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23 Proliferative Glomerular Disease Flashcards

1
Q

Clinical presentation of proliferative glomerular diseases

  • Proliferative glomerular diseases usually present as either…
  • Major differences
A
  • Proliferative glomerular diseases usually present as either…
    • Acute nephritic syndrome
    • Rapidly Progressive Glomerulonephritis (RPGN)
      • Cannot be applied to any GN in which renal failure develops rapidly
      • Crescents must be seen in a high proportion of the glomeruli for the disease to be termed RPGN
  • Major differences
    • How rapidly the disease develops
    • Long-term extent of renal function impairment
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2
Q

Clinical presentation of proliferative glomerular diseases:
Acute nephritic syndrome

  • Characterized by…
  • Due to…
  • Classic presentation
A
  • Characterized by…
    • Inflammatory damage of the glomerular capillaries
    • –> hematuria/proteinuria, HTN, and azotemia
  • Due to…
    • Secondary GN related to infectious disease
      • Ex. post-streptococcal GN or other bacterial/viral illnesses
    • Other systemic disease
      • Ex. lupus, vasculitis, Henoch Schonlein purpura, Goodpasture’s syndrome
    • Primary glomerular disease
      • Ex. IgA nephropathy
  • Classic presentation
    • Ppost-streptococcal
    • Other post-infectious forms of GN
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3
Q

Clinical presentation of proliferative glomerular diseases:
Rapidly progressive glomerulonephritis (RPGN)

  • RPGN
  • Characterized by…
  • Necessary feature to diagnosis RPGN
  • Etiologies
    • Type I
    • Type II
    • Type III
  • Critical to avoid ESRD
  • Renal pathology
A
  • RPGN
    • Subtype of the acute nephritic syndrome
  • Characterized by…
    • Fulminant progressive downhill course
    • Associated oliguria or anuria
    • Decline in GFR occurs over days to weeks
      • If untreated, RPGN –> ESRD
    • Causes: primary & secondary
  • Necessary feature to diagnosis RPGN
    • Many crescents are seen on renal biopsy
  • Etiologies
    • Type I: Anti-GBM disease/Goodpasture’s syndrome
    • Type II: Immune complex mediated
      • E.g. membranoproliferative GN, lupus nephritis, cryoglobulin associated GN, Ig A nephropathy, etc.
    • Type III: Pauci immune ANCA associated vasculitis
      • E.g. Wegner’s Granulomatosis, microscopic polyangiitis, pauci immune crescentic GN
  • Critical to avoid ESRD
    • Rapid diagnosis with a renal biopsy and institution of therapy
  • Renal pathology
    • Variable
    • Common feature: necrotizing lesions or crescents in a variable % of glomeruli
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4
Q

Glomerular diseases associated w/ cellular proliferation

  • Glomerular cellular proliferation is related to…
  • Degree of cell proliferation depends on…
  • The degree of complement activation
    • Chemotaxis
    • Serum complement
    • Hypocomplementemia
  • Diseases associated with hypocomplementemia
  • Glomerular proliferation tends to be associated w/…
A
  • Glomerular cellular proliferation is related to…
    • Deposition of immune complexes or antibodies in the mesangial subendothelial system &/or the glomerular BM
  • Degree of cell proliferation depends on…
    • Rate of accumulation of complexes
  • The degree of complement activation
    • Chemotaxis
      • Some complexes readily activate complement –> chemotaxis of inflammatory cells
        • E.g. post-infectious GN
      • Other deposits don’t cause the same degree of chemotaxis
        • Ex. IgA nephropathy
    • Complement activation may be reflected in serum complement levels
      • If severe enough –> hypocomplementemia
    • Pts w/ hypocomplementemia almost always have a proliferative glomerulonephritis
      • But not all proliferative GN is hypocomplementemic
      • Some deposits (ex. IgA) –> significant mesangial proliferation w/o lowering serum complement
  • Diseases associated with hypocomplementemia (COMPS)
    • Cryoglobulinemia
    • AtherOemboli
    • Membranoproliferative Glomerulonephritis
    • Post infectious glomerulonephritis
    • Systemic Lupus erythematosus
  • Glomerular proliferation tends to be associated w/…
    • A nephritic syndrome including hematuria & RBC casts
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5
Q

