Abstract
Glucose is an osmotic agent in the peritoneal dialysis fluid (PDF) to absorb water, sodium and other toxins. Glucose absorption from PDF to blood impairs peritoneal dialysis (PD) efficiency and cause glycemic burden. This extra glycemic load leads to poor glycemic control in diabetic dialysis patients with PD program. Studies have shown sodium-glucose co-transporter (SGLT)-2 expression in peritoneal mesothelial cells. Blockade of peritoneal SGLT reduced blood glucose increment and increased peritoneal glucose retention in mice. In rat models, it was shown that high glucose PDF promotes the peritoneal fibrosis by upregulating the expression of glucose transporter (GLUT) and SGLT, and addition of phlorizin to PDF leads to downregulation of GLUT and SGLT expression and reduced peritoneal degeneration. According to these information, we want to share our experience of using empagliflozin in a poor glycemic controlled type 2 diabetic patient, who was on PD program for end-stage renal disease. We hypothesized that if we administer empagliflozin to our patient we can reduce glycemic burden caused by PDF and increase the ultrafiltration volume.
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