The laboratory studies the chronic kidney disease-mineral bone disorder (CKD-MBD) syndrome, chronic kidney disease (CKD), and mechanisms of its complications. Our focus has been in the high cardiovascular mortality associated with CKD. We have discovered that the skeletal disorder caused by CKD contributes to this mortality. This has lead to the naming of a CKD associated syndrome, CKD-MBD. In the CKD-MBD, we have discovered that kidney diseases directly cause vascular calcification and diminish bone formation early in their course despite normal calcium, phosphorus, PTH and vitamin D. Increased tubular fluid phosphate stimulates secretion of fibroblast growth hormone 23 (FGF23), which is a skeletal hormone regulating phosphorus excretion and calcitriol production. Besides stimulation of FGF23, the early pathogenesis of the CKD-MBD, which we have shown in stage 2 CKD, results from release of factors including Wnt inhibitors from the injured kidney during attempted repair. Systemic Wnt inhibition causes vascular disease producing vascular stiffness/calcification, and cardiac hypertrophy. Skeletal anabolic factors, such as neutralization of Wnt inhibition and bone morphogenetic protein 7 (BMP-7), increase bone formation and inhibit vascular calcification in the early CKD. Additionally, BMP-7 restores the normal osteoblast phenotype in the dystrophic condition, osteitis fibrosis. Thus, BMP-7 and skeletal anabolics hold promise in as therapies for the CKD-MBD, and BMP-7, through its renal actions, as a therapy for CKD itself. The CKD-MBD is associated with excess bone resorption which contributes to hyperphosphatemia in CKD. We have shown that hyperphosphatemia is a direct stimulus to osteoblastic differentiation of cells in the neointima of atherosclerotic plaques causing stimulation of vascular calcification (VC) in CKD. This mechanism added to observational studies strongly suggests that phosphorus is a cardiovascular risk factor. We have discovered that members of the bone morphogenetic protein (BMP) family differentially affect lineage allocation of mesenchymal stem cells. While BMP-7 and BMP-2 support endochondral osteogenesis, their actions differ, and BMP-13 favors chondrogenesis. This is critical in the pathogenesis of vascular calcification because BMP-2 is causative of VC, while BMP-7 is therapeutic, capable of reversing established calcification. BMP-7 is a critical renal morphogen. It is expressed in the adult kidney, and its expression is reduced by renal injuries. BMP-7 exhibits therapeutic potential against renal fibrogenesis and diabetic nephropathy, and for vascular calcification and renal osteodystrophy as discussed above. Furthermore, we have discovered that the chondrogenic program represented by autocrine factors, including BMP-13, produced by juvenile chondrocytes is sufficient for the entire differentiation program of the articular cartilage. These data support juvenile articular tissue as potential allograft sources for repair of cartilage injuries. The latter concepts have been taken to clinical trial as have the studies of phosphorus as a cardiovascular risk factor. Other studies in basic bone cell biology in the laboratory are focused on the lineage commitment of mesenchymal stem cells and novel mechanisms of osteoclastogenesis by microRNAs.