Specific proliferative glomerular diseases:
Acute post-infectious glomerulonephritis

  • Path description
  • Incidence
  • Post streptococcal GN
    • Incidence
    • Cause
    • Among…
    • Typical features
A
  • Path description
    • Diffuse endocapillary proliferative and exudative GN
  • Incidence
    • 9.5 – 28.5 per 100,000
    • Usually occurs in healthy children (can also occur in adults)
  • Post streptococcal GN
    • Incidence
      • Most common cause of post-infectious GN
      • Occurs after a streptococcal sore throat or impetigo
        • Secondary form of GN
    • Caused by Group A, beta-hemolytic Streptococci
      • Particularly those of “nephritogenic” strains - Types 1, 4, & 12 (throat) and types 49 & 2 (skin)
    • Among the prototypic immune complex diseases
      • Streptococcal antigen is only rarely identified
    • Typical features
      • Acute onset of gross hematuria (cola colored) or microscopic hematuria after latent period of 10-14 d
      • Salt and water retention –> edema & HTN
      • Urinary sediment is nephritic (w/ blood & RBC casts)
      • Proteinuria present but
      • GFR is usually depressed
        • Elevated serum creatinine
        • Occurs suddenly (within days)
        • Decreased serum complements
        • Increased antistreptolysin O (ASO) titers w/ a preceding throat infection
          • Elevated Antihyaluronidase titers (AHT) and anti-DNAse B titers are common with preceding skin infection
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6
Q

Specific proliferative glomerular diseases:
Acute post-infectious glomerulonephritis

  • Other causes of acute post infectious GN
  • Pathogenesis
  • Pathology
    • LM
    • IF
    • EM
  • Treatment
A
  • Other causes of acute post infectious GN
    • Staphylococcal infection of heart valves (endocarditis) or ventricular shunts
    • Visceral abscesses
    • All associated w/ protracted infection w/ continuous release of antigen into the circulation.
  • Pathogenesis
    • Due to an immune response to infection w/ nephritogenic Group A beta-hemolytic streptococcus
    • Deposited antibodies may be directed at streptococcal antigens and/or intrinsic glomerular epitopes (ex. ECM)
    • Inflammation is caused by local activation of the complement cascade, IL-6, ICAM-1, and the plasmin-plasminogen system
  • Pathology
    • LM
      • Glomerular tufts are enlarged & hypercellular w/ leukocytes in glomerular capillaries
      • Diffuse proliferative and exudative GN
      • Edothelial/mesangial cell proliferation
      • Intracapillary luminal neutrophils
    • IF
      • IgG and C3 with “lumpy, bumpy” pattern (sparse, coarsely granular)
    • EM
      • Subepithelial “hump” deposits, “Flame like deposits” and some mesangial deposits
  • Treatment
    • Supportive: Na restriction & BP control
    • Dialysis if necessary (uncommon)
    • Most patients recover normal renal function and don’t have progressive renal failure
    • Renal biopsy is generally not required as the diagnosis can be made on the basis of the clinical presentation & serologic tests
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7
Q

Specific proliferative glomerular diseases:
IgA predominant immune complex glomerulonephritis (IgA nephropathy, Berger’s disease)

