The KNOW-CKD study: evidence for a link between proteinuria and alterations of mineral metabolism

Renal disease has become endemic worldwide. In addition to the risk of terminal renal failure and renal replacement therapy, renal disease carries an increased risk of fatal or severe cardiovascular (CV) events before the initiation of renal replacement therapy. Over the last few years, a very strong association between proteinuria and renal–CV complications of chronic kidney disease (CKD) has been highlighted in several populations. Proteinuria is now recognized as a main prognostic factor in kidney disease. The pathway linking renal disease progression with proteinuria likely involves albumin-mediated tubular cell toxicity, but the mechanisms by which proteinuria influences CV risk and mortality are less clear. Phosphate retention and abnormalities in the mineral endocrine system [Klotho, Fibroblast Growth Factor 23 (FGF23), parathormone] are epidemiologically associated with CV and bone complications of CKD as well as progression of renal disease, and pathophysiological links have been demonstrated