The understanding how complement relates to glomerular diseases
has evolved considerably during the last years. Substantial
evidence has accumulated that explain how a defective or
deregulated complement system results in kidney diseases. The
combination and close interaction of basic research with clinical
medicine has demonstrated an important role of complement effector
and regulatory proteins in pathological settings of the kidney.
A large panel of distinct human kidney diseases such as hemolytic
uremic syndrome (HUS), membrano proliferative glomerulonephritis
(MPGN), systemic lupus erythematosus (SLE) and in ischemic
reperfusions injury and transplantation are caused by defective
complement control. Genetic analyses have identified mutations in
complement regulators that are associated with these diseases.
Mutations have been identified in the fluid phase alternative
pathway regulator Factor H and the membrane regulator Membrane
Cofactor Protein MCP (CD46). The functional characterization of the
mutant proteins allows to define the pathophysiological events on a
molecular level. These new concepts and data on disease mechanisms
already allowed to establish new diagnostic and novel promising
therapeutic approaches for several human kidney diseases.
"synopsis" may belong to another edition of this title.
It is evident that a defective or deregulated complement system results in kidney diseases. An important role of complement effector and regulatory proteins in pathological settings of the kidney has been demonstrated. A large panel of distinct human kidney diseases is caused by defective complement control. Genetic analyses have identified mutations in complement regulators that are associated with these diseases. Mutations have been identified in the fluid phase alternative pathway regulator Factor H and the membrane regulator Membrane Cofactor Protein MCP (CD46). The functional characterization of the mutant proteins allows to define the pathophysiological events on a molecular level. These new concepts and data on disease mechanisms allowed establishing new diagnostic and promising therapeutic approaches for several human kidney diseases. Molecular biology, clinics and therapy are discussed in this volume.
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Buch. Condition: Neu. This item is printed on demand - it takes 3-4 days longer - Neuware -It is evident that a defective or deregulated complement system results in kidney diseases. An important role of complement effector and regulatory proteins in pathological settings of the kidney has been demonstrated. A large panel of distinct human kidney diseases is caused by defective complement control. Genetic analyses have identified mutations in complement regulators that are associated with these diseases. Mutations have been identified in the fluid phase alternative pathway regulator Factor H and the membrane regulator Membrane Cofactor Protein MCP (CD46). The functional characterization of the mutant proteins allows to define the pathophysiological events on a molecular level. These new concepts and data on disease mechanisms allowed establishing new diagnostic and promising therapeutic approaches for several human kidney diseases. Molecular biology, clinics and therapy are discussed in this volume. 236 pp. Englisch. Seller Inventory # 9783764371661
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Gebunden. Condition: New. Dieser Artikel ist ein Print on Demand Artikel und wird nach Ihrer Bestellung fuer Sie gedruckt. Role of genetic mutations in regulator proteinsNew therapies in human kidney diseasesProf. Zipfel is a well renowned scientist in this area of researchThe understanding how complement relates to glomerular diseaseshas evolved con. Seller Inventory # 5279624
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