  • IgA nephropathy
  • Clinical findings
  • Incidence
  • Prevalence
  • Pathology
    • LM
    • IF
    • EM
  • Treatment
A
  • IgA nephropathy
    • Most common type of GN in countries w/ routine renal biopsies
    • Associated with chronic severe liver disease, psoriasis, inflammatory bowel disease (IBD), and HIV disease
  • Clinical findings
    • Hematuria (micro- or macroscopic) often precipitated by flu-like illnesses or vigorous exercise
      • May or may not be associated with flank pain
    • Urinary protein excretion < 2 g/day
      • Some pts have nephrotic range proteinuria (poor prognosis)
    • Some pts have fulminant course w/ rapid deterioration of renal function.
  • Incidence
    • 15 – 40 per million per year
  • Prevalence
    • 2 – 10% of renal biopsies –> 38% in Native Americans from New Mexico
    • Highest in Asia where prevalence is 20-40% of all renal biopsies
  • Pathology
    • LM: > 1 of…
      • Normal
      • Diffuse mesangial cell/matrix proliferation
      • Focal segmental mesangial and endocapillary cell proliferation
      • Necrosis/crescents
    • IF
      • Predominantly IgA, C3
      • IgG and IgM can be present
    • EM
      • Mesangial electron dense deposits
      • Rare subendothelial electron dense deposits in necrotizing forms
  • Treatment
    • No known treatment
    • Fish oil for pts w/ progressive renal failure
    • Immunosuppressive therapy: not beneficial
    • Steroids: possible treatment
    • 20 yr renal survival approximately 50% to 70%
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8
Q

Specific proliferative glomerular diseases:
Henoch-Schönlein Purpura (HSP)

  • Mediated by…
  • Form of…
  • Involves…
  • Occurs…
  • Incidence
  • Cause
  • Prognosis
  • Biopsy
  • Renal involvement
  • Morphology
A
  • Mediated by…
    • IgA
  • Form of…
    • hypersensitivity angiitis
  • Involves…
    • Skin (purpuric rash over buttocks, lower extremities)
    • Joints (arthralgias)
    • GI tract (GI bleeding common)
    • Kidneys
  • Occurs…
    • At any age
    • Most common: children 3-10yo
  • Incidence
    • Rare: 20 / 100,000 children / year
  • Cause
    • Antecedent infection is common (often streptococcal URI)
  • Prognosis
    • Most children recover in 4-6 weeks with no lasting kidney damage
    • Adults recover more slowly and less completely
    • Pts w/ nephrotic syndrome or crescentic GN renal failure may supervene within the first 6 months
  • Biopsy
    • Necrotizing, leukocytoclastic vasculitis
    • Fibrinoid necrosis of vascular walls which contain fragments of neutrophilic debris
  • Renal involvement
    • Present in ~50% of pts
    • Varies from mild hematuria to nephrotic syndrome to fulminant renal failure
  • Morphology
    • Similar to IgA nephropathy
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9
Q

Specific proliferative glomerular diseases:
Membranoproliferative (mesangiocapillary) glomerulonephritis (MPGN)

  • Incidence
  • Presentation
  • Therapy
  • Forms
    • Primary (idiopathic)
    • Secondary (associated with other diseases)
  • Pathology
    • Characterized by…
    • LM
A
  • Incidence
    • Rare group of disorders (2-3 / 1,000,000 / year)
  • Presentation
    • Proteinuria (often nephrotic range)
    • Hematuria
    • HTN
    • Nephrotic or nephritic syndrome
    • Low C3 (< 70% of cases)
    • Often progresses to renal failure
  • Therapy
    • No accepted therapy
  • Forms
    • Primary (idiopathic)
      • Type I: mesangiocapillary glomerulonephritis
      • Type II: Dense Deposit Disease
      • Type III: Mixed features of Type I and membranous GN
    • Secondary (associated with other diseases)
      • With immune complexes
        • Autoimmune diseases like SLE
        • Infections like hepatitis C, endocarditis, infected ventricular shunt, etc.
        • Dysproteinemia like cryoglobulinemia associated with CLL, lymphoma
      • Without Immune deposits
        • HUS/TTP, transplant glomerulopathy
  • Pathology
    • Characterized by…
      • 1 of 3 alterations in the GBM
      • Proliferation of glomerular cells (mainly mesangial cells)
    • LM
      • Global hypercellularity
      • Accentuation of the glomerular segments or lobules (–> lobular GN)
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10
Q

