Fig.14.17 ).Astrikingadditionalfindingisthepresenceofproteinaceouscastsinthedistaltubulesandcollectingducts,whichconsistofTamm-Horsfallprotein(normallysecretedbytubularepithelium)alongwithhemoglobinandotherplasmaproteins.WhencrushinjurieshaveproducedATI,thecastsalsocontainmyoglobin.Theinterstitiumusuallyshowsgeneralizededemaalongwithamildinflammatoryinfiltrateconsistingofneutrophils,lymphocytes,andplasmacells.Thehistologicpictureinnephrotoxic ATI isbasicallysimilar,withsomedifferences.OvertnecrosisisusuallymoreprominentintheproximaltubulethaninischemicATI,andthetubularbasementmembranesgenerallyarespared.
Ifthepatientsurvives,epithelialregenerationbecomesapparentintheformofalowcuboidalepithelialcoveringandmitoticactivityinthesurvivingtubularepithelialcells.Insomecases,forreasonsthatarenotentirelyclear,acutekidneyinjurywithunderlyingacutetubularinjuryasitscausemayresultintubularatrophyandinterstitialfibrosisratherthanrepair.
The clinical course of ischemic ATI initially is dominated by the inciting medical, surgical or obstetric event. Affected patients often present with manifestations of acute kidney injury, including oliguria and decreased GFR. Not all patients have oliguria; both anuric and non-oligouric forms are seen. The clinical picture is often dominated by electrolyte abnormalities, acidosis, and the signs and symptoms of uremia and fluid overload. The prognosis varies depending upon the severity and nature of the underlying injury and comorbid conditions. In the absence of supportive treatment or dialysis, patients may die. When the cause of acute kidney injury is ATI, repair and tubular regeneration lead to gradual clinical improvement. With supportive care, patients who survive have a good chance of recovering renal function, but a single severe episode of ATI also may result in chronic kidney disease. In those with preexisting chronic kidney disease, complete recovery is less frequent, and progression to end-stage renal disease is unfortunately common.
Fig. 14.17 Acutetubularepithelialcellinjurywithblebbingattheluminalpole,detachmentoftubularcellsfromtheirunderlyingbasementmem-branes,andgranularcasts.
ATIisthemostcommoncauseofacutekidneyinjury;itsclinicalmanifestationsareelectrolyteabnormalities,acidosis,uremia,andsignsoffluidoverload,oftenwitholiguria.
ATIresultsfromischemicortoxicinjurytorenaltubules,andisassociatedwithintrarenalvasoconstrictionresultinginreducedGFRanddiminisheddeliveryofoxygenandnutrientstotubularepithelialcells.
ATIischaracterizedmorphologicallybyinjuryornecrosisofsegmentsofthetubules(typicallytheproximaltubules),proteinaceouscastsindistaltubules,andinterstitialedema.
Nearly all diseases of the kidney affect the renal blood vessels secondarily. Systemic vascular diseases, such as various forms of vasculitis, also involve renal blood vessels, and often produce clinically important effects on renal function (Chapter 10). Conversely, the kidney is intimately involved in the pathogenesis of both essential and secondary hypertension. This section covers the renal lesions associated with hypertension.