MCO Membranes and FGF-23: Advancing Dialysis Strategies for Better Outcomes?

In the last years, several studies have highlighted the impact of fibroblast growth factor-23 (FGF-23) on in- creased morbidity and mortality among patients with chronic kidney disease (CKD). FGF-23 is produced in bone by osteocytes and plays a pivotal role in renal handling of phosphate, vitamin D metabolism, and PTH secretion. FGF-23 levels increase early during the course of CKD in parallel with the decline in glomerular fil- tration rate, leading to reductions in calcitriol and ele- vations of PTH [1, 2]. While FGF-23 production is in- duced by an increase in PTH, phosphate, 1,25(OH) 2 D, and calcium, none of these classical factors fully explain the early rise in FGF-23 observed in CKD patients, as elevations in FGF-23 levels precede these abnormalities in bone and mineral metabolism [3, 4]. Hence, the derangement of mineral metabolism in CKD is not the sole trigger for FGF-23 production.