Specific proliferative glomerular diseases:
Membranoproliferative (mesangiocapillary) glomerulonephritis (MPGN):
Type I

  • Predominantly…
  • Silver stain
  • Presence of immune complex deposits
  • IF
  • EM
  • Complement levels
  • Immune complexes
A
  • Predominantly…
    • Mesangial (and variable endocapillary) cell proliferation
    • Circumferential extension of the mesangium into the subendothelial space of the capillary wall (mesangial interposition or mesangialization)
    • –> thickening of the peripheral capillary wall
  • Silver stain
    • Double contour in the capillary walls (tram tracking)
    • Corresponds to reduplicated subendothelial lamina densa
  • Presence of immune complex deposits
    • Occurs in most cases of Type I MPGN including the primary form
  • IF
    • Mesangial & capillary loop granular positivity for IgG and C3
    • Not infrequently C4 and C1q suggesting complement activation by the classical pathway
  • EM
    • Mesangial interposition
    • Reduplication of the lamina rara interna and mesangial
    • Subendothelial electron dense deposits
  • Complement levels
    • Variably decreased
  • Immune complexes
    • Formed & deposited predominantly in the subendothelial space of the capillary wall
    • Stimulates mesangial ingrowth & new BM formation to isolate & remove the deposits
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11
Q

Specific proliferative glomerular diseases:
Membranoproliferative (mesangiocapillary) glomerulonephritis (MPGN):
Cryoglobulinemia

  • Specific form of…
  • Generic descriptive term given to…
  • 3 types recognized by immunoelectrophoresis
    • Type 1
    • Type 2
    • Type 3
  • Frequently occur in association w/…
  • Clinical syndrome: >1 of…
  • Renal disease
    • Acute phase
    • Chronic phase
A
  • Specific form of…
    • Type I MPGN
  • Generic descriptive term given to…
    • Igs that precipitate on cooling and resolubulize on warming
  • 3 types recognized by immunoelectrophoresis
    • Type 1 - monoclonal Ig (usually IgM)
    • Type 2 - monoclonal Ig (usually IgM) directed against Fc portion of a polyclonal (usually IgG)
    • Type 3 - polyclonal Ig (usually IgM) directed against Fc portion of a polyclonal Ig (usually IgG).
  • Frequently occur in association w/…
    • Other diseases such as plasma cell dyscrasias and hepatitis C
  • Clinical syndrome: _>_1 of…
    • Purpura, weakness, neuropathy, arthralgias, & frequently glomerular disease (20-55%)
  • Renal disease
    • Acute phase
      • Proliferative & variably necrotizing GN associated w/ neutrophilic exudation and cryoglobulin “thrombi” (subendothelial and mesangial electron dense deposits)
    • Chronic phase
      • Cryoglobulin deposition produces a type I membranoproliferative pattern of injury
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12
Q

Specific proliferative glomerular diseases:
Membranoproliferative (mesangiocapillary) glomerulonephritis (MPGN):
Type II & III

  • Type II
    • General
    • IF
    • Etiologic agent
  • Type III
A
  • Type II
    • General
      • Similar to types I and III by its H&E LM appearance only
      • Lamina dense is transformed into a diffusely thickened & electron dense structure –> “dense deposit disease”.
    • IF
      • C3 and properdin are deposited on either side of the abnormal lamina densa, but not within it
    • Etiologic agent
      • Serum autoantibody: C3 nephritic factor (C3NeF)
        • Present in 70% of patients
        • Stabilizes the alternative pathway C3 convertase (C3bBb), preventing its normal degradation by factors H and I
        • –> constitutive alternative pathway complement activation.
      • Serum C3 levels are often depressed w/ a normal C4 level
      • Dense deposit disease has a predilection to recur in renal transplants
      • Dense deposit disease is associated with partial lipodystrophy
  • Type III
    • Similar to Type I, except subepithelial deposits are also seen
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13
Q

