Phosphorus is essential for life and exists in the body as phosphate. It is mainly intracellular (70%), about 29% resides in the bones and less than 1% circulates in the serum. Phosporous balance is regulated by kidneys (Figure 1A). It is filtered freely in the glomerulus and then it is reabsorbed in the proximal tubule under the effect of various hormones. The amount of reabsorbed phosphorus is the main regulator of the serum phosphorus levels in subjects with normal renal function, or moderately reduced glomerular filtration rate. Despite its importance, the accumulation of phosphate can produce deleterious effects. In Chronic Kidney Disease (CKD) the kidneys fail to excrete the phosphorus and the result is a positive phosphorus balance. However, the skeleton through the disorders of the bone that accompany CKD, contributes to this hyperphosphatemic state as it cannot handle the phosphorus excess. This leads to a need for new phosphorus reservoir and this is soft tissue organs including vasculature.1 The final result is vascular calcification that is frequently observed in end stage renal disease. The vascular and valvular calcifications are predictors of cardiovascular diseases and mortality in patients with chronic renal failure.2 To consider the pathogenesis of hyperphosphatemia in CKD, it is useful to understand the mechanisms of phosphate homeostasis in normal physiological conditions, along with the pathologic processes related to altered phosphate balance which conspire to result in more accentuated kidney damage and increased cardiovascular mortality and morbidity.