Prolonged Dietary Calcium Restriction: A Diagnostic Approach in Idiopathic Hypercalciuria

Abstract

Background: Although frequently observed, the etiology of idiopathic hypercalciuria (IHC) remains largely unknown. A common hypothesis postulates intestinal hyperabsorption and/or a primary renal leak as the pathophysiological basis. The aim of our study was to investigate the regulation pattern of calcium homeostasis in patients with IHC by using a prolonged period of calcium restriction. Methods: Twenty-seven patients with IHC were investigated. After a 3-week run-in period (dietary calcium content 700–1,000 mg/24 h), a standard calcium reduced diet (300 mg/24 h) was given for 4 weeks. Thereafter, the participants received again a normal calcium-containing diet. Values for urinary calcium, PTH and calcitriol levels of all participants were obtained at different phases of the study. Forty-three healthy persons served as controls. Results: During calcium restriction, two distinct groups were identified. One group displayed an increase (n = 12) in urinary calcium excretion, the second (n = 15) a marked reduction, respectively. In both groups, the values during calcium restriction were significantly different from baseline (p < 0.01). In the first group, the increase of urinary calcium excretion was accompanied by an increase of PTH and calcitriol. These values were also significantly different from baseline values (p < 0.01). The control group showed decreasing calcium excretion during oral restriction (p < 0.01). Conclusion: Prolonged calcium restriction proved to be useful in distinguishing apparently two major forms of IHC. The fact that one group displayed the same excretion pattern as the control group raises the question if this group just represents the upper limit of a physiological range. These findings may shed new light on diagnosis, pathogenesis and treatment of patients with IHC.

Other Secondary Hyperparathyroid States

“…22 Recent trials have focused on differentiating subtypes of idiopathic hypercalciuria using prolonged dietary calcium restriction (300 mg/24 h for 3 weeks, 700-1000 mg/24 h for 4 weeks); this revealed that one subset of subjects responded to a low-calcium diet with increasing urinary calcium loss and compensatory rise in PTH, while another subset responded with normalized urinary calcium excretion. 23 The molecular basis for these differences remains unclear. Studies of families with idiopathic hypercalciuria have revealed genetic loci that may be linked to hypercalciuric nephrolithiasis: chromosome 1q23.3-q24, which contains the human soluble adenylyl cyclase gene; chromosome 12q12-q14, which contains the vitamin D receptor gene; chromosome 9q33.3-q34.2, with candidate gene as yet undetermined.…”