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This Concept Map, created with IHMC CmapTools, has information related to: Kidney II, Renal Pathology II Renal Calculi/Stones UROLITHIASIS -mostly in kidney -MEN>wm, 20-30yo -fam, hereditary predisposition -IEMs-gout, cystinuria, etc. -mucoprotein in all -most imp't factor-concentration of stones' constituents in urine 4 types: Calcium Oxalate--75%-radiopaque -hypercalcemia, hypercalciuria -uric acid can nucleate Ca stones Struvite-'triple stones'-Mg-NH3-PO4 -after urea-splitting bac-Proteus ->largest-staghorn calculi Uric Acid-gout, rapid cell TO (leukemia) -most w/ NL urate amt-low urine pH -radiolucent Cystine-genetic defects in Cys reabsorp OTHER, RENAL CELL CA - OLD MEN (Hypernephroma, AdenoCA) 85% of renal CA Risk fx: smoking, esp pipe/cigar, obesity, HTN, unopposed estrogen Tx, asbestos, petroleum products, heavy metals -CRF, acquired cystic dz, tuberous sclerosis -mostly sporadic, some familial AD in younger -Von Hippel-Lindau syndrome-2/3 pts->RCC -hemangioblastomas or CBLM, retina -VHL gene->familial & sporadic clear cell -Hered (fam) clear cell CA-VHL w/ just CA -Hered papillary CA-AD-multiple bilateral CA -MET protooncogene mutations MORPH-can fungate into coll system->ureter OR R vein->IVC->rt heart -sarcomatoid changes in all infreq'ly-ominous CLINICAL-hematuria, CVA pain, palpable mass -in only 10% ->silent til big enough->constitutional Sx MIMICS-ABNL hormone production=>polycythemia, HTN, hepatic dysfcn, hyperCa, feminize, masc'ize, Cushing syndrome, eosinophilia, amyloidosis, leukemoid rxns WIDE METS->lungs>bones>regional LNs>liver >adrenals>brain Px-5yr-45-70% survival w/out mets -renal vein, perirenal fat involved-15-20% Tx-nephrectomy Classification Collecting duct CA-rare -irregular channels -atyp epith w/ hobnail pattern, Renal Pathology II Diseases of Vessels BENIGN NEPHROSCLEROSIS -sclerosis of renal aa'oles, small aa ->focal ischemia -BLACKS>whites, w/ HTN, DM PATHOGENESIS- -medial & intimal thickening -genetic or due to hemodynamics -hyaline deposition (injured epith) MORPH-NL or moderately smaller size -fine, even granularity on surface (Grain leather resemblance) -interlobular, arcuate aa -fibroelastic hyperplasia->narrowing ->some ischemic atrophy-tub atrophy, interstit fibrosis, collapsed GBMs, coll deposits in Bowman->sclerosis CLINICAL-unusually->renal insuff, uremia RISK-BLACKS, higher HTN, DM, Renal Pathology II Diseases of Vessels MALIGNANT NEPHROSCLEROSIS -via MALIG/ACCELERATED HTN -in scleroderma pts->uremia -YOUNG BLACK MEN Pathogenesis -vasc dmg to kidneys (long-standing HTN) ->increase perm to fibrinogen, other PPs ->fibrinoid necrosis (w/ plts, injury) (PAS(+)) (can->necrotizing arteriolitis) ->intravasc thrombosis ->hyperplastic arteriolosclerosis -interlobular aa-onion-skinning ->necrotizing glomerulitis ->ischemic kidneys->RENIN MORPH-flea-bitten kidney (pinpoint hemorrhs) CLINICAL -diastolicmmHg+endo organ dmg (eye, brain, CV, kidney) -increased ICP->HA, N/V, visual scotomas -HTNive crises-lose consciousness, convulse -proteinuria w/ renal failure -medical emergency Px-75% survive 5 yrs, 50% w/ precrisis