It is well known that some patients with renal lithiasis due to idiopathic hypercalciuria (IH) may exhibit decreased bone mineral density (BMD). We have studied a large group of children with IH and related their BMD values to several renal function parameters and calcium and bone metabolism markers. Children with IH had higher osteocalcin and calcitriol levels and higher urinary excretion of magnesium and prostaglandin E2, as well as lower tubular reabsorption of phosphate, urinary excretion of ammonium, maximum urinary PCO2, and BMD compared with control group of children. In children with IH we observed a negative correlation between BMD and age. We found osteopenia in 22 of 73 children with IH (30.1%); these children showed lower citraturia levels and higher fractional excretion of uric acid than children with normal BMD. In osteopenic children there was a negative correlation between BMD and calcitriol levels. Several possible pathogenetic factors have been proposed for the bone mass loss. Our results demonstrate that, at least in some cases, it may be related to high levels of calcitriol, which has a wellknown resorption ability. Whether a certain degree of intracellular acidosis or a higher production of prostaglandin E2 could play a role in some cases is still an open question. In children with normal BMD we observed a direct correlation between osteocalcin and tartrate-resistant acid phosphatase levels; this correlation did not hold for children with osteopenia.

Our results showed that the prevalence of hypercalciuria was greater in paediatric patients with VUR than in the general population. Urolithiasis in patients with VUR had a metabolic origin. Hypercalciuria was inherited as an autosomal dominant trait although with a higher probability to be inherited from the mother.

Background/Aims: Idiopathic hypercalciuria (IH) is associated with a decreased bone mineral density (BMD) both in children and adults. It is being increasingly recognized that IH may be a contributing factor to osteopenia and/or osteoporosis in adults. We studied BMD in girls with IH and in their mothers, also affected with IH, in order to evaluate the influence of genetic background on bone mass in the setting of IH. Methods: BMD was evaluated in 40 girls with IH and in their premenopausal mothers from whom they had inherited this disease. Urinary creatinine and calcium were measured by standard laboratory methods. BMD was determined by dual X-ray absorptiometry scanning of the lumbar spine (LS) and the femoral neck (FN), and values are expressed as Z- and T-scores. Results: A Z-score of <–1 at the LS was found in 42.5% of the girls, whilst in the mothers, a Z score of <–1 at the LS and/or FN was observed in 47.5% and a T-score of <–1 at the LS and/or FN in 62.5%. The Z-score at the LS was significantly lower in girls and their mothers compared to controls, although this finding did not apply for the Z-score at the FN in the mothers. Z-scores in the girls of mothers with osteopenia were significantly lower or there was a trend for the score to be lower than in the girls of mothers with normal BMD. There was a significant relationship between the Z-score of the girls and the T-score at the LS in the mothers (r = 0.32, p < 0.05). Conclusion: We have observed a high prevalence of osteopenia in our population affected by IH, both in girls and in their mothers. We suggest that BMD should be measured during the third or fourth decades of life in those individuals with nephrolithiasis or with children diagnosed as having IH.

We studied 34 asymptomatic children who were born with a very-low-birth-weight (VLBW) and had no perinatal history of acute renal failure nor treatment with furosemide. The study was done at preschool or school age, looking for echographic changes and renal tubular disturbances which are known to predispose to renal lithiasis. The results were compared with those of a control group of 18 children who had been born at term with a body weight >2,500 g. One or more renal tubular disturbances were found in 64.70% of the VLBW children. Most frequently found were decreased ammonium excretion in response to furosemide (38.23%), enhanced N-acetylglucosaminidase excretion (35.29%), hypercalciuria (26.47%), and hypocitraturia (23.53%). Echography revealed renal cortical hyperechogenicity (17.65%) and renal lithiasis (8.82%) in some of the VLBW children. We found a significant positive correlation (r = 0.7) between the perinatal level of plasma phosphate and the total amount of H⁺ excreted in response to furosemide at preschool or school age. Because these renal tubular anomalies may be precursors of future lithiasis, and the renal function and echography tests are not invasive, we suggest that renal tubular function be measured and followed up in every VLBW child, particularly when perinatal hypophosphatemia has occurred.

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