Abstract The precise point at which growth ends and no longer influences physiologic mechanisms is unknown. Mineral metabolism in each period of growth appears to be unique although related in concept to all other periods, including adult life. Differences, when present, may be related to supply and demand. For example, rapid bone growth in the fetus theoretically would be enhanced by the combined low PTH and elevated calcitonin activity during this period. Similarly, renal maintenance of serum [Pi] at levels normal for adults would not favor mineralization of bone matrix in the growing child. Thus, with the possible important addition of growth hormone, the pathways and mechanisms schematized in Fig. 1 can be applied throughout life. The objective of the review articles in this symposium is to discuss current knowledge of the role of the kidneys in mineral homeostasis during maturation. Because research on developmental aspects of mineral metabolism has lagged, some apparent differences in adult and pediatric mineral homeostasis ultimately may be proven false. For example, the majority of studies on renal phosphate handling in early life present data as fractional excretion or percent tubular reabsorption among others, a practice now considered physiologically inappropriate. Serum [Pi] in adults is set by Tmphos/GFR, and similar studies in infants have not been published. Thus, the current assumption that renal Pi excretion or, more correctly, Tmphos/GFR, does not regulate serum [Pi] in infants may be incorrect. Similarly, there has been only one published study of intestinal calcium absorption in the neonate using Ussing-type apparatus with removal of electrical and chemical gradients to investigate mechanisms related to epithelial transport; therefore, studies that demonstrate non-vitamin D-dependent intestinal calcium absorption in the neonate must also be questioned. Idiopathic hypercalciuria occurs during childhood; however, its effect on calcium balance is not known, and appropriate studies to determine values for diagnosis of absorptive or renal hyper-calciuria in children have not been published. Protocols for investigation of this subject will be complex in view of prior demonstration of a relationship between age and intestinal calcium absorption in childhood. Many important questions related to the role of the kidney in mineral homeostasis during maturation could not be included in this symposium. Undoubtedly, future research will raise as many new questions as answers for prevailing questions. We believe that the reviews and individual viewpoints presented in this issue of Seminars in Nephrology emphasize the importance of continuing as well as expanding clinical and laboratory research on developmental aspects of vitamin D and mineral homeostasis.