Diet, phosphate and management of hyperphosphatemia in dialysis patients: Survey Results
by Prof. Denis Fouque
Most readers correctly answered C, with a fixed proportion of 13 mg phosphorus per gram protein. However, it has been showed recently that phosphate from vegetal protein may not be absorbed as well due to a potential binding with fibers in the intestine. But E was also true, since certain food (sausages, processed food) and beverages (colas) may content a quite important phosphorus content. Phosphate is not influenced by seasonal variation of food content, which mainly applies to fruit and vegetables.
According to current guidelines, protein intake in a dialysis patient should be 1.1 g/kg per day, which represent between 65 to 90 g protein times 13, which equals 800 to 1200 mg phosphate/day. Among this, between 40 to 70% will be absorbed by the gut, partly positively regulated by calcitriol level and negatively by phosphate binders. There are large differences between meals (meat and dairy products bring the largest phosphate amount) and among countries.
Quite easy question with 60 + % correct answers, except for D which is true. Indeed nicotinamide (also called niacine or vitamin PP or B3) is a strong inhibitor of phosphate transport into the intestinal cell, and has been successfully used to reduce serum phosphate.
Above are listed the different amounts of phosphate cleared by dialysis. On a daily basis, the net elimination is approximately 300 mg whereas the net intake is between 400 to 800 mg, resulting in a positive balance. This is why an intestinal binding is mandatory to limit the positive phosphate balance and tissue accumulation. The most powerful way to increase phosphate elimination is the duration of the dialysis session, followed by daily hemodialysis and hemodiafiltration.
This was a quite difficult question about the recently discovered fibroblast growth factor-23/Klotho system. Although much remains to be discovered about it, we already know that phosphate metabolism is strongly influenced by FGF-23 : serum FGF-23 rises at a very early stage of CKD to increase tubular phosphate excretion. In addition, FGF-23 downregulates the renal 1-alpha hydroxylase expression, which in turns reduces calcitriol and further limits intestinal phosphate absorption. Serum FGF-23 is increased by phosphate intake, and also by protein intake and is reduced by phosphate binders. High levels of serum FGF-23 are associated with increased mortality in maintenance dialysis patients without any pathophysiological clues so far.
A few correct answers surprisingly. Whereas it is well known that serum phosphate is positively associated with mortality and serum phosphate is increased with high intakes of protein (note that a high serum phosphate can also be present in case of bone disease and low protein intake), high protein intakes are associated with lower mortality and reducing protein intake may increase mortality in response to superimposed protein energy wasting (PEW). Thus, in general it is not advisable to reduce protein intake to try to correct hyperphosphataemia. Finally, no prospective randomised trial has shown until now that lowering serum phosphate by the use of phosphate binders reduces patients mortality.
Cheese phosphate content is high but mainly depends on density (ie, the inverse of hydration). Thus cooked and concentrated cheese such as beaufort, gruyere, abondance, appenzeller have the highest content, eg, 800 mg phosphate per 100 g cheese. Camembert, St Nectaire and gouda have about 300 mg/100 g and fresh white cheese only brings 60 mg/100 g. A regular dry cheese portion should be 30 g, whereas for white cheese and yoghurt, is about 100-150 g.