Kidney stones are very common in industrialized countries and the lifetime risk is about 10 to 15% in this population. Men are more affected than women and the mean age of the patients is be-tween the fourth and sixth decade of life. Notably, a considerable percentage of patients experience recurrent kidney stones with a relapse rate of 50% in 5-10 years complicated by pain and urinary tract infections and potential loss of functional renal parenchyma with development of chronic renal failure in the long term. 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. Among all factors, abnormal urinary pH and calcium excretion are predominant findings in stone formers and seem to play a major role in the pathogenesis of stone formation (1-5). Moreover, a significant percentage of patients with calcium nephrolithiasis and normal parathyroid function show hypophosphatemia and reduced renal phosphate reabsorption i.e. a renal phosphate leak (6-8) with resulting hyperphosphaturia. To date, little is known on fibroblast growth factor (FGF23) levels in patients with calcium nephrolithiasis (6). The authors demonstrated that FGF23 was increased in stone formers with renal phosphate leak when compared to controls. Also serum FGF23 concentration was strongly inversely associated with serum phosphate levels and rate of tubular phosphate re-absorption, respectively. This study suggests a role of FGF23 in the pathogenesis of calcium nephrolithiasis, however, more studies are necessary to confirm these findings. More, the influence of other novel factors involved in hyperphosphaturia has not been identified yet, such as Klotho.