Pathophysiology: severe hypertension → acute thrombotic microangiopathy → thrombosis of glomerular capillaries and red blood cell extravasation and fragmentation as well as luminal thrombosis of arterioles → infarction and necrosis of endothelial and mesangial cells → decreased glomerular blood flow → acute kidney damage
Histopathologic patterns
Fibrinoid necrosis: Cell death and excessive fibrin deposition within the arteriolar walls is visible as circumferential, amorphous, pink material with smudged, necrotic endothelial cells that lack cytologic detail.
Hyperplastic arteriolosclerosis: Over time, activated platelets and injured endothelial cells release growth factors, which induce concentric hyperplasia and layering of smooth muscle cells and collagen, resulting in intimal thickening and an “onion-skin” appearance.