Arterionephrosclerosis: Progressive,chronicrenaldamageassociatedwithhypertension.Characteristicfeaturesarehyalinearteriolosclerosisandnarrowingofvascularluminawithresultantcorticalatrophy.
Malignant hypertension: Acutekidneyinjuryassociatedwithsevereelevationofbloodpressure.Arteriesandarteriolesshowfibrinoidnecrosisandhyperplasiaofsmoothmusclecells;petechialhemorrhagesappearonthecorticalsurface.
Thrombotic microangiopathies: Disorderscharacterizedbyfibrinthrombiinglomeruliandsmallvesselsresultinginacutekidneyinjury.TypicalHUSisusuallycausedbyendothelialinjurybyanE. coli toxin;TTPisoftencausedbyabnormalitiesinvonWillebrandfactorleadingtoexcessivethrombosis,withplateletconsumption.ThemostcommoncauseofatypicalHUSiscomplement-mediatedendothelialinjuryduetocomplementdysregulation.
Chronic kidney disease is a broad term that describes the final common pathway of progressive nephron loss resulting from any type of kidney disease. Alterations in the function of remaining intact nephrons are ultimately maladaptive and cause further scarring. This eventually results in an end-stage kidney with sclerosed glomeruli, tubules, interstitium and vessels, regardless of the anatomic site of the original injury. Unless the disorder is treated with dialysis or transplantation, death from uremia, electrolyte disturbances, or other complications of end-stage renal disease results.
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As progressive renal damage destroys more and more nephrons, adaptive mechanisms are initated that try to maintain renal function. Among such adaptive mechanisms, glomerular hyperfiltration tends to compensate for decreased glomerular filtration rate resulting from the loss of nephrons. An increase in the rate of excretion of solutes per nephron via increased plasma concentrations (for creatinine), decreased tubular reabsorption (for sodium, phosphate, and calcium), or increased tubular secretion (for potassium and hydrogen ions) helps to maintain homeostasis until the late stages of chronic kidney disease. The rate of functional decline varies based on the original disease; however, renal function often deteriorates progressively even when the original insult is controlled. Uncontrolled hypertension, regardless of the etiology, results in more rapid renal functional decline.
MORPHOLOGYClassically,thekidneysaresymmetrically contracted, andtheirsurfacesarered-brownanddiffusely granular whentheunderlyingdisorderaffectsbloodvesselsorglomeruli.Kidneysdamagedbychronicpyelonephritisaretypicallyunevenlyinvolvedandhavedeepscars.Microscopically,thefeaturecommontoallcasesisadvancedscarringoftheglomeruli,sometimestothepointofcompletesclerosis(
Fig.14.20 ).Thisobliteration of the glomeruli istheendpointofmanydiseases,anditisimpossibletoascertainfromsuchkidneysthenatureoftheinitiallesion.Therealsoismarkedinterstitial fibrosis, associatedwithatrophyanddropoutofmanyofthetubulesinthecortex,anddiminutionandlossofportionsoftheperitubularcapillarynetwork.Thesmall-andmedium-sizedarteriesfrequentlyarethick-walled,withnarrowedlumina,secondarytohypertension.Lymphocytic(and,rarely,plasmacell)infiltratesarepresentinthefibroticinterstitialtissue.Asdamagetoallstructuresprogresses,itmaybecomedifficulttoascertainwhethertheprimarylesionwasglomerular,vascular,tubular,orinterstitial.Suchmarkedlydamagedkidneyshavebeendesignatedend-stage kidneys.