Path HY Flashcards
nephrOtic syndromes
- podocyte effacment
- hyperlipidemia
- frothy urine
- proteinuria > 3.5 g/day
- edema
name the nephrotic syndromes
- minimal change disease
- FSGS
- amyloidosis
- diabetic nephropathy
- MPGN
- membranous nephropathy
minimal change disease
- flat podocytes (cytokines)
- Hodgkin Lymphoma
- SELECTIVE proteinuria (albumin only)
- Tx: steroids
FSGS
- unknown cause of flat podocytes
- severe version of minimal change disease
- HIV, sickle cell
- no response to steroids
membranous nephropathy
- immune complexes deposit in BM (PLA2R on podocytes)
- subEPIthelial
- tumor, hepatitis, RA
- spike + dome appearance
- IF: IgG, C3 (granular)
diabetic nephropathy
- glycosylation of BM
- proteinuria
- sclerosis of EA leads to sclerosis of glomeruli
- Kimmelstiel Wilson bodies
- nodular mesangial sclerosis
- Tx: ARB, ACEi
amyloidosis
- extracellular buildup of amyloid paraproteins
- apple green biorefringence
- mesangial sclerosis
membranoproliferative (MPGN)
- thick BM
- hypercellularity of mesangial cells
- TRAM TRACK
Type 1- subendothelial IgG, C3 (hepatitis, lupus)
Type 2- BM C3, hypocomplementemia
type 1 MPGN
- subendothelial deposits
- IgG, C3
- hep b/c, SLE
- tram track
type 2 MPGN
- deposits in BM
- C3 only
- hypocomplementemia
- C3 nephritic factor
nephrItic syndromes
- hematuria
- proteinuria <3.5 g/day
- RBC casts
- oliguria
- decr GFR
- hypertension
name the nephritic syn
- post infectious GN
- IgA nephropathy (Henoch, Berger)
- Lupus Nephritis (4 - DPGN)
- cresentic/RPGN
- MPGN
- Alport
post-infectious GN
- 2/3 weeks after infection
- subENDOthelial deposition (but see subEPIthelial humps)
- HYPOCOMPLEMENTEMIA
- hypercellular glomeruli (neutrophils)
- IF: IgG, C3
- Tx: supportive only
IgA nephropathy
- 2/3 DAYS after infection
- IgA response to trigger (URI)
- mesangioproliferative bc IgA deposits in mesangium
- activates complement, but only weakly, so no hypocomplementemia
- IF: IgA granular
Henoch Schonlein has extra renal involvement (skin, GI, joints)
Berger is renal only
Lupus Nephritis 4/ DPGN
- subENDOthelial deposits
- hypercellular
- thickened capillary loops
- IF: “full house” IgG, IgA, IgM, C3, C1q
- fever, rash, arthritis
RPGN
- cresentic
- macrophages + fibrin
Type 1: antiGBM antibodies, goodpasture (linear IF)
Type 2: hypersensitivity, SLE, post strep GN (granular IF)
Type 3: ANCA positive (pauci immune)
type 1 RPGN
- antiGBM antibodies
- LINEAR IF
- goodpastures
type 2 RPGN
- hypersensitivity
- SLE, post strep
- GRANULAR IF
type 3 RPGN
- ANCA positive
- pauci immune IF
- lymphocyte release
Alport Syn
- genetic type 4 collagen defect
- can’t see, can’t pee, can’t hear a bee (eyes, ears, renal)
- x linked
- lamellation of GBM
thin basement membrane disease
- non progressive hematuria
- benign
- AD
- defect in type 4 collagen (make less)
acute interstitial nephritis
- hypersensitivity rxn (EOS, PMNs)
- trigger: PCN, sulfas, NSAIDS, diuretics
- assoc w: sarcoidosis, sjogren, SLE
- fever, rash, AKI
- WBC casts
- EOS
- can lead to papillary necrosis
chronic interstitial nephritis
- chronic use of NSAIDs, phenacetin, caffeine
- papillary necrosis (slough off, obstruct)
- large calcified scars
papillary necrosis
- classic feature of analgesic nephropathy
- coagulative necrosis of papillae
- sloughing of tissue
- hematuria
- painless
- normal renal fxn
causes: chronic drug use, diabetes, acute pyelonephritis, sickle cell anemia