The peritoneum consists of the parietal peritoneum –
a heterogeneous, serous, semi-permeable membrane that lines the abdominal wall – and the visceral peritoneum, which covers the abdominal organs (Figure 1). Its surface area is approximately 1-2 m2. In males, the peritoneum is a closed-sac system, whereas in females it is an open-sac system with the fallopian tubes and ovaries connecting to the peritoneal cavity. The parietal peritoneum derives its blood supply from the abdominal wall (lumbar, intercostals, and epigastric regions) and drains into the inferior vena cava, while the visceral peritoneum receives its blood supply from the superior mesenteric artery and drains into the portal vein. The total peritoneal blood flow ranges from 50–150 mL/min. The peritoneal cavity, located between the parietal and visceral peritoneum2, contains approximately 100 mL of serous fluid1 and becomes the dialysate compartment during peritoneal dialysis (PD) from which exchange of solutes with the blood can occur1,2. Drainage of the peritoneal cavity is mainly accomplished by the lymphatic system. Importantly, the subdiaphragmatic lymphatic system is responsible for 70-80% of the lymphatic flow from the peritoneal cavity. The lymphatic system also serves as a pathway for the removal of foreign substances and macromolecules. In stable patients undergoing PD, the rate of lymphatic flow varies from 7-20 mL/hr with total fluid losses between 60-91 mL/hr3.
Six Layers of the Peritoneum
The peritoneal membrane is comprised of six layers consisting of the capillary fluid film, capillary endothelium, endothelial basement membrane, interstitium, mesothelium, and the fluid film (Figure 2). It was previously thought that all six layers provided different levels of resistance to solutes, and the mesothelial layer with its large surface area functioned as the dialyzer. However, the three-pore model (below) suggests that the peritoneal capillary is the critical barrier to peritoneal transport.
The Three-Pore Model
The three-pore model (TPM) of the peritoneum defines solute and water transport across the peritoneal capillary through pores of three different sizes: Large, small, and ultra-small pores4. This model has been validated by clinical observations5,6. The large pores range from 10-20 nm (100-250 A°) in size and are formed by clefts between endothelial cells. Large pores are small in numbers, < 0.01% of total pores, and account for < 10% of solute removal (macromolecules). Small pores are more numerous, also formed by clefts between endothelial cells, account for > 90% of solute removal (small solutes) and water, and range from 4-6 nm in diameter. Ultra-small pores, comprised mainly of Aquaporin-1, range in size from 0.4-0.6 nm and are transcellular channels in the endothelial cells that transport water only and provide 0% of solute removal. The transport of water via the Aquaporin-1 is also known as “free-water transport” and contributes to ~50% of the ultrafiltration in PD4,7.
Although this model suggests that the interstitium may also contribute to resistance to solute transport, there is no resistance from the mesothelium itself or from stagnant fluid layers. Additional research has expanded on this model. Ronco proposed that the peritoneal vasculature, particularly the surface area of the peritoneal capillaries, rather than the entire surface area of the peritoneum and the interstitium, is responsible for facilitating solute transport8. Specifically, the distance of each peritoneal capillary from the mesothelium determines that capillary’s relative contribution to effective surface area and the resistance properties of the membrane. This concept is called the “nearest capillary hypothesis”, where the capillaries closer to the mesothelium experience a greater osmotic effect compared to those farther away. Since patients with the same total peritoneal surface area may have very different degrees of peritoneal vascularity, their effective peritoneal surface areas would also vary widely. Moreover, in a single patient, peritoneal surface area may be altered by specific events such as episodes of peritonitis9.
- Blake PG, Daugirdas JT. Physiology of Peritoneal Dialysis. In: Daugirdas JT, Blake PG, Ing TS, eds. Handbook of Dialysis. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007:323-338.
- Flessner MF. Peritoneal transport physiology: insights from basic research. J Am Soc Nephrol. 1991;2(2):122-35. www.ncbi.nlm.nih.gov/pubmed/1954325
- Flessner MF. Solute and water transport across the peritoneal membrane. In: Ronco C, Bellomo R, Kellum JA, eds. Critical Care Nephrology. 2nd ed. Philadelphia, PA: Saunders Elsevier; 2009:1472-1478.
- Devuyst O, Rippe B. Water transport across the peritoneal membrane. Kidney Int. 2014;85(4):750-8. www.ncbi.nlm.nih.gov/pubmed/23802191
- Rippe B, Stelin G. Simulations of peritoneal solute transport during CAPD. Application of two-pore formalism. Kidney Int. 1989;35(5):1234-44. www.ncbi.nlm.nih.gov/pubmed/2770105
- Rippe B, Stelin G, Haraldsson B. Computer simulations of peritoneal fluid transport in CAPD. Kidney Int. 1991;40(2):315-25. www.ncbi.nlm.nih.gov/pubmed/1942781
- Ipema KJR, van der Schans CP, Vonk N, de Vries JM, Westerhuis R, Duym E, Franssen CFM. A difference between day and night: protein intake improves after the transition from conventional to frequent nocturnal home hemodialysis. J Ren Nutr. 2012;22(3):365-72. www.ncbi.nlm.nih.gov/pubmed/22054873
- Ronco C. The “nearest capillary” hypothesis: a novel approach to peritoneal transport physiology. Perit Dial Int. 1996;16(2):121-5. www.ncbi.nlm.nih.gov/pubmed/9147543
- Holmes CJ. Abnormalities of Host Defense Mechanisms During Peritoneal Dialysis. In: Nissenson AR, Fine RN, eds. Dialysis Therapy. 3rd ed. Philadelphia, PA: Hanley & Belfus; 2002:235-238.
P/N 102479-01 Rev. A 12/2014