Phosphate control in end-stage renal disease: barriers and opportunities

Abstract

Hyperphosphatemia is a nearly universal complication of end-stage renal disease that is widely recognized as one of the most important and most challenging clinical targets to meet in the care of dialysis patients. Left untreated, it can lead to bone pain, pruritus and worsening secondary hyperparathyroidism. Data from observational studies demonstrate that an elevated serum phosphorus level is an independent risk factor for mortality, and that treatment with phosphate binders is independently associated with improved survival. Experimental studies provide support for the epidemiologic findings: phosphate excess promotes vascular calcification, induces endothelial dysfunction and may contribute to other emerging chronic kidney disease-specific mechanisms of cardiovascular toxicity. On the basis of this evidence, clinical practice guidelines recommend specific targets for serum phosphorus levels in the dialysis population. The purpose of this review is to summarize common challenges in meeting these targets and to identify potential opportunities for improvement.

Phosphate Removal During Long Nocturnal Hemodialysis/Hemodiafiltration: A Study With Total Dialysate Collection

“…Regarding the total mass of phosphate removed, nocturnal HD is the superior method compared to conventional HD and peritoneal dialysis . Our results showed a much higher total phosphate reduction per session compared to reductions between 600 and 1200 mg per session found in the literature . However, these results are from a study conducted by Musci et al in 1994/95 .…”

Effects of systematic nursing instruction on a low‐phosphorus diet, serum phosphorus level and pruritus of patients on haemodialysis

“…Hyperphosphataemia causes pruritus, renal osteodystrophy, hyperparathyroidism and calcification of the heart and blood vessels and increases mortality. Statistics showed that mortality increases when SPVs are higher than 5Á5 mg/dl (Kestenbaum et al 2005, Spasovski 2007, Waheed et al 2013.…”

“…Although the mechanism underlying uraemic pruritus (UP) is poorly understood, multiple factors have been proposed as pruritogenic substrates, among which vitamin A, parathyroid hormone, histamine, and calcium and magnesium salts may induce itching (Narita et al 2008, Mettang & Kremer 2015. Furthermore, hyperphosphataemia and secondary hyperparathyroidism have been related to pruritus (Chou et al 2000, Virga et al 2002, Waheed et al 2013.…”

A Role of Intestinal Alkaline Phosphatase 3 (Akp3) in Inorganic Phosphate Homeostasis

“…An elevated serum inorganic phosphate (Pi) level is an independent risk factor for mortality, and treatment with Pi binders is independently associated with improved survival in chronic kidney disease (CKD) patients [1,2]. Findings from experimental studies support the epidemiologic findings: clinical practice guidelines recommend specific targets for serum Pi levels in dialysis patients [3][4][5].…”