Abstract
Abstract BACKGROUND AND AIMS Reduction and normalization of calciuria in children with idiopathic hypercalciuria (IH) was published by Aladjem et al. (1996). The association between IH and hypocitraturia was described in two Brazilian studies; however, further studies are needed to determinate the caracteristics of its relation. We studied calcium and citrate urinary excretion in children diagnosed with IH and followed up until adulthood. METHOD: A total of 34 patients (12 M and 22 F) were studied. IH diagnosis was performed at the age of 7.9 ± 3 years (range: 1–14). Hypercalciuria was defined as urinary calcium excretion of >4 mg/kg/day in two successive samples. Calciuria and citraturia were collected in the first urine sample of the day at the same time as bone densitometry was performed. Three determinations were made: the first (D1) at age 10.5 ± 2.7 years (range: 6.5–16.8), the second (D2) at age 14.5 ± 2.7 years (range: 9.9–19.5) and the third (D3) at age 28.2 ± 2.8 years (range: 24.1–35.9). RESULTS: Calcium/creatinine ratio (P = 0.005) and citrate/creatinine ratio (P < 0.001) reduction during follow up was observed. In addition, we observed an increase in the calcium/citrate ratio (P = 0.008). Patients with a calcium/creatinine ratio higher than 0.20 mg/mg decreased from 100% at diagnosis to 52.9% (18/34) on D1 and to 26.5% (9/34) on D2 and 23.5% (8/34) in adulthood (D3). Lithogenetic risk decreased from diagnosis (15/28; 53.6%) to D1 (13/32; 40.6%) and D2 (8/28; 28.6%) but increased in adulthood (21/30; 70%). CONCLUSION It is difficult to explain why some IH patients present a decrease in both calcium and citrate excretion in adolescence and early adulthood, which has an impact on lithogenic risk. The interpretation of these results is complex. Bone is the largest reservoir of alkaline salts in the body. Our hypothesis is that late hypocitraturia observed in patients with IH would be an indirect sign of high functional osteoblastic activity. Increased proximal tubular citrate reabsorption would denote an increased bicarbonate production, which is necessary as osteoblastic activity increases, thus requiring increased inputs of alkali, calcium (normalized calciuria) and phosphate. Another option could be the development of incomplete distal renal tubular acidosis.
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