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.