG (10.3 +/- 0.9 mg/g Cr) and citrate (235.2 +/- 52.3 mg/24 h) excretion may precipitate stone formation in the presence of a high urinary Ca excretion. Thus, it is reasonable to suggest that patients with hematuria and IH may not develop overt renal stone due to the presence of normal levels of renal stone inhibitors.

Metabolic disturbance as a cause of recurrent hematuria in children. To evaluate metabolic disturbance as a cause of hematuria, 250 children, aged eight months to fourteen years, with recurrent hematuria were studied. In the present series, metabolic disturbance was mainly due to idiopathic hypercalciuria (IH), the most common etiology of hematuria without proteinuria in childhood. Sixty-seven (27%) of the children had IH, ten children (4%) had hyperuricosuria, and 27 (11%) had nephrolithiasis. To better characterize the IH into renal (RH) or absorptive hypercalciuria (AH) subtypes, 45 of the 67 children (ranging age from six to twelve years) were further submitted to an oral calcium load test. Eighteen patients (40%) had AH, 7 (15.5%) RH and 20 (44.4%) could not be classified as having AH or RH [indeterminant (ID) idiopathic hypercalciuria group]. Intravenous pyelography or ultrasound were normal in all children. The oral calcium load test may be useful in characterizing the subtype of IH in some children; however, a great number of the IH children were characterized as indeterminant. Also hyperuricosuria, recently described as another metabolic disturbance associated with hematuria, may be an important cause of recurrent hematuria in children.

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