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32 Cards in this Set

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Basic Histopathological Changes of Glomerulonephritis
Cellular Proliferation
Leukocytic Infiltration
"Membranous" Change
Hyalinization
Thrombosis, Necrosis, Deposition of Fibrin
Minimal Change Disease
(lipoid nephrosis)
NEPHROTIC
Loss of charge barrier --> leakage of protein
No hematuria, NORMAL filtration function
Occurs more often in children than in adults
Histology is NORMAL
Effacement (FUSION) of podocytes
Almost all patients respond to steroids (kids > adults)
Steroid-resistant respond to cyclophosphamide
Associated with Hodgkin's disease and NSAID use
Etiology is unknown
Focal Segmental Glomerular Sclerosis
NEPHROTIC
Some may have microscopic hematuria
Loss of renal function (ALL eventually require transplant)
Deep, juxtmedullary glomeruli are affected first
POOR or NO RESPONSE TO STEROIDS
IF may show IgM and C3 trapped in the mesangium
Epithelial cell vacuolization, Variable podocyte fusion
Focal sclerosis is also associated with urinary reflux, and IV drug abuse
Etiology is unknown
Effects blacks > whites
Membranous Nephropathy
NEPHROTIC (most common cause in adults)
Etiology is IN SITU IC (IgG) DEPOSITION (Sub-epithelial)
Primary -- most common
Secondary -- assoc. w/ cancer, drugs, HEP B, SLE, infections
Adults of any age (peak 4th-5th decade); RARE in kids
Female > Male
Histology -- diffuse CAPILLARY WALL THICKENING
Silver stain - spikes of GBM between deposits
IF makes IgG (C3) deposits look linear, BUT THEY'RE NOT
Responds to withdrawal of treatment of infection that caused the disease
Stage I and 50% of Stage II respond to steroids
Different stages of Membranous Nephropathy
Stage I -- GBM has normal thickness
Stage II -- GBM spikes between deposits
Stage III -- Intramembranous dposits
Stage IV -- Deposits disappearing (losing electron density)

Stages II, III, IV show GBM thickening
Diabetic Glomerulosclerosis
NEPHROTIC
Hyperglycemina appears to be the major cause
Non-enzymatic glycosylation: LYSINE residues
Cross-linking of matrix and GBM proteins
Earliest manifestation is MICROALBUMINURIA
ESRD in 30% of juvenile diabetics
Two types:
Diffuse glomerulosclerosis
Nodular glomerulosclerosis (Kimmelstiel-Wilson)
Kimmelstiel-Wilson Disease
NEPHROTIC
Found in pts. with microaneurysms of the retina (bad prognosis)
ACELLULAR NODULES IN THE MESANGIUM
PAS and Silver stain POSITIVE
IF shows LINEAR highlighting of IgG (trapped)
Amyloidosis
NEPHROTIC
Mesangial deposition of EC proteins; CONGO RED positive
AL AMYLOID -- secondary to MONOCLONAL GAMMOPATHY
(light chain deposition [LAMBDA])
AA AMYLOID -- assoc. w/ inflammatory diseases
(RA, infections, Tb, osteomyo, Hodgkin's)
Green bi-refringence when stained (under polarized light)
HYPOcellular glomeruli
ESRD is inevitable
Acute Proliferative GN
NEPHRITIC
Pts. (usually kids) present after Strep infection (TYPES 12, 4, 1)
Hematuria, Oliguria, EDEMA, Hypertension
Believed to be IC mediated (kidneys are STERILE)
C3 levels are initially low, ASO titer is elevated
HYPERcellular glomeruli
EM shows electron dense deposits (humps)
Overall cure rate is 75% (kids ~100%; adults not so good)
Slow progression to chronic GN
Rapidly Progressive GN Types
RPGN with anti-GBM Ab
RPGN with Immune Complexes
"Pauci-Immune" RPGN
Rapidly Progressive GN
(A.K.A. Crescentic GN)
Associated with acute renal failure
Diagnosis based on finding of epithelial crescent
FIBRIN is often deposited in Bowman's space
Therapy is with CYCLOPHOSPHAMIDE
RPGN with anti-GBM Ab
Less than 5% of RPGN
Serum anti-GBM Ab (negative test does NOT rule out)
IF shows LINEAR deposits of IgG
NO electron dense deposits
Treatment is supportive
RPGN with Immune Complexes
May be a sequel to post-infectious GN
Other forms of IC GN cal also present as this, with crescents
"Pauci-Immune" RPGN
NO GBM Abs or ICs
Can occur as GN OR as changes in vasculitis
(Ex. microangiitis, Wegener's)
Pts. frequently have POSITIVE ANCA
P-ANCA Ab
Peri-nuclear staining
In patients with Pauci-immune GN (with or without vasculitis)
C-ANCA Ab
Cytoplasmic staining
In patients with Wegener's
Patients alo have sinusitis, often with nose bleed/hemoptysis
Membranoproliferative GN
Nephritic OR Nephrotic
Both kids and adults
Selective depletion in C3, 5, 6, 7
Some pts. have C3 NeF -- IgG AUTO-Ab to C3b
INTERPOSITION of mesangial cells --> splitting of the GBM
IgA Nephropathy
NEPHRITIC ("HEMATURIA is the rule")
Histo -- mesangial enlargement
IF shows abundant IgA in the mesangium
Prognosis is usually good
No specific treatment - control hypertension
Henoch-Schoenlein Allergic Purpura
Children and young adults are affected
Focal GN (presents as hematuria)
PURPURA; ARTHRITIS; ACUTE ABDOMINAL PAIN
Prognosis is fair to good
Cryoglubulinemic GN
NEPHRITIC
Proteins that deposit are cryoglobulins
Most pts. hematuria, proteinuria, HYPOcomplementemia