renal fcn, Renal Pathology II Diseases of Vessels THROMBOTIC MICROANGIOPATHIES -thrombosis in caps, aa'oles thruout body CLINICAL-microangiopathic hemolytic anemia, TCP, renal failure (plt-fibrin thrombi in interlob aa, gloms, necrotic, thickened of vessel walls) MORPH-like malignant HTN, but not necessarily w/ HTN PATHOGENESIS->distal ischemia via: dz -ɭ. endoth injury->thrombosis -less PGI2, NO; activated endoth -ɮ. plt aggregation-via lots of vWF, calpain (cysteine protease), THROMBOTIC MICROANGIOPATHIES -thrombosis in caps, aa'oles thruout body CLINICAL-microangiopathic hemolytic anemia, TCP, renal failure (plt-fibrin thrombi in interlob aa, gloms, necrotic, thickened of vessel walls) MORPH-like malignant HTN, but not necessarily w/ HTN PATHOGENESIS->distal ischemia via: dz -ɭ. endoth injury->thrombosis -less PGI2, NO; activated endoth -ɮ. plt aggregation-via lots of vWF, calpain (cysteine protease) Diseases IDIOPATHIC HUS/TTP-WOMEN មyo -fever, neuro Sx, hemolytic anemia, TCP purpura, thrombi in glom caps/aff aa'ols -classic TTP-CNS -dominant Sx -renal in 50% -eosinophilic granular thrombi -mostly plts Tx-exchange transfusion, corticosteroids, Renal Pathology II Benign Tumors RENAL FIBROMA/HAMARTOMA -features of renal interstitial cells (Renomedullary Interstit Cell tumor) -small foci fo gray-white firm tissue əcm diameter in pyramids -fibroblast-like cells, collagenous tissue, THROMBOTIC MICROANGIOPATHIES -thrombosis in caps, aa'oles thruout body CLINICAL-microangiopathic hemolytic anemia, TCP, renal failure (plt-fibrin thrombi in interlob aa, gloms, necrotic, thickened of vessel walls) MORPH-like malignant HTN, but not necessarily w/ HTN PATHOGENESIS->distal ischemia via: dz -ɭ. endoth injury->thrombosis -less PGI2, NO; activated endoth -ɮ. plt aggregation-via lots of vWF, calpain (cysteine protease) Diseases ADULT HUS/TTP 1. w/ infx-typhoid, E.coli septicemia, shigellosis, Endotoxin, Shiga toxin 2. antiphospholipid syndrome-SLE (lupus anticoagulant) 3. preg complications or post-partum =post-partum renal failure -MA hemo anemia, olig-,anuria, HTN ->grave prognosis 4. vasc renal diseases-scleroderma, malig HTN 5. CTX, immunosupps-mitomycin, cyclosporin, bleomycin, cisplatin, THROMBOTIC MICROANGIOPATHIES -thrombosis in caps, aa'oles thruout body CLINICAL-microangiopathic hemolytic anemia, TCP, renal failure (plt-fibrin thrombi in interlob aa, gloms, necrotic, thickened of vessel walls) MORPH-like malignant HTN, but not necessarily w/ HTN PATHOGENESIS->distal ischemia via: dz -ɭ. endoth injury->thrombosis -less PGI2, NO; activated endoth -ɮ. plt aggregation-via lots of vWF, calpain (cysteine protease) Diseases CLASSIC (CHILDHOOD) HUS -75% after EHEC (O157:H7) -verocytotoxin (bac)->injury -similar to Shiga toxin ->WBC adhesion, loss of NO ->inc'd endothelin->constrict -one of main causes of ARF in kids CLINICAL - HTN in half of pts -acute after GI, flu-like prodrome -hematemesis, melena -severe oliguria, hematuria -anemia->neuro changes in some MORPH-renal cortical necrosis -thickened glom cap walls -fibrin-like deposits in caps, subendoth, mesang -fibrinoid necrosis, int hyperplasia -interlobular, aff