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<p>Assessing buffer base kinetics in dialysate using the three-pore model of peritoneal transport is not enough to predict changes to the acid-base equilibrium in blood during peritoneal dialysis (PD). We complemented the three-pore model with a model of acid-base homeostasis to evaluate differences between PD sessions using dialysis fluid buffered with lactate (PD4) or bicarbonate/lactate (B/L). Six patients underwent two 4-hour dwells with either B/L or PD4; blood and peritoneal fluid sampling was used to quantify intraperitoneal volume—using a radioiodinated albumin as volume marker—and solute concentrations. The integrated model describes CO<sub>2</sub> and O<sub>2</sub> transport across central circulation and tissues, predicting changes in acid-base equilibrium driven by peritoneal transport of bicarbonate, lactate, and dissolved CO<sub>2</sub>. The model accurately predicted dialysate concentrations of bicarbonate and dissolved CO<sub>2</sub>, with errors in the range 5–10% of measured values for both fluids, and with similar prediction errors for plasma concentrations despite tuning the model to dialysate data only. Estimated transport parameters fell into the expected ranges and were generally comparable between fluids. These results validate our understanding of transport kinetics and acid-base homeostasis during PD, demonstrating that different buffer compositions do not appear to impact small solute transport nor mechanisms of acid-base regulation.</p>

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Mathematical modeling of peritoneal buffer transport and acidosis correction in patients on peritoneal dialysis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月4日

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  • M. Pietribiasi,
  • J. Stachowska-Pietka,
  • J. Waniewski,
  • B. Lindholm,
  • O. Heimbürger

摘要

Assessing buffer base kinetics in dialysate using the three-pore model of peritoneal transport is not enough to predict changes to the acid-base equilibrium in blood during peritoneal dialysis (PD). We complemented the three-pore model with a model of acid-base homeostasis to evaluate differences between PD sessions using dialysis fluid buffered with lactate (PD4) or bicarbonate/lactate (B/L). Six patients underwent two 4-hour dwells with either B/L or PD4; blood and peritoneal fluid sampling was used to quantify intraperitoneal volume—using a radioiodinated albumin as volume marker—and solute concentrations. The integrated model describes CO2 and O2 transport across central circulation and tissues, predicting changes in acid-base equilibrium driven by peritoneal transport of bicarbonate, lactate, and dissolved CO2. The model accurately predicted dialysate concentrations of bicarbonate and dissolved CO2, with errors in the range 5–10% of measured values for both fluids, and with similar prediction errors for plasma concentrations despite tuning the model to dialysate data only. Estimated transport parameters fell into the expected ranges and were generally comparable between fluids. These results validate our understanding of transport kinetics and acid-base homeostasis during PD, demonstrating that different buffer compositions do not appear to impact small solute transport nor mechanisms of acid-base regulation.