Quantification Using Target Marker VEGFR2 for the Effect of Peritoneal Dialysis and Treatments to Inhibit Angiogenesis
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End stage renal disease leaves patients with only two options in order to survive: receive a kidney transplant or go on dialysis. Patients who choose peritoneal dialysis (PD) generally want more autonomy because it allows them to carry out their regular daily living in opposition to hemodialysis. The major limitation of PD as a technique is failure of the peritoneal membrane to continue to clear poisons from the blood (e.g. dialyze) or failure of the membrane to excrete fluid (ultrafiltration). Hypervascularity and angiogenesis contribute to these failures because the increased vessel growth causes the dialysate glucose to get absorbed back in the blood. The present study aimed to use a cell marker, VEGFR2, that causes vessel growth and quantify its levels in PD along with various treatments. VEGFR2 is known to play a key role in angiogenesis. Its expression levels were measured in rats under 6 different conditions. Three of the conditions, rats were treated with dialysis and either losartan, JAK inhibitor, or both losartan and JAKi. JAKi is used to counteract the membrane injury that PD causes. After treating the rats for four months in these conditions, immunohistochemistry was done in order to stain for the VEGFR2. Quantification of the cells was done through a program called Qu Path then the data was averaged, and the results were compared across groups. In our findings, there was increased VEGFR2 expression in the dialysis group compared to controls and the groups that received treatments. Allow conclusions can’t be made this follows our hypothesis that VEGFR2 plays a key role in the decreased membrane functionality and angiogenesis observed in PD patients. Small sample size may have influenced the statistical outcome. Future research would benefit from a larger sample size. Other factors that lead to peritoneal membrane failure in PD should also be explored.