Abstract
In patients with chronic kidney disease higher phosphatemia is not only a cardiovascular risk factor, but it also contributes to the progression of chronic kidney disease and interferes with the renoprotective action of the angiotensin converting enzyme inhibitors. Interventions aimed at the reduction of phosphatemia (e.g. restriction of dietary phosphate intake, phosphate binders) could thus also slow down the progression of renal failure and enhance the efficacy of the blockade of the renin-angiotensin system.
Proteinuria-induced increased tubular reabsorption of phosphate could contribute to the increased cardiovascular risk in patients with unremitting nephrotic syndrome.