Kidney stones are very common in industrialized countries and the lifetime risk is about 10 to 15% in this population. Kidney stones are composed of inorganic and organic components. Calcium containing stones are the most common stone type accounting for more than 80% of kidney stones. Many factors predispose or contribute to the development of kidney stones, including genetic variants or mutations, diet, environmental factors, and behavior. To date, little is known on fibroblast growth factor (FGF23) levels in patients with calcium nephrolithiasis. FGF23 is crucial for phosphate homeostasis including physiological and pathophysiological conditions such as X-linked hypophosphatemic rickets and it seems that FGF23 is probably the most important regulator of serum phosphate and calcitriol (1,25(OH)2D3) levels in addition to parathyroid hormone (PTH) produced by the parathyroid gland. Novel factors such as Klotho and Sclerostin, which are involved in the bone-kidney-parathyroid endocrine axis, have been identified recently. Klotho is a putative aging suppressor gene and its deficiency results in osteopenia, hyperphosphaturia, and calcification. Klotho is mainly expressed in the kidney but also in the parathyroid gland and acts as a FGF23 specific co-receptor mediating FGF23 participation in the bone-kidney-parathyroid endocrine axis as described above. Sclerostin is a protein secreted by osteocytes that inhibits bone formation by osteoblasts. However, the potential role of FGF23, Klotho, and Sclerostin in nephrolithiasis is still poorly under-stood or even unexplored. The aim of this study is to test if levels of FGF23, Klotho, and Sclerostin are differentially regulated in kidney stone formers.