Prolonged use of the tyrosine kinase inhibitor in a peritoneal dialysis patient with metastatic renal cell carcinoma: possible beneficial effects on peritoneal membrane and peritonitis rates

Increased submesothelial collagen deposition, loss of mesothelial cells and increased peritoneal vascularization of peritoneal membrane with vasculopathy leads to peritoneal fibrosis in a patient on long-term peritoneal dialysis (PD). This vascular proliferation within the peritoneum is associated with an increased expression of vascular endothelial growth factor (VEGF), which in turn leads to functional loss or deterioration of the peritoneal membrane over time. Vascular endothelial growth factor inhibitors may slow or even prevent vascular proliferation and subsequent loss of membrane function in peritoneal dialysis patient. We have observed the anti-VGEF effects of a tyrosine kinase inhibitor, sunitinib maleate, in a patient who was on this medication for renal cell carcinoma with extensive abdominal metastasis. The patient had also been on PD for 26 months at the time of the study. In this patient, the tyrosine kinase inhibitor helped to stabilize the abdominal metastasis as well as the thickness of the peritoneal membrane. The D/P creatinine ratio also remained stable. These observations suggest that this tyrosine kinase inhibitor may have prevented peritoneal membrane angiogenesis. We also observed that the patient did not have any further episode of peritonitis from gut-derived organisms, suggesting that stabilization of the intestinal metastasis prevented the transmural migration of bacteria from the gut, thereby preventing peritonitis.