Calcium and phosphate combine to form insoluble precipitates in both inorganic and organic materials. This property is useful biologically and has been used by numerous organisms to create hard tissues, a process referred to as biomineralisation [1]. In humans, calcium and phosphate combine to form useful crystal structures largely composed of calcium hydroxyapatite [Ca10(PO4)6(OH)2] and these are essential in the growth, maintenance and strength of parts of the skeleton and other structures like teeth. However, it remains unclear how the body achieves the exquisite specificity involved in biomineralisation. In ageing and disease, these pathways are perturbed, resulting in ectopic calcium crystal deposition impairing tissue function and, interestingly, frequently accompanied by simultaneous loss of mineral from sites where it is useful (e.g. bone). One paradigm for this maladaptive situation is renal failure; a situation that we know is associated with vascular stiffening and calcification, along with mineral loss from the skeleton. Mineral trafficking is a loose term used to describe the movements of calcium salts around the body, and new insights into these pathways may explain some of the problems of previous models of bone mineral disease in renal failure and point to potential future therapeutic strategies.