A pathophysiologic link exists between proteinuria and renal phosphate handling, say researchers. An analysis of 1,738 patients with chronic kidney disease identified albuminuria ≥300 mg per 24 h as an independent predictor of high phosphate levels. Using both rat and mouse animal models, the researchers showed that proteinuria-induced phosphate retention was partly caused by enhanced sodium-dependent phosphate transport protein 2A expression and decreased fibroblast growth factor (FGF)-23 activity. They suggest that high levels of phosphate and FGF-23 in patients with proteinuria might contribute to their increased risk of cardiovascular disease.