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.