Epidemiology
Etiology
Pathophysiology
Clinical features
- Renal: Acute hypertensive nephrosclerosis (formerly malignant nephrosclerosis)
- Acute kidney injury (azotemia and/or oliguria, edema) and microhematuria
- 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.
Diagnostics
Treatment
- The drugs most commonly used to treat hypertensive emergencies are nitroprusside, labetalol, and nicardipine.