Complement and Kidney Disease by Peter F Zipfel

By Peter F Zipfel

The knowledge how supplement pertains to glomerular illnesses has advanced significantly over the past years. giant proof has collected that specify how a faulty or deregulated supplement approach leads to kidney illnesses. The mixture and shut interplay of uncomplicated examine with medical medication has tested an enormous function of supplement effector and regulatory proteins in pathological settings of the kidney. a wide panel of designated human kidney illnesses corresponding to hemolytic uremic syndrome (HUS), membrano proliferative glomerulonephritis (MPGN), systemic lupus erythematosus (SLE) and in ischemic reperfusions harm and transplantation are as a result of faulty supplement regulate. Genetic analyses have pointed out mutations in supplement regulators which are linked to those illnesses. Mutations were pointed out within the fluid section 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 strategies and information on ailment mechanisms already allowed to set up new diagnostic and novel promising healing techniques for a number of human kidney illnesses.

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Example text

A more recent study using P-selectin inhibition in C3-deficient mice found that treatment with anti-P-selectin antibody to reduce the neutrophil-mediated renal I/R injury was equally effective in the absence of C3, suggesting that complement- and P-selectin-mediated pathways of renal I/R injury are mutually independent [13]. Thus, complement and P-selectin may pose distinct targets for therapy. Besides investigation in complement-deficient animals, renal I/R injury has also been studied using complement inhibitory reagents, which include a membrane-targeted portion of the complement regulator CR1, C5aR antagonist, anti-C5 mAb and Crry-Ig.

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Renal I/R injury has also been studied in mice with deficiency in complement inhibitors CD55 (decay accelerating factor, DAF) and CD59 [30, 31]. CD55 inhibits complement activation by promoting the breakdown of activated C3 and accelerating decay of the C3 converting enzyme complexes; CD59 protects against complement-mediated cell injury by blocking the formation of the MAC. These two studies showed that mice lacking either CD55 or CD59 are highly susceptible to renal I/R injury [30, 31]. Moreover, double deficiency of CD55/CD59 significantly exacerbates the injury [30].

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