The complement system is considered to be an important part of innate immune system with a significant role in inflammation processes. The activation can occur through classical, alternative, or lectin pathway, resulting in the creation of anaphylatoxins C3a and C5a, possessing a vast spectrum of immune functions, and the assembly of terminal complement cascade, capable of direct cell lysis. The activation processes are tightly regulated; inappropriate activation of the complement cascade plays a significant role in many renal diseases including organ transplantation. Moreover, complement cascade is activated during ischemia/reperfusion injury processes and influences delayed graft function of kidney allografts. Interestingly, complement system has been found to play a role in both acute cellular and antibody-mediated rejections and thrombotic microangiopathy. Therefore, complement system may represent an interesting therapeutical target in kidney transplant pathologies.

• Keywords
• antibody-mediated rejection, anticomplement therapy, complement, ischemia/reperfusion injury, kidney transplantation,
• Publication type
• Journal Article MeSH
• Review MeSH

Angiogenesis is a vessel development process that maintains the vascular supply for organ function. Regulation of angiogenesis is provided by positive factors, such as vascular endothelial or basic fibroblast growth factors, and negative factors, such as thrombospondin and macrophage-derived inflammatory cytokines. While the role of angiogenesis in the wound healing, embryogenesis, tumor growth and proliferative diseases is clear, in organ transplantation it is not yet well established. Herein we discuss the potential role of angiogenesis in chronic renal disease and in transplant settings.

• MeSH
• Angiopoietins physiology   MeSH
• Models, Biological MeSH
• Fibroblast Growth Factor 2 physiology   MeSH
• Neovascularization, Physiologic * MeSH
• Hepatocyte Growth Factor physiology   MeSH
• Kidney blood supply   injuries   MeSH
• Humans MeSH
• Ribonuclease, Pancreatic physiology   MeSH
• Neovascularization, Pathologic * MeSH
• Graft Rejection MeSH
• Transforming Growth Factor beta physiology   MeSH
• Transforming Growth Factor beta1 MeSH
• Organ Transplantation * MeSH
• Vascular Endothelial Growth Factor A physiology   MeSH
• Animals MeSH
• Check Tag
• Humans MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Review MeSH
• Names of Substances
• angiogenin MeSH Browser
• Angiopoietins MeSH
• Fibroblast Growth Factor 2 MeSH
• Hepatocyte Growth Factor MeSH
• Ribonuclease, Pancreatic MeSH
• TGFB1 protein, human MeSH Browser
• Transforming Growth Factor beta MeSH
• Transforming Growth Factor beta1 MeSH
• Vascular Endothelial Growth Factor A MeSH