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This Concept Map, created with IHMC CmapTools, has information related to: Kidney I, Renal Pathology GLOMERULAR DZS Clinical Manifestations 5 Syndromes: -Acute Nephritic Syndrome -RPGN -Nephrotic Syndrome -Chronic Renal Failure -(-)Sx hema or proteinuria, Tubulointerstitial Nephritis PYELONEPHRITIS-inflam of collecting system -renal pelvis, tubules, interstitium Mostly via E. coli, other gram (-) bac from GI -Proteus, Klebsiella, Enterobacter, Strep fecalis Mostly via ASCENDING INFX -entrance (catheter, etc,)->bladder (multiply) ->vesicoureteral reflux (key to entering kidney) (should be compressed while peeing) ->intrarenal reflux (upper, lower poles) Types TIN NSAID-ass'd Nephropathy= -hemodynamically-induced ARF -inhibited vasodilatory PGs -esp w/ other volume-depleting renal d/os -acute hypersensitivity interstit nephritis->ARF -acute interstit nephritis, lipoid nephrosis ->renal failure AND nephrotic syndrome -MGN w/ nephrotic syndrome, Renal Pathology TUBULES, INTERSTITIUM Tubulointerstitial Nephritis PYELONEPHRITIS-inflam of collecting system -renal pelvis, tubules, interstitium Mostly via E. coli, other gram (-) bac from GI -Proteus, Klebsiella, Enterobacter, Strep fecalis Mostly via ASCENDING INFX -entrance (catheter, etc,)->bladder (multiply) ->vesicoureteral reflux (key to entering kidney) (should be compressed while peeing) ->intrarenal reflux (upper, lower poles), Renal Pathology Renal Transplantation CHRONIC XPLANT GLOMERULOPATHY -segmental ischemic collapse -diffuse mesangial sclerosis -thickened cap loops -mesangial interposition -lucent subendoth zone, Renal Pathology CONGENITAL ANOMALIES AGENESIS -unilateral can survive -other side is big, can sclerose -not bilateral HYPOPLASIA-usually unilateral ɞ renal lobes or pyramids -oligomeganephronia-few, big nephrons ECTOPIC-usually around pelvis HORSESHOE-1:500-1000 autopsies -90% fused at lower pole, Renal Pathology GLOMERULAR DZS Histological Alterations -Hypercellularity -BM Thickening-mostly due to IC subepith deposition-MGN -Hyalinization->Sclerosis, Tubulointerstitial Nephritis PYELONEPHRITIS-inflam of collecting system -renal pelvis, tubules, interstitium Mostly via E. coli, other gram (-) bac from GI -Proteus, Klebsiella, Enterobacter, Strep fecalis Mostly via ASCENDING INFX -entrance (catheter, etc,)->bladder (multiply) ->vesicoureteral reflux (key to entering kidney) (should be compressed while peeing) ->intrarenal reflux (upper, lower poles) Types CHRONIC PYELONEPHRITIS Chronic inflam, scarring in calyces/pelvis CHRONIC OBSTRUCTIVE -recurrent infx->recurrent scarring REFLUX NEPHROPATHY-MORE COMMON -in early childhood due to UTI on reflux MORPH-scar overlies blunted calyx -Thyroidization-dilated tubs w/ colloid casts -in HTN-hyaline arteriosclerosis -chronic infiltrate, can have acute superimposed Xanthogranulomatous Pyelonephritis -accum foamy cells w/ WBCs-Proteus -can make large yellow nodules (resemble CA) CLINICAL-insidious or just like acute -pyuria, bacteriuria-can see scarring on X-ray -bacteriuria absent later on -common cause of HTN in kids -proteinuria mild, but can->FSGS->nephrotic syn -due to renal ablation nephropathy (atrophy) -indicates poor Px->ESRF, Renal Pathology Renal Transplantation CYCLOSPORIN A NEPHROTOXICITY acute sudden creatinine elevation isomorphic vacuolization thrombotic microangiopathy chronic progressive creatinine elevation striped fibrosis arteriolar hyalinosis, Tubulointerstitial Nephritis PYELONEPHRITIS-inflam of collecting system -renal pelvis, tubules, interstitium Mostly via E. coli, other gram (-) bac from GI -Proteus, Klebsiella, Enterobacter, Strep fecalis Mostly via ASCENDING INFX -entrance (catheter, etc,)->bladder (multiply) ->vesicoureteral reflux (key to entering kidney) (should be compressed while peeing) ->intrarenal reflux (upper, lower poles) Types TUBULOINTERSTITIAL NEPHRITIS Acute (Allergic) Drug-Induced TIN ->ARF -begins 15d after exposure to drug ->fever, eosinophilia, RASH -renal->hematuria, mild proteinuria, WBCuria, rising S creatinine, oliguria MORPH-ABNL intersitium -edema, mononuc infiltrate, also PMNs -methicillin, thiazides->granulomas -NL glom (except w/ NSAID-induced MCD) Pathogenesis-not fully understood -immune-hypersensitivity; not dose-related -IgE late-phase hypersens or DTH rxn Tx-just withdraw the drug! -normalize in a couple months DRUGS: PCNs, cephalosporins, diuretics, dilantin, NSAIDs, antacids, Renal Pathology TUBULES, INTERSTITIUM MULTIPLE MYELOMA Bence-Jones proteinuria, Cast Nephropathy -some light chains directly toxic to epith -B-J + Tamm-Horsfall protein->cast ->inflammation-large, distinct ->acute or chronic renal failure Amyloidosis-6-24% of MM pts-AL amyloid Light-Chain Nephropathy (Deposition Dz) -deposit in non-fib forms in glom (glom'pathy) or around tubs (TIN) -can look like diabetic GS by light Hypercalcemia, Hyperuricemia Vascular Dz-esp in elderly UT obstruction, 2ndary pyelonephritis MORPH-B-J casts-pink-blue masses -can be laminated, surr'd by giant cells -necrotic epith, can be eroded by cast CLINICAL-Chronic RF most common -OR ARF w/ oliguria -ppt factors-dehydration, hypercalcemia, infx, nephrotoxic ABX, Tubulointerstitial Nephritis PYELONEPHRITIS-inflam of collecting system -renal pelvis, tubules, interstitium Mostly via E. coli, other gram (-) bac from GI -Proteus, Klebsiella, Enterobacter, Strep fecalis Mostly via ASCENDING INFX -entrance (catheter, etc,)->bladder (multiply) ->vesicoureteral reflux (key to entering kidney) (should be compressed while peeing) ->intrarenal reflux (upper, lower poles) Types TIN Analgesic Abuse Nephropathy -chronic TIN w/ papillary necrosis -very common in some of Australia Drugs: phenacetin, ASA, caffeine, codeine -mixture of two antipyretics+water depletion PATHOGENESIS -pap. necrosis FIRST->cortical TIN -phenacetin-met'd->acetaminophen -covalent binding, oxidative dmg -ASA inhibits vasodilation->ischemia MORPH-papillae varied in necrotic stage, size -cortex-atrophy of tubules, calcification -analgesic microangiopathy- -PAS(+) BM thickening of CLINICAL-WOMEN>men -HA, anemia, GI Sx, HTN -colic from excreting chunks of papillae Can->transitional papillary CA of renal pelvis, Renal Pathology CONGENITAL ANOMALIES CYSTIC RENAL DYSPLASIA-sporadic -abnl metanephric diff'ation -abnl structures: cartilage, undiff mesenchyme, immature collecting ducts, abnl pelvic organization -most have uteropelvic obstruction, ureteral agenesis, or atresia -mostly cystic-lined by flattened epith CLINICAL-flank mass -unilateral-most common -can survive after removal -bilateral-eventually->renal failure, Renal Pathology TUBULES, INTERSTITIUM ACUTE TUBULAR NECROSIS -destoyed tub epith cells -acutely suppressed renal fcn MOST COMMON CAUSE OF ARF -acute GFR decline, oliguria, rising BUN/creat -reversible Ischemic ATN-inadequate blood flow-shock hepatorenal syndrome, rhabdomyolysis -also via transfusions, Hgb-uria Nephrotoxic ATN-aminoglycosides (genta), AmpB, CCl4, X-ray contrast, poisons, Hg, eth glycol -necrotic in PCT, PST-more extensive PATHOGENESIS -1.tubular injury -2.persistent disturbances in blood flow Hypoperf->necrosis of tub cells->sloughed cells ->tubule obstruction->increased pressure -->decreased GFR->Aff aa. vasoconstriction MORPH-skip areas of apop, necrosis -CASTS in distal lumens (granular AND hyaline) -with Tamm-Horsfall proteins -tubulorrexis (rupture) -distalization-prox tub dilates, epith flattens -regenerative changes-mitoses, nuc hyperchromasia CLINICAL- 3 stages Initiating-36 hrs-slight oliguria, elevated BUN Maintenance-oliguria (40-400mL/day), salt, water overload, rising BUN, meta acidosis Recovery-increased urine (up to 3L/d) -hypokalemia (still dmged, so lots of stuff leaving) 50% may not have oliguria-esp nephrotoxins, Renal Pathology Renal Transplantation CHRONIC REJECTION-mos-yrs -progressive azotemia, oliguria, HTN, wt gain -not responsive to Tx Histo-intimal sclerosis/aa. prolif -interstitial fibrosis-most severe -tubular atrophy, Renal Pathology Renal Transplantation HYPERACUTE REJECTION-min-hrs -preformed AB -anuria, pain, fever Tx-TAKE OUT KIDNEY Gross-mottling, cyanosis, poor turgor Histo-vasc congestion, fibrin-plt thrombi -neutrophilic vasculitis, fib necrosis -interstitial edema -neutrophilic infiltrates, Renal Pathology CONGENITAL ANOMALIES ACQUIRED CYSTIC DZ -pts w/ ESRD after lots of dialysis -hyperplastic or flattened tub epith -often w/ Ca-oxalate crystals, clear fluid -probably form after obstruction -fibrosis or crystals -mostly (-)Sx, but can have hematuria -can -> renal cell CA in walls of cyst, Renal Pathology Clinical Manifestions NEPHROTIC SYNDROME -heavy proteinuria (ɯ.5 gm/d) -hypoalbuminemia, edema -hyperlipidemia, lipiduria, Renal Pathology Clinical Manifestions ACUTE RENAL FAILURE -oliguria or anuria -recent azotemia CHRONIC RENAL FAILURE -prolonged S/Sx of uremia -end result of all renal dzs Stages: Diminished Renal Reserve-GFR=50% NL -no azotemia, (-)Sx, more suscep to dz Renal Insufficiency-GFR=20-50% -azotemia, usually anemia, HTN -polyuria, nocturia (can't concentrate) Renal Failure-GFRង-25% -can't regulate volume or solutes ->edema, meta acidosis, hypocalcemia -can->uremia->neuro, GI, CV problems ESRD-GFRɝ%-terminal stage, Renal Pathology TUBULES, INTERSTITIUM HYPERCALCEMIA, NEPHROCALCINOSIS -hyperparathyroidism, MM, vit D intox, mets bone dz, excess Ca intake ->stones, deposition of Ca in kidney 1st problem-mitochon dysfcn in tub epith ->Ca deposits->obstruction->atrophy ->fibrosis, chronic inflam -scarring of entire cortical areas CLINICAL-1st-can't concentrate urine -tub acidosis, salt-losing nephritis ->renal insufficiency due to nephrocalcinosis, also stones/infx, TIN Analgesic Abuse Nephropathy -chronic TIN w/ papillary necrosis -very common in some of Australia Drugs: phenacetin, ASA, caffeine, codeine -mixture of two antipyretics+water depletion PATHOGENESIS -pap. necrosis FIRST->cortical TIN -phenacetin-met'd->acetaminophen -covalent binding, oxidative dmg -ASA inhibits vasodilation->ischemia MORPH-papillae varied in necrotic stage, size -cortex-atrophy of tubules, calcification -analgesic microangiopathy- -PAS(+) BM thickening of CLINICAL-WOMEN>men -HA, anemia, GI Sx, HTN -colic from excreting chunks of papillae Can->transitional papillary CA of renal pelvis Papillary Necrosis Also in DM, Sickle Cell Anemia or trait, Renal Tuberculosis, Urinary Tract Obstruction