0.0 0.5 1.0 1.5 2.0 2.5 3.0 Relative microvessels area (%)
Figure 5 Correlation between the relative microvessels area and D/P b2 microglobulin (rho = 0.52, p = 0.018, n = 22).
nine, but not with RVN and RVA/RVN. No correlation was found between D/P albumin (large molecule) and RVA (Figure 6) or RVN. These observations cannot be explained only by the presence of microvessel dilatation, and therefore other pathology may be present in the PD peritoneum as well.
Increased microvessel surface area may be well reflected by the perfusion volume. In the study mentioned earlier, it was not possible to take into consideration the possible influence of the actual perfusion state of the microvessels. The various microvascular networks are open or closed at different times, and this might have an impact on the transport properties of the membrane. Recently intravital microscopy was introduced in the PD field. It may be helpful to clarify the peritoneal microvessels status during PD.
In PD animal models, the peritoneum has been reported to gain in thickness, and presumably this occurs also in patients on PD. Thus, it can be speculated that the thickening of the peritoneum may provide an increase in the total capillary length, while the density of microvessels does not decrease. However, this has not been elucidated in the clinical study.
The main pathology that alters the vasculatures of the PD peritoneum has not been clarified in patients on PD. However, accumulating studies have reported the important role of some cytokines.
Based on the experimental study, vascular endothelial growth factor (VEGF) is assumed to be the main factor enhancing angiogenesis and vascular permeability. It is expressed in the endothelium lining peritoneal capillaries in the human peritoneal membrane. VEGF is detected in the dialysate from both PD rat model and PD patients. In the rat model it was reported that the dialysate level of VEGF correlates with small-solute transport. Furthermore, VEGF concentration in the effluent is increased as a function of time on CAPD, and it is very closely related with PSTR in PD patients. It was reported that VEGF blockade normalized PSTR in streptozotosin-induced diabetic rats.
VEGF stimulates nitric oxide synthase (NOS) production, leading to the production of nitric oxide (NO). Endothelial NOS (eNOS) is required for angiogenesis and vascular permeability driven by VEGF, and VEGF upregu-lates eNOS production. Therefore, NO plays an important role in the regulation of vascular tone and permeability. In fact, it is reported that NOS production is increased in the peritoneum of long-term CAPD patients. There is an interesting recent report that eNOS4(a/b) gene polymorphism is associated with PSTR at the start of PD in uremic Chinese patients.
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