Phosphate Control in Peritoneal Dialysis Patients: Issues, Solutions, and Open Questions

Abstract

Hyperphosphatemia is a common complication in advanced chronic kidney disease and contributes to cardiovascular morbidity and mortality. The present narrative review focuses on the management of phosphatemia in uremic patients receiving peritoneal dialysis. These patients frequently develop hyperphosphatemia since phosphate anion behaves as a middle-size molecule despite its low molecular weight. Accordingly, patient transporter characteristics and peritoneal dialysis modalities and prescriptions remarkably influence serum phosphate control. Given that phosphate peritoneal removal is often insufficient, especially in lower transporters, patients are often prescribed phosphate binders whose use in peritoneal dialysis is primarily based on clinical trials conducted in hemodialysis because very few studies have been performed solely in peritoneal dialysis populations. A crucial role in phosphate control among peritoneal dialysis patients is played by diet, which must help in reducing phosphorous intake while preventing malnutrition. Moreover, residual renal function, which is preserved in most peritoneal dialysis patients, significantly contributes to maintaining phosphate balance. The inadequate serum phosphate control observed in many patients on peritoneal dialysis highlights the need for large and well-designed clinical trials including exclusively peritoneal dialysis patients to evaluate the effects of a multiple therapeutic approach on serum phosphate control and on hard clinical outcomes in this high-risk population.

Management of serum phosphorus over a 1-year follow-up in patients on peritoneal dialysis prescribed sucroferric oxyhydroxide as part of routine care: a retrospective analysis

“…These data suggest the need for increased attention to PB dose titration in patients with the most rapid decreases in residual kidney function. They also support the potential importance of efforts to maintain residual kidney function and individualizing PD prescriptions to optimize phosphate management [ 22 ].…”

“…Residual kidney function is a key factor impacting phosphate clearance and balance in patients on PD [ 6 , 22 ] and can influence the perceived efficacy of PB. Reductions in K ru have been significantly correlated with increases in sP [ 23 ].…”

Magnesium inhibits peritoneal calcification as a late-stage characteristic of encapsulating peritoneal sclerosis

“…In the present study, Ca overload augmented high-phosphate-induced calcification of the extracellular matrix in cultured MeT5A cells, suggesting that the simultaneous unloading of phosphate and Ca could protect against peritoneal calcification. Dietary phosphate restriction, phosphate binder use, and the use of calcimimetics to prevent secondary hyperparathyroidism may prevent hyperphosphatemia and decrease transperitoneal phosphate exposure, ultimately slowing the progress of peritoneal calcification 56 . Regarding Ca unloading, we should reduce the Ca concentration of the dialysate and minimize the use of vitamin D receptor activators and Ca-based phosphate binders 23 , 57 , 58 .…”

Hyperphosphatemia in Chronic Kidney Disease: The Search for New Treatment Paradigms and the Role of Tenapanor

“…This implies that phosphate transport through peritoneal membrane is noticeably influenced by patient transporter features and dialysis modality and prescription and that phosphate binders and a proper diet are essential to improve serum phosphate control also in this population. 56 The aforementioned considerations are supported by recent observational data showing that, despite a strict dietary regimen and the use of phosphate-lowering medications, many CKD patients, especially on dialysis therapy, fail to adequately control serum phosphate levels. 57 Accordingly, there is a need for novel pharmacological approaches enabling to better handle hyperphosphataemia and ameliorate clinical outcomes of CKD patients.…”

“…This implies that phosphate transport through peritoneal membrane is noticeably influenced by patient transporter features and dialysis modality and prescription and that phosphate binders and a proper diet are essential to improve serum phosphate control also in this population. 56 …”