Injury resulting from long-standing hypertension causes increased permeability of the 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., platelet-derived growth factor) and plasma cause intimal hyperplasia of vessels, resulting in hyperplastic arteriosclerosis. Because of the luminal narrowing, the kidneys become markedly ischemic, which leads to further elevation of blood pressure via the renin-angiotensin system.
MORPHOLOGYThekidneymaybenormalinsizeorshrunken,dependingonthedurationandseverityofthehypertensivedisease.Small,pinpoint petechial hemorrhages mayappearonthecorticalsurfacefromruptureofarteriolesorglomerularcapillaries,givingthekidneyapeculiar,flea-bitten appearance.
Themicroscopicchangesreflectthepathogeneticeventsdiscussedearlier.Damagetothesmallvesselsismanifestedasfibrinoid necrosis ofthearterioles(
Fig.14.19A ).Thevesselwallsshowahomogeneous,granulareosinophilicappearancemaskingunderlyingdetail.Intheinterlobulararteriesandlargerarterioles,proliferationofintimalcellsafteracuteinjuryproducesanonion-skin appearance(see
Fig.14.19B ).Thisnameisderivedfromtheconcentricarrangementofcellswhoseoriginisbelievedtobeintimalsmoothmuscle,althoughthisissuehasnotbeenfinallysettled.Thislesion,calledhyperplastic arteriolosclerosis, causesmarkednarrowingofarteriolesandsmallarteries,tothepointoftotalobliteration.Necrosisalsomayinvolveglomeruli,withmicrothrombiwithintheglomeruliaswellasnecroticarterioles.Similarlesionsareseeninindividualswithacutethromboticmicroangiopathies(discussedlater),andinpatientswithsclerodermainrenalcrisis.
The full-blown syndrome of malignant hypertension is characterized by papilledema, encephalopathy, cardiovascular abnormalities, and renal failure. Most often, the early symptoms are related to increased intracranial pressure and include headache, nausea, vomiting, and visual impairment, particularly the development of scotomas, or “spots” before the http://ebooksmedicine.net
Fig. 14.19 Malignanthypertension.(A)Fibrinoidnecrosisofafferentarteriole(periodicacid–Schiffstain).(B)Hyperplasticarteriolosclerosis(onion-skinlesion).(Courtesy of Dr. H. Rennke, Department of Pathology, Brigham and Women’s Hospital, Boston, Massachusetts.) eyes. At the onset of rapidly mounting blood pressure, there is marked proteinuria and microscopic, or sometimes macroscopic, hematuria but no significant alteration in renal function. Soon, however, acute kidney injury develops. The syndrome represents a true medical emergency that requires prompt and aggressive anti-hypertensive therapy before irreversible renal lesions develop. About 50% of patients survive at least 5 years; 90% of deaths are caused by uremia, and the other 10% are caused by cerebral hemorrhage or cardiac failure.