Platelets in Immune Mediated Glomerular Disease

Abstract

Platelets are recognized for their role in hemostasis, but may also act as proinflammatory cells capable of releasing vasoactive, chemotactic, proliferative, and proteolytic factors or enzymes. Platelet activation and localization to glomeruli can be demonstrated in numerous experimental and human glomerular diseases, especially in diseases associated with endothelial cell or mesangial cell injury. Proposed roles for platelets in glomerular injury include initiating glomerular thrombosis, facilitating immune complex deposition, modulating hemodynamic changes and mediating glomerulosclerosis. We have recently demonstrated a critical requirement for platelets in neutrophil-mediated glomerulonephritis. The mechanism may involve an augmentation of neutrophil injury by the platelet or platelet products. Platelets also mediate mesangial cell proliferation in immune complex nephritis. The effect involves a platelet-mediated induction of platelet-derived growth factor (PDGF) and PDGF-receptor synthesis by the mesangial cell, and is also associated with the acquisition by the mesangial cell of a smooth muscle phenotype. Thus, the platelet has important and diverse roles in glomerular inflammation. Platelets can mediate direct effects, such as in the formation of platelet-fibrin thrombi, but may effect glomerular inflammation indirectly via their ability to interact with neutrophils and glomerular mesangial cells.