Specific proliferative glomerular diseases:
Systemic lupus erythematosus (SLE)

  • General
  • Incidence
  • Mostly involves the following organ systems
  • Lab findings
  • Renal involvement
    • Incidence
    • Presentation
    • Immune complex deposition
    • Clinical signs
A
  • General
    • Multisystem, autoimmune disease w/ antibodies directed against cellular constituents
    • Most important: antibodies to native double stranded DNA (anti-ds DNA)
  • Incidence
    • Predominantly young women (women : men :: 6 : 1)
  • Mostly involves the following organ systems
    • Skin, joints, serous membranes, heart, neurologic, blood (cytopenias, coagulation disorders), & kidneys
  • Lab findings
    • Antinuclear antibodies (ANA)
    • Depression of C3, C4, CH50
    • Circulating immune complexes.
  • Renal involvement
    • ~4.4 / 100,000
    • Can present w/ both nephrotic (heavy proteinuria) & nephritic (hematuria, hypertension, azotemia) syndrome
      • Some present w/ tubulointerstitial nephritis
    • Immune complex deposition can be detected in 90-95%
      • 1/3 not sufficiently extensive to give rise to symptoms
    • Clinical signs (hematuria, proteinuria, azotemia) occur when the level of deposits reach threshold
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14
Q

Specific proliferative glomerular diseases:
Systemic lupus erythematosus (SLE)

  • 2 principal patterns of immune complex deposition
  • Other pathology features
    • LM
    • IF
    • EM
  • Treatment
    • Depends upon…
    • Class IV
A
  • 2 principal patterns of immune complex deposition
    • Mesangial-subendothelial
      • Preformed immune complexes deposit in mesangium first
      • Later may extend into the subendothelial space
    • Membranous-smaller complexes
      • Formed in situ within the BM or subepithelial space
      • –> typical subepithelial deposits
  • Other pathology features
    • LM
      • Interstitial nephritis; hyaline thrombi; vasculitis-rare; fibrinoid necrosis; wire loop lesions (confluent subendothelial IC deposits); hematoxylin bodies (LE Cells)
    • IF
      • TBM staining (“full house”)
      • Stains with all Igs including IgM, IgG, Ig A and complements
    • EM
      • “Fingerprint”; tubuloreticular inclusions (endothelial cells); rings and cylinders; TBM deposits
  • Treatment
    • Depends upon the class of disease
      • The patient can transform from one class to other over the course of the disease
        • Pt can initially present w/ class III & can transform to Class V w/o going through class IV
      • Why pts usually require multiple renal biopsies during the course of the disease to determine the histological class
    • Class IV (most aggressive form)
      • Steroid & cyclophosphamide
      • Resistant cases: other immunosuppressants like Mycophenolate mofetil, cyclosporine and rituximab
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15
Q

Specific proliferative glomerular diseases:
WHO classification of lupus nephritis (LM, IF, & EM for each)

  • Class I
  • Mesangial (Class II)
  • Focal Proliferative (Class III)
  • Diffuse Proliferative (Class IV)
  • Membranous (Class V)
  • Sclerosing GN (Class VI)
A
  • Class I - rare
    • LM: Normal
    • IF: Negative Staining
    • EM: No Deposits
  • Mesangial (Class II) 25%
    • LM: Loops normal; mesangium increase cells and matrix
    • IF: Mesangial
    • EM: Mesangial
  • Focal Proliferative (Class III) 20%
    • LM
      • < 50% of glomeruli affected
      • Segmental increase cells; adhesions; small crescents
    • IF: Mesangial & loop> than changes by light
    • EM: Mesangial and segmental small subendothelial
  • Diffuse Proliferative (Class IV) 35-40%
    • LM
      • > 50% of glomeruli affected
      • Marked hypercellularity and matrix increase; crescents; necrotizing lesions
    • IF: Mesangial and loop
    • EM: Mesangial and large subendothelial
  • Membranous (Class V) 15%
    • LM: Thick loops; minimal hypercellularity
    • IF: Loop
    • EM: Subepithelial; occasional mesangial
  • Sclerosing GN (Class VI)
    • LM: Advanced sclerosing lesions
    • IF: ±Immune deposits
    • EM: ±electron dense mesangial, subendothelial and subepithelial
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16
Q

