What is the pathophysiology of malignant hypertension?
A rapid and sustained rise in blood pressure causes endothelial dysfunction and then frank arteritis, leading to platelet and fibrin deposition within the vessel and eventually fibrinoid necrosis.
The juxtaglomerular apparatus of the kidney releases renin when it senses relative ischemia, which increases circulating angiotensin II levels and causes severe vasoconstriction. The kidney responds to the elevated blood pressure with natriuresis, causing relative volume depletion and further activating the renin-angiotensin-aldosterone system. These events typically reinforce each other and lead to the “vicious cycle” of increasing blood pressure and worsening vascular function.