Nephrosclerosis refers to sclerosis of small renal arteries and arterioles that is strongly associated with hypertension. The characteristic morphologic alterations of the small arterioles are called hyaline arteriolosclerosis, while the arteries show fibrous intimal and medial thickening often resulting in luminal narrowing. The vascular changes cause ischemia, which leads to various combinations of interstitial fibrosis, tubular atrophy, and focal global glomerulosclerosis. Some degree of nephrosclerosis, albeit mild, is present in many individuals older than 60 years of age. The frequency and severity of the lesions are increased at any age when hypertension or diabetes are present. Of note, many renal diseases cause hypertension, which in turn is associated with nephrosclerosis. Thus, this renal lesion often is superimposed on other primary kidney diseases.
The arterial lesions associated with hypertension are the result mainly of endothelial dysfunction and platelet activation (Chapter 10). Two processes participate in the arterial lesions of nephrosclerosis: http://ebooksmedicine.net
Medial and intimal thickening, as a response to hemodynamic changes, aging, genetic defects, or some combination of these
Hyalinization of arteriolar walls, caused by extravasation of plasma proteins through injured endothelium and by increased deposition of basement membrane matrix
MORPHOLOGYGrossly,thekidneysaresymmetrically atrophic. Typicallytherenalsurfaceshowsdiffuse,finegranularitythatresemblesgrainleather.Microscopically,themostprominentchangeishyalinethickeningofthewallsofthearterioles,knownashyaline arteriolosclerosis. Thisappearsasahomogeneous,pinkhyalinethickening,attheexpenseofthevessellumina,withlossofunderlyingcellulardetail(
Fig.14.18 ).Thenarrowingofthelumenresultsinmarkedlydecreasedbloodflowthroughtheaffectedvessels,withconsequentischemiaandrenalatrophy.Inadvancedcasesofarterionephrosclerosis,theglomerulartuftsmaybecomesclerosed.Diffusetubularatrophyandinterstitialfibrosisarepresent,butinflammatoryinflltratesareabsentorscant.Thelargerbloodvessels(interlobarandarcuatearteries)showintimalthickeningwithreplicationofinternalelasticlaminaalongwithfibrousthickeningofthemedia(fibroelastic hyperplasia).
This renal lesion alone rarely causes damage severe enough to produce renal failure, except in individuals from some, possibly genetically susceptible, groups, such as African Americans, in whom it may lead to uremia and death. However, all patients usually show some functional impairment, such as loss of concentrating ability or a variably diminished GFR. A mild degree of proteinuria is a frequent finding.
Fig. 14.18 Benignnephrosclerosis.High-powerviewoftwoarterioleswithhyalinedeposition,markedthickeningofthewalls,andanarrowedlumen.
(Courtesy of Dr. M.A.Venkatachalam, Department of Pathology, University of Texas Health Sciences Center, San Antonio,Texas.)
Malignant hypertension, defined as blood pressure usually greater than 200/120 mm Hg, is far less common in the United States than essential hypertension and occurs in only about 5% of hypertensive individuals. It may arise de novo (i.e., without preexisting hypertension), or it may appear suddenly in an individual who had mild hypertension. The prevalence of malignant hypertension is higher in developing countries. It may present with severe acute kidney injury and renal failure. Renal changes are confined to the vasculature and may include thrombotic microangiopathy.
The renal changes are related to hypertension and the reactions to it.