aa'oles Tx-dialysis-recover in weeks -many w/ later renal failure (15-25yrs), Renal Pathology II Benign Tumors ANGIOMYOLIPOMA -vessels, sm. mm., fat -25-50% of tuberous sclerosis pts -lesions of cerebral cortex ->epilepsy, MR, skin ABNLities, RENAL CELL CA - OLD MEN (Hypernephroma, AdenoCA) 85% of renal CA Risk fx: smoking, esp pipe/cigar, obesity, HTN, unopposed estrogen Tx, asbestos, petroleum products, heavy metals -CRF, acquired cystic dz, tuberous sclerosis -mostly sporadic, some familial AD in younger -Von Hippel-Lindau syndrome-2/3 pts->RCC -hemangioblastomas or CBLM, retina -VHL gene->familial & sporadic clear cell -Hered (fam) clear cell CA-VHL w/ just CA -Hered papillary CA-AD-multiple bilateral CA -MET protooncogene mutations MORPH-can fungate into coll system->ureter OR R vein->IVC->rt heart -sarcomatoid changes in all infreq'ly-ominous CLINICAL-hematuria, CVA pain, palpable mass -in only 10% ->silent til big enough->constitutional Sx MIMICS-ABNL hormone production=>polycythemia, HTN, hepatic dysfcn, hyperCa, feminize, masc'ize, Cushing syndrome, eosinophilia, amyloidosis, leukemoid rxns WIDE METS->lungs>bones>regional LNs>liver >adrenals>brain Px-5yr-45-70% survival w/out mets -renal vein, perirenal fat involved-15-20% Tx-nephrectomy Classification PAPILLARY CA-10-15% sporadic-trisomies 7, 16, 17, t(X;1) PRCC on chrom 1-in kids familial-trisomy 7-MET-protooncogene MORPH-multifocal, bilateral -hemorrhagic, cystic -papillae-golden yellow flakes -cuboidal or low col cells -interstitial foam cells in pap cores -can have psammoma bodies -scanty, highly vascularized stroma, Renal Pathology II Benign Tumors RENAL PAPILLARY ADEMONA -origin in renal tubules -found at autopsy in 7-22% MORPH-small, cortex -pale, yellow-gray -complex, branching, papillomatous structures -cuboidal-polygonal cells -small central nuclei -clear cytoplasm -looks like low-grade pap RCadenoCA -trisomies 7, 17 -possible early CAs until proven o/w, RENAL CELL CA - OLD MEN (Hypernephroma, AdenoCA) 85% of renal CA Risk fx: smoking, esp pipe/cigar, obesity, HTN, unopposed estrogen Tx, asbestos, petroleum products, heavy metals -CRF, acquired cystic dz, tuberous sclerosis -mostly sporadic, some familial AD in younger -Von Hippel-Lindau syndrome-2/3 pts->RCC -hemangioblastomas or CBLM, retina -VHL gene->familial & sporadic clear cell -Hered (fam) clear cell CA-VHL w/ just CA -Hered papillary CA-AD-multiple bilateral CA -MET protooncogene mutations MORPH-can fungate into coll system->ureter OR R vein->IVC->rt heart -sarcomatoid changes in all infreq'ly-ominous CLINICAL-hematuria, CVA pain, palpable mass -in only 10% ->silent til big enough->constitutional Sx MIMICS-ABNL hormone production=>polycythemia, HTN, hepatic dysfcn, hyperCa, feminize, masc'ize, Cushing syndrome, eosinophilia, amyloidosis, leukemoid rxns WIDE METS->lungs>bones>regional LNs>liver >adrenals>brain Px-5yr-45-70% survival w/out mets -renal vein, perirenal fat involved-15-20% Tx-nephrectomy Classification CLEAR CELL (nonpap) CA -70-80% RCCs -fam, sporadic, or VHL syn -deletion/translocation of VHL gene -chrom 3p-t. suppressor gene->elongin MORPH-solitary lesions-upper