229© Springer Nature Switzerland AG 2021 B A Warady et al (eds ), Pediatric Dialysis, https //doi org/10 1007/978 3 030 66861 7 14 Peritoneal Dialysis Solutions Elizabeth Harvey Introduction The perit[.]
Peritoneal Dialysis Solutions 14 Elizabeth Harvey Introduction The peritoneal dialysis solution (PDS) is the cornerstone of peritoneal dialysis (PD), responsible for both fluid removal and metabolic control As eloquently stated by Rippe, “the optimal electrolyte composition of a dialysis solution is that which best serves the homeostatic needs of the body” [1] The absolute requirements for a PDS are a buffer to manage acidosis, an osmotic agent to produce ultrafiltration (UF), and electrolytes including sodium, chloride, calcium, and magnesium to maintain homeostasis and prevent metabolic bone disease Yet more than half a century since the introduction of PD as a chronic therapy for replacement of renal function, the ideal PDS remains elusive This likely reflects the diverse nature and diet of patients on PD, the need to customize treatment based on individual peritoneal transport characteristics, the type of dialysis (continuous ambulatory peritoneal dialysis (CAPD) versus automated peritoneal dialysis (APD)), dwell time, residual renal function, age and growth requirements, and accumulating data on the beneficial and harmful effects of PDS including their interaction with other components of CKD management [2] E Harvey (*) Hospital for Sick Children, Department of Pediatrics, University of Toronto, Toronto, ON, Canada e-mail: elizabeth.harvey@sickkids.ca This chapter will review PD solutions including biocompatibility, key composition, specific solutions, new solutions, and membrane preservation strategies Biocompatibility Increasing length of time on PD has been associated with an increase in small solute transport and decreased ultrafiltration, both of which are associated with an increased risk of technique failure and death The pathological correlate of these functional changes was first elucidated by Williams et al in their landmark description of the changes in the peritoneal membrane associated with uremia and PD. These changes were characterized by loss of the mesothelial layer, marked increase in the thickness of the submesothelial compact collagenous zone, and a progressive hyalinizing vasculopathy, with worsening of severity correlating with duration of PD [3] UF failure was associated with increased blood vessel density These changes were attributed in part to the use of “bio-incompatible” PD fluids, characterized by low pH (