Influence of Calcium Intake on Calcitriol Levels in Idiopathic Hypercalciuria in Children

Abstract

Twenty-four children with idiopathic absorptive hypercalciuria (IAH) and a control group (CG) of 11 healthy children were studied. Plasma 1,25-hydroxyvitamin D₃ (calcitriol), parathyroid hormone (PTH), calcium (Ca) and phosphate (P) levels were measured during dietary manipulation. The three diets analized were: (A) calcium-restrictive diet (400 mg/l.73 m²day) for 7 days; (B) supplemented diet (1,000 mg/l.73 m²day) for 3 days; (C) supplemented diet continued for 15 days. The IAH group had higher levels of serum calcitriol than the control group for all three diets. Serum calcitriol levels in the IAH group decreased in diet B compared to diet A, and returned to levels observed with diet A during diet C. Serum Ca, P and plasma PTH levels did not vary throughout the study in either group. In IAH, two subgroups were observed. In one, serum calcitriol levels were elevated and in the other, serum calcitriol levels were not different from the controls. This second group had a lower P and maximum rate of tubular reabsorption of phosphate per 100 ml of glomerular filtrate than the IAH group with elevated serum calcitriol levels and the control group. These results suggest that IAH in children may be related both to increased serum calcitriol levels and to an altered Tmp/GFR.

Urinary excretion of endothelin-1 in children with absorptive idiopathic hypercalciuria

“…AIH patients are considered to be in a positive Ca balance. In these patients increased serum levels of 1,25-dihydroxyvitaminD [17,18], low or normal serum concentrations of PTH, a finding confirmed by this study as well as by others [19], and excessive intestinal Ca absorption [20] are compatible with a state of Ca excess. Thus it could be expected that in AIH patients the renal ET-1 synthesis might be increased.…”

Effects of Thiazide on the Expression of TRPV5, Calbindin-D28K, and Sodium Transporters in Hypercalciuric Rats

“…Despite being named by Albright about 50 yr ago (8), the pathophysiology is still unclear and diagnosis remains exclusive. Proposed pathogenic mechanisms are increased intestinal calcium reabsorption, increased renal loss, and augmented bone resorption (9, 10). …”