The key findings were the clear signs of progressive glomerular endothelial and immune cell activation already in an early phase of disease pathogenesis, and included severely distended glomerular capillaries, aneurysms and microthrombi, increased glomerular endothelial glycocalyx thickness and immune cell homing, and albumin leakage through the damaged GFB. The gene discussed is ALB; the disease is aneurysm.