Rapidly progressive glomerulonephritis (RPGN):
Type I: RPGN (Anti-GBM GN, Goodpasture’s Syndrome)

  • Incidence
  • Antibodies directed against antigens in the…
  • Presentation
  • Diagnosis
  • Renal involvement
  • Pathology
  • Treatment
A
  • Incidence
    • Rare condition
    • Mainly involves young males
      • Can occur in both genders & at all ages
  • Antibodies directed against antigens in the…
    • Glomerular BM –> type I RPGN
    • Pulmonary alveolar BM –> hemoptysis
  • Presentation
    • GN w/ rapidly deteriorating renal function
    • Associated pneumonitis w/ hemoptysis, cough, & SOB
  • Diagnosis
    • Based on renal biopsy
  • Renal involvement
    • Characterized by crescentic GN w/ progressive (sometimes fulminant) renal failure
  • Pathology
    • Caused by antibodies directed against a glomerular BM type IV collagen that’s uniformly distributed within the glomerular BM
    • Linear deposits are seen on IF, usually IgG
    • Increased anti-GBM antibody titer
  • Treatment
    • Plasmapheresis to remove the anti-GBM antibodies
    • Steroids and cyclophosphamide
    • Poor prognosis if diagnosed at advanced stage (serum creatinine >6mg/dl)
17
Q

Rapidly progressive glomerulonephritis (RPGN):
Type III RPGN

  • General
  • Pauci immune vasculitis includes…
  • AntiNeutrophil Cytoplasmic Antibodies (ANCA)
  • 2 ANCA patterns recognized by indirect IF
  • Incidence
  • Usual presentation
  • Presentation in pts w/ granulomatosis with polyangiitis (GPA)
A
  • General
    • Pauci-immune proliferative & necrotizing GN w/ or w/o systemic involvement
    • Lack of glomerular immune deposits on IF and EM
  • Pauci immune vasculitis includes…
    • Granulomatosis with polyangiitis (GPA) (formerly Wegener’s)
    • Churg-Strauss disease
    • Microscopic polyangiitis (MPA)
  • AntiNeutrophil Cytoplasmic Antibodies (ANCA)
    • Antibodies o lysosomal enzymes of neutrophils and monocytes are commonly present
  • 2 ANCA patterns recognized by indirect IF
    • C-ANCA … Cytoplasmic ANCA …Antiproteinase 3
      • Usually seen in pts w/ granulomatosis w/ polyangiitis (GPA)
    • P-ANCA… Perinuclear ANCA …Antimyeloperoxidase
      • More commin in microscopic polyangiitis (MPA)
  • Incidence
    • 5th - 6th decades
  • Usual presentation
    • Prodrome lasting for weeks to months during which they may have intermittent fever, arthralgia, weight loss, shortness of breath, middle ear effusion
  • Presentation in pts w/ granulomatosis with polyangiitis (GPA)
    • Symptoms involving upper airway like sinusitis, epistaxis, and saddle nose deformity
18
Q

Rapidly progressive glomerulonephritis (RPGN):
Type III RPGN

  • Urine analysis
  • Renal biopsy
  • Pathology
    • LM
    • IF
    • EM
  • Pathogenesis of pauci-immune GN/vasculitis
  • Treatment
A
  • Urine analysis
    • Moderate proteinuria & active urine sediments w/ RBC casts
  • Renal biopsy
    • Usually needed to confirm the diagnosis
  • Pathology
    • LM: necrotizing lesions of the glomerular tuft along with crescents
    • IF: little or no immunoprotein deposits as shown below
    • EM: few or no deposits (hