All are seen in malignant hypertension except -
Malignant hypertension, defined as blood pressure usually
greater than 200/120 mm Hg, is far less common in the
United States than so-called “benign” hypertension and
occurs in only about 5% of persons with elevated blood
pressure. It may arise de novo (i.e., without preexisting
hypertension), or it may appear suddenly in a person who
had mild hypertension.
Pathogenesis
The basis for this turn for the worse in hypertensive subjects
is unclear, but the following sequence is suggested: The initial
event seems to be some form of vascular damage to the
kidneys. This most commonly results from long-standing
hypertension, with eventual injury to the arteriolar walls. The
result is increased permeability of the small vessels to fibrinogen
and other plasma proteins, endothelial injury, and platelet
deposition. This leads to the appearance of fibrinoid
necrosis of arterioles and small arteries and intravascular
thrombosis. Mitogenic factors from platelets (e.g., plateletderived
growth factor) and plasma cause intimal hyperplasia
of vessels, resulting in the hyperplastic arteriolosclerosis
typical of organizing injury of malignant hypertension and of
morphologically similar thrombotic microangiopathies (see
later) and further narrowing of the lumina. The kidneys
become markedly ischemic.
Fibrinoid necrosis
Hyaline arteriolosclerosis
Necrotizing glomerulonephritis
Hyperplastic arteriolosclerosis