pole -spherical, sharply-defined, 3-15cm -parts can be cystic -most well-diff'd -some ischemic, hemorrhagic areas -solid, trabecular, or tubular growth -clear cells w/ glycogen, lipids in cyto, Renal Pathology II Malignant Tumors RENAL CELL CA - OLD MEN (Hypernephroma, AdenoCA) 85% of renal CA Risk fx: smoking, esp pipe/cigar, obesity, HTN, unopposed estrogen Tx, asbestos, petroleum products, heavy metals -CRF, acquired cystic dz, tuberous sclerosis -mostly sporadic, some familial AD in younger -Von Hippel-Lindau syndrome-2/3 pts->RCC -hemangioblastomas or CBLM, retina -VHL gene->familial & sporadic clear cell -Hered (fam) clear cell CA-VHL w/ just CA -Hered papillary CA-AD-multiple bilateral CA -MET protooncogene mutations MORPH-can fungate into coll system->ureter OR R vein->IVC->rt heart -sarcomatoid changes in all infreq'ly-ominous CLINICAL-hematuria, CVA pain, palpable mass -in only 10% ->silent til big enough->constitutional Sx MIMICS-ABNL hormone production=>polycythemia, HTN, hepatic dysfcn, hyperCa, feminize, masc'ize, Cushing syndrome, eosinophilia, amyloidosis, leukemoid rxns WIDE METS->lungs>bones>regional LNs>liver >adrenals>brain Px-5yr-45-70% survival w/out mets -renal vein, perirenal fat involved-15-20% Tx-nephrectomy, THROMBOTIC MICROANGIOPATHIES -thrombosis in caps, aa'oles thruout body CLINICAL-microangiopathic hemolytic anemia, TCP, renal failure (plt-fibrin thrombi in interlob aa, gloms, necrotic, thickened of vessel walls) MORPH-like malignant HTN, but not necessarily w/ HTN PATHOGENESIS->distal ischemia via: dz -ɭ. endoth injury->thrombosis -less PGI2, NO; activated endoth -ɮ. plt aggregation-via lots of vWF, calpain (cysteine protease) Diseases Atherosclerotic Ischemic Renal Dz -bilateral renal atherosclerosis ->renal insuff, can be w/out HTN Atheroembolic Renal Dz-from Ao or RA -elderly w/ AbdAo surgery -cholesterol clefts-in arcuate, intralobular aa ->ARF in elderly w/ compromised renal fcn SCD Nephropathy-in dz and trait -accel'd sickling w/ more hypoxia ->hematuria, dec'd concentrating ability -can->patchy PAPILLARY NECROSIS->scars -dz->proteinuria or nephrotic syndrome, MPGN, THROMBOTIC MICROANGIOPATHIES -thrombosis in caps, aa'oles thruout body CLINICAL-microangiopathic hemolytic anemia, TCP, renal failure (plt-fibrin thrombi in interlob aa, gloms, necrotic, thickened of vessel walls) MORPH-like malignant HTN, but not necessarily w/ HTN PATHOGENESIS->distal ischemia via: dz -ɭ. endoth injury->thrombosis -less PGI2, NO; activated endoth -ɮ. plt aggregation-via lots of vWF, calpain (cysteine protease) Diseases Diffuse Cortical Necrosis-after OB emergency (abruptia placenta), septic shock, surgery -if diffuse, bilateral->sudden anuria->uremic death -microthrombi in some->renal dmg, necrosis -CAUSED by DIC, vasoconstriction MORPH-ONLY cortex, like acute ischemic nec. -glom hemorrs, fibrin in caps CLINICAL-if patchy, unilateral->survival Renal Infarcts-mostly embolic-LV/A mural thrombosis -also from advanced atherosclerosis, acute PAN -also emboli from vege endocarditis, Ao aneurysms MORPH-white, wedge-shaped infarcts -hemorrhagic discoloration w/ hyperemia ->depressed gray scars -ischemic coagulation necrosis CLINICAL-(-)Sx to CVA pain w/ hematuria -large infarcts in one kidney-HTN, Renal Pathology II Urinary Tract Obstruction ->infx, stones, renal atrophy = HYDRONEPHROSIS (OBSTRUCTIVE NEPHROPATHY) Causes: 1. Congenital Anomalies- 2. Urinary Calculi 3. BPH 4. Tumors 5 Inflammation 6. Sloughed papillae, blood clots 7. Normal pregnancy 8. Uterine prolapse, cystocele 9. Functional d/os-neurogenic, etc MORPH-dilation of pelvis, calyces -filtration still present (reabsorb through lymph, vv) ->tub atrophy-reversible acutely ->compression of medulla, vasc ->interstit inflam, fibrosis ->blunted pyramids->cupped -->thin-walled cystic form CLINICAL -acute-pain due to distention -can be (-)Sx for a long time -bilateral-can't concentrate urine -polyuria, nocturia -distal tub acidosis, salt wasting, 2ndary calculi, TIN->HTN -complete bilateral-olig/anuria -treat soon or die -after Tx->massive diuresis, RENAL CELL CA - OLD MEN (Hypernephroma, AdenoCA) 85% of renal CA Risk fx: smoking, esp pipe/cigar, obesity, HTN, unopposed estrogen Tx, asbestos, petroleum products, heavy metals -CRF, acquired cystic dz, tuberous sclerosis -mostly sporadic, some familial AD in younger -Von Hippel-Lindau syndrome-2/3 pts->RCC -hemangioblastomas or CBLM, retina -VHL gene->familial & sporadic clear cell -Hered (fam) clear cell CA-VHL w/ just CA -Hered papillary CA-AD-multiple bilateral CA -MET protooncogene mutations MORPH-can fungate into coll system->ureter OR R vein->IVC->rt heart -sarcomatoid changes in all infreq'ly-ominous CLINICAL-hematuria, CVA pain, palpable mass -in only 10% ->silent til big enough->constitutional Sx MIMICS-ABNL hormone production=>polycythemia, HTN, hepatic dysfcn, hyperCa, feminize, masc'ize, Cushing syndrome, eosinophilia, amyloidosis, leukemoid rxns WIDE METS->lungs>bones>regional LNs>liver >adrenals>brain Px-5yr-45-70% survival w/out mets -renal vein, perirenal fat involved-15-20% Tx-nephrectomy Classification CHROMOPHOBE RCC-5% -prominent cell membs -pale eosinophilic nucleus -HALO AROUND NUCLEUS -multiple chrom losses-hypodiploidy -from intercalated cells of coll ducts Px-excellent! MORPH-solid sheets, largest cells around vessels, Renal Pathology II Malignant Tumors UROTHELIAL CAs OF PELVIS -5-10% of primary renal tumors -can be benign-ish to frank CA -apparent quickly b/c in pelvis -fragment->hematuria, flank pain -can ->hydronephrosis MORPH-just like in bladder -50% pts also have bladder uroth tumor -increased risk w/ analgesic nephropathy -commonly infiltrates wall Px-50-70% 5-yr survival - low-grade -10% for hi-grade, Renal Pathology II Diseases of Vessels RENAL ARTERY STENOSIS -ɮ-5% of HTN Unilateral RA constriction ->renin-->-->HTN -Most common cause-atheroma -MEN>wm, AGE, DM -2nd-fibromusc dysplasia -intimal, med, advent hyperplasia -YOUNGER WOMEN MORPH-plaque at origin of RA -smaller kidney, diffuse atrophy, interstit fibrosis -arterioles-MILD arteriolosclerosis -CONTRALATERAL KIDNEY HTN->hyaline arteriolosclerosis CLINICAL-like essential HTN -can have bruit over RA Dx-elevated renin, ACE-I response, renal scans, IV pyelography -arteriography Tx-surgery-70-80% cure rate