Dietary Phosphorus and Metabolic Health in CKD and ESKD

The contribution of dietary phosphate (P) in the pathogenesis of CKD-associated mineral bone disease and the management of P intake in patients with CKD are essential to slow down disease progression and improve patient outcomes. In patients with CKD, and most likely in the general population, P retention and overload can affect four critical aspects of the cardiovascular system: increased arterial BP, vascular and valvular calcification, and left ventricular hypertrophy. All of these factors contribute to increased cardiovascular risk and mortality. Intestinal absorption of P from a mixed diet is approximately 60%-70% of the dietary P content, with lower rates for organic P from plant sources and higher rates for inorganic P from processed foods containing additives. The widespread use of phosphate additives in processed foods and the high consumption of animal protein in the Western diet have led to a steady increase in phosphate consumption in recent decades. Although it is unclear whether this high P intake has adverse effects in people with normal kidney function, several studies have found that increased dietary P contributes to the progression of CKD and cardiovascular damage. High P intake may be detrimental, but there is no clear evidence that it should be avoided in the general population. On the contrary, kidney function impairment is the setting in which modulation of P intake is justified and easy to implement by restricting/reducing protein intake. However, it is quite difficult to implement P restriction in patients on dialysis because of the conflicting recommendation of high protein intake. Educational approaches, together with solid motivation and adherence by patients and caregivers, are needed to achieve the goal of successful dietary phosphate management in patients with CKD.