Download Complement and Kidney Disease by Peter F Zipfel PDF

By Peter F Zipfel

ISBN-10: 3764371668

ISBN-13: 9783764371661

ISBN-10: 3764374284

ISBN-13: 9783764374280

It is clear faulty or deregulated supplement approach ends up in kidney illnesses. a big position of supplement effector and regulatory proteins in pathological settings of the kidney has been tested. a wide panel of particular human kidney illnesses is attributable to faulty supplement keep watch over. Genetic analyses have pointed out mutations in supplement regulators which are linked to those ailments. Mutations were pointed out within the fluid part substitute pathway regulator issue H and the membrane regulator Membrane Cofactor Protein MCP (CD46). The sensible characterization of the mutant proteins permits to outline the pathophysiological occasions on a molecular point. those new ideas and information on disorder mechanisms allowed developing new diagnostic and promising healing methods for a number of human kidney illnesses. Molecular biology, clinics and treatment are mentioned during this volume.

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Extra resources for Complement and Kidney Disease

Example text

Am J Transplant 4: 1562–1566 Lederer SR, Kluth-Pepper B, Schneeberger H, Albert E, Land W, Feucht HE (2001) Impact of humoral alloreactivity early after transplantation on the long-term survival of renal allografts. Kidney Int 59: 334–341 Mauiyyedi S, Pelle PD, Saidman S, Collins AB, Pascual M, Tolkoff-Rubin NE, Williams WW, Cosimi AA, Schneeberger EE, Colvin RB (2001) Chronic humoral rejection: identification of antibody-mediated chronic renal allograft rejection by C4d deposits in peritubular capillaries.

In membranoproliferative glomerulonephritis type I, complement deposition is dominated by C3, though C1q deposition is regularly found. An overview of site and character of complement deposition in various forms of glomerulonephritis is summarized in Table 1. The absence of detectable C1q in the presence of glomerular staining for IgG and C3 does not exclude that the classical pathway is responsible for the complement deposition in these kidneys. Since C1q does not undergo covalent binding to its ligands, in contrast to C4b and C3b, it may have a short half-life and can be difficult to detect.

All of these events are associated with the development of nonspecific inflammatory injury and antigen-specific immune response in the organ graft and recipient. Given the functions in both the innate and adaptive immune responses, complement may play an important role in renal transplantation. Role of complement in renal I/R injury I/R injury is an important form of injury that occurs upon reperfusion of vascularized tissue after an extended period of ischemia. It is an unavoidable event in organ transplantation.

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Complement and Kidney Disease by Peter F Zipfel


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