The kidney kallikrein-kinin system plays important roles in inflammation, coagulation, angiogenesis, and regulation of vessel tone and permeability. In this issue of the JCI, Liu et al. provide data that suggest a protective role for kallikrein in animal models of anti–glomerular basement membrane (GBM) antibody–induced nephritis, an experimental model of Goodpasture disease (see the related article beginning on page 911). Furthermore, human systemic lupus erythematosus and lupus nephritis were shown to be associated with kallikrein 1 (KLK1) and the KLK3 promoter. The authors suggest that kallikrein genes are involved in the development of SLE and lupus nephritis and may exert a renoprotective role. It is possible, however, that the kallikrein-kinin system may play dual roles: protecting the kidney against ischemia and interstitial fibrosis while also mediating vasodilation, inflammation, and activation of the innate immune response
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