Loss of heparin-binding protein prevents necrotizing glomerulonephritis: first clues hint at plasminogen activator inhibitor-1.

The orchestration of acute inflammatory kidney injury is subject to widespread influences and involves cytokines as well as chemokines released by resident as well as infiltrating cells. Although intense research efforts have been made in the field, it still unravels yet novel key molecules involved in the pathogenesis of this kidney disease. A heparin-binding growth factor denoted midkine is expressed by various cell types following stress of tissue damage. Specific functions relate to orchestration of reparative and inflammatory processes by promoting migration of leucocytes and release of chemokines with ensuing angiogenesis. Midkine appears as a double-edged sword with beneficial or harmful effects in injured tissues. Here, we discuss a recent publication that provides evidence for the beneficial role of midkine in progressive glomerulonephritis, most likely due to blockade of plasminogen activator inhibitor-1 release.