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Purinergic signaling by 5\u2032-ectonucleotidase, CD73, an enzyme that converts AMP to adenosine on the extracellular surface, can suppress inflammation. The role of CD73 in progressive kidney fibrosis has not been elucidated. We evaluated the effect of deletion of CD73 from kidney perivascular cells (including pericytes and\/or fibroblasts of the Foxd1<jats:sup>+<\/jats:sup>lineage) on fibrosis. Perivascular cell expression of CD73 was necessary to suppress inflammation and prevent kidney fibrosis in Foxd1CreCD73<jats:sup>fl\/fl<\/jats:sup>mice evaluated 14 days after unilateral ischemia-reperfusion injury or folic acid treatment (250 mg\/kg). Kidneys of Foxd1CreCD73<jats:sup>fl\/fl<\/jats:sup>mice had greater collagen deposition, expression of proinflammatory markers (including various macrophage markers), and platelet-derived growth factor recepetor-\u03b2 immunoreactivity than CD73<jats:sup>fl\/fl<\/jats:sup>mice. Kidney dysfunction and fibrosis were rescued by administration of soluble CD73 or by macrophage deletion. Isolated CD73<jats:sup>\u2212\/\u2212<\/jats:sup>kidney pericytes displayed an activated phenotype (increased proliferation and \u03b1-smooth muscle actin mRNA expression) compared with wild-type controls. In conclusion, CD73 in perivascular cells may act to suppress myofibroblast transformation and influence macrophages to promote a wound healing response. 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