Two broad groups:
Those associated with ICs
Those associated with monoclonal gammopathy
Essential Mixed Cryoglobulinemic GN
Most common form
Composed of monoclonal IgM
MAJOR ASSOCIATION WITH HEP C
Palpable purpura on lower extremities
Leg ulcers, arthralgias, hepatosplenomegaly
Monoclonal Cryoglobulinemic GN
Assoc. w/ underlying LYMPHOPROLIFERATIVE disorders
IF shows glomerular deposit only having one of the light chains (lambda)
Histology is like MPGN
Thin GBM Disease
Patients are usually women
Hematuria only
Etiology is unknown
Segments of the GBM are abnormally thin, all else is normal
NO treatment necessary
All patients do well
GN of SLE
Nephritic or Nephrotic
Almost 100% of pts. have anti-nuclear Abs
Ag-Ab complex disease
Serum Complement C3 is depressed
Different classifications resemble different GNs
Mesangial Lupus Nephritis
Resembles IgA Nephropathy
Presents with hematuria
Usually respond well to steroid therapy (good prognosis)

NOTE: can progress to more serious forms of lupus GN
Membrane Lupus GN
Resembles Membranous GN
Severe Proteinuria
Diffuse Membranoproliferative Lupus GN
Known as Type IV (very serious)
BOTH hematuria and proteinuria, freq. assoc. w/ ARF
IV CYCLOPHOSPHAMIDE is given in a bolus
Electron dense deposits are adjacent to GBM
Some SLE complexes have a finger print pattern on them
Wire Loop
Significant thickening of the BM in capillary loops
Associated with Lupus GN type IV
Hematoxylin Body
Round, glass-like basophilic deposit adjacent to necrosis
Represent naked cell nuclei that have reacted with ANA
Nephrotic GNs
Minimal Change
FSGN
Membranous
Diabetic
Amyloidosis
MPGN (can be nephritic also)
SLE (can be nephritic also)
Nephritic GNs
Acute Proliferative
IgA Nephropathy
Cryoglobulinemic
Henoch-Schonlein Allergic Purpura
Vasculitis
MPGN (can be nephrotic also)
SLE (can be nephrotic also)
Renal Diseases assoc. w/ ARF
RPGN
ATN
Interstitial Nephritis