Renal diseases

dktrumble's version from 2016-04-18 14:29

Section 1

Question Answer
Angiomyolipomaassoc with tuberous sclerosis; Tan/brown, maybe areas of hmg and yellow adipose tissue Variable amts of blood vessels, sm musc, fat
OncocytomaSolid, mahogany brown, central scar, large (up to 12cm) Nests of cells with abundant granular eosinophilic cytopl and bland nuc; numerous mito
Clear cell carcinoma chromchrom 3p deletion (von Hippel Lindau)
Clear cell carcinomaGross: nodular mass, birght yellow, areas of hmg and necrosis Micro: clear cell-clear cytopl cells arranged in nests and sheets, bland nuc;
Papillary carcinoma chromtrisomy chrom 7
Papillary carcinomaGross: nodular mass, birght yellow, areas of hmg and necrosis; micro:papillary-cuboidal, low columnar cells in papillary formations, prominent macphs
Wilm’s Tumor epiMalig renal tumor of kids 2-5yo, mutation on chrom 11 for WT1 gene Assoc with WAGR syndrome and Denys-Drash syndrome
Wilm’s TumorGross: nodular gray/white soft fleshy mass Micro: malig of primitive renal blastema with epith and stromal components; prim blastema-small, dark, undiffx cells; epith-abortive tubules and glom; stroma-heterologous elements; anaplasia with pleomorphism/hyperchrom nuc, mitotic figures; nephrogenic rests-clusters of primitive cells
Urothelial carcinoma of renal pelvisGross: papillary-exophytic mass with papillary fronds; flat-reddened/ granular appearance Micro: papillary-fronds with vasc cores lined by prolif of malig uroth cells; flat-no papillary growth pattern, cells w/ malig features Infiltrates adjacent calyces and renal parenchyma
Urinary bladder cancermales, 50-80yo, assoc with smoking, chemical carcinogens (arylamines), Schistosoma (squam cell), cyclophosphamide (transit epith), analgesics, radiation

Section 2

Question Answer
Pre-renal disease/ renal hypoperfusionBUN:Cr>20:1 FENa<1% UA: High spec grav, no prot/blood/WBC; Sed-bland, no casts/cells
Intrinsic renal dz-Tubulointerstitial dz ATN labsBUN:Cr = 10-15:1 FENa >2% UA: isosthenuric, spec grav ~1.01 Sed: muddy brown granular casts
Intrinsic Renal dz- Tubulointerstitial dz Acute Interstitial Nephritis (Allergic) causesNSAIDs, penicillin, cephalosporins, sulfas, vanco Cipro, PPI, diuretics, Sjogrens, sarcoidosis, Legionella, leptospira, CMV
Intrinsic Renal dz- Tubulointerstitial dz Acute Interstitial Nephritis (Allergic)Acute rise in Cr Periph eosinophilia on blood smear Eosinophiluria>1% Proteinuria Sed: WBCs, WBC casts Triad: Fever, rash, eosinophilia
Intrinsic renal dz-Tubulointerstitial dz ATNCaused by ischemia (hypotn, sepsis, prolonged vol depletion), toxins (radiocontrast, aminoglycosides, amphotericin B, heme and myoglobin pigments [rhabdo])
Intrinsic Renal dz- Tubulointerstitial dz Acute Tubular Obstructioncast nephropathy multiple myeloma, P containing enemas, meds: acyclovir, methotrexate
Intrinsic Renal-Vascular renal atheroembolic dzSerum Cr rises 2-8 weeks following manip/procedure
Post-renal/ obstructive uropathyRenal US will show hydronephrosis BUN:Cr>20:1 Sed: bland

Section 3

Question Answer
Minimal change dzKids<5, less common in adults Causes: idiopathic, NSAIDs, Hodgkins dz, lymphoma, leukemia
Minimal change dz microLight micro: normal/minimal Immunofluoro: negative Elec micro: diffuse effacement of podocyte foot processes; no immune complexes, normal GBM
Minimal change dz etiologyproteinuria, Podocyte injury-->T cell dysfxn
Focal segmental glomerulosclerosis epiMost common cause in adults, 2nd in kids, inc incidence in males and AfAms Causes: idiopathic, genetic/familial, secondary due to renal injury and systemic dz
Focal segmental glomerulosclerosis microLight micro: focal glomeruli show sclerosis/scarring of part of glom tuft, may have collagen/matrix material, foam cells, protein material/hyaline Immunofluoro: no specific immune complex deposition, nonspecific trapping of igs and comp in areas of sclerosis Elec micro: no iimmune deposits, obliteration of segment of glom by accum of matrix cells, diffuse podocyte foot process effacement in primary; patchy in secondary
Focal segmental glomerulosclerosishematuria, proteinuria, Primary: immune dysreg/T cell dysfxn, circ toxin Seconary: hyperfiltr and inc glom cap htn (reduced renal mass, obesity, Sickle cell); direct injury to podocyte from virus (HIV)
Membranous nephropathySecond most common in adults, males>40yo Primary/idiopathic 70%; secondary 30% (penicillamine, captopril, gold, NSAIDs, malig, SLE, hep B)
Membranous nephropathy microLight micro: diffuse thickening of glom cap loops, small spikes of GBM Immunofluoro: fine granular immune deposits along glom cap walls-usually IgG, C3, kappa and lambda Elec micro: numerous small electorn dense immune deposits along subepith GBM, reactive spikes of GBM, diffuse podocyte effacement
Diabetic nephropathyMost common cause of ESRD, in both type I and II, Latinos, AfAms, NatAms
Diabetic nephropathy microProteinuria, microalbuminuria, Light micro: diffusely thickened GBM, inc mesangial matrix leads to formation of large nodules of matrix material, thick tubular BMs, progressive fibrosis, intimal sclerosis, hyalinosis Immunofluoro: pseudolinear staining of glom and tubular BM with IgG and albumin due to stickiness of BMs Elec micro: diffuse thickening of GBM due to inc lamina densa, nodules of matrix material, podocyte effacement
AmyloidosisLight micro: amorphous pale eosinophilic material irreg distrib in mesangium and along glom cap loops, Congo red stain positive Immunofluoro: may see light chain if AL Elec micro: deposition of haphazard arranged fibrils in mesangium and GBM, podocyte effacement

Section 4

Question Answer
Bladder Cystitis bugsE Coli, Proteus, Klebsiella, Enterobacter, candida, schistosoma
Bladder CystitisACUTE: Gross: hyperemia of mucosa, exudate, hmg Micro: neut infiltrate, hmg, ulceration of mucosa, large areas of ulceration-ulcerative cystitis CHRONIC: gross: may have hyperemia of mucosa often nonspec Micro: infiltrate of Ls and plasma cells, heaped up rxtive appearing epith, fibrosis and thickening of musc propria MALACOPLAKIA: gross: soft yellow raised mucosal plaques; micro: large foamy macphs with giant cells and Ls, Michaelis Gutman bodies (laminated Ca within macphs and btw cells)
Acute pyelonephritisAscending infxn from bladder >95% of time E Coli, Klebsiella, Enterobacter, Proteus, can be nosocomial
Acute pyelonephritis microLeukocytosis with left shift, leukocyte casts, pos urine culture, pos blood culture, Gross: focal abscess in acute; scarring in late Micro: neut infiltrate (patchy) in early; mixed infiltrate of PMNs, Ls, plasma cells in later, glom not involved; viral inclusions in polyomavirus
Chronic pyelonephritisMost cases assoc with chronic reflux-early in childhood usually; can be due to recurrent infxns superimposed on obstruction
Chronic pyelonephritis microGross: coarse, discrete corticomedullary scars overlying dilated blunted or deformed calyxes Micro: chronic interstitial inflm and fibrosis, tubular atrophy, hyaline casts

Section 5

Question Answer
Membranoproliferative glomerulonephritis causesHep C, multiple myeloma, leukemia, Low C3, C4 in serum
Membranoproliferative glomerulonephritisLM: glom diffusely hypercellular with lobulated appearance, duplication of GBM (tram track) Immunofluoro: IgG, IgM, C3 deposits in mesangium subendoth EM: elec dense immune deposits in mesangium and subendoth GBM, duplication of GBM (tram track)
Dense Deposit Disease (type II MPGN)Drusen in retina mbr, lipodystrophy, Only C3 low in serum, normal C4
Dense Deposit Disease (type II MPGN) microLM: glom diffusely hypercellular with lobulated appearance, PMNs Immunofluoro: irreg staining of mesangium with C3 only EM: linear deposition of elec dense material in ribbon like pattern on GBM
C3 glomerulonephritisLow C3 in serum, normal C4
IgA nephropathyMost common casue of glomnephritis, 2nd-3rd decade, Asians, Caucasians Mucosal infxns triggered by enviro ags drive IgA immune complexes, may follow upper resp or GI illness (Celiac), genetics
IgA nephropathy microLM: diffuse inc in mesangial matrix cellularity, mesangial prolif Imunofluoro: mesangial deposits of IgA and C3 EM: depostis in mesangium
Post infectious glomerulonephritisMost common casue of acute nephritic syndrome, more common in devel countries, peak incidence in kids 5-12 and adults>60
Post infectious glomerulonephritis UADysmorphic RBCs, RBC casts, WBCs, WBC casts Low C3, C4 normal Positive streptozyme test
Post infectious glomerulonephritis microLM: glom hypercellular, influx of large #s of inflm cells Immunofluoro: large granular deposits of IgG or C3 (starry sky) in mesangium and cap walls EM: elec dense immune deposits on subepith side of GBM, large hump like appearance
Lupus nephritisPts with SLE, women, Af Amers, genetic, environmental, immune (loss of tolerance and polyclonal B activation)
Lupus nephritis labsANA, antidsDNA, antiSmith, low C3, low C4 Active urine sed
Lupus nephritis microLM: variable based on class; Class III-focal prolif pattern with active lesions with wire loops of thick caps due to subendoth deposits; Class IV-diffuse prolif pattern, most severe type; class V-mbrous, similar histo to idiopathic mbrous nephropathy (loops with spikes) IM: full house: IgA, IgM, IgG, C3, C1 all in mesangium and cap loops EM: varies accord to class; large deposits in all compartmetns of glom, small subepith deposits in mbrous
Rapidly progressive glomerulonephritis type IantiGBM-acute nephritis, hemoptysis, abs to type IV coll, target pulm alveoli, all ages
Rapidly progressive glomerulonephritis Pauci Immunesmall vessel vasculitis; cytoplasmic or perinuclear
Rapidly progressive glomerulonephritis Pauci Immune antibodiescANCA (Wegener’s granulomatosis w polyangities; target ag proteinase 3) pANCA (target ag myeloperoxidase; microscopic polyangitis)
Rapidly progressive glomerulonephritisLM: necrosis of glom caps, formation of crescents, rupture of glom cap loops, rxtive prolifof cells inurinary space; antiGBM/Pauci gloms appear normal; immune comples depends on underlying cause Immunofluoro: linear stainig for IgG along GBM (antiGBM); Pauci negative; immune complex depends EM: antiGBM and Pauci absent or scant immune deposits, may see rupture; immune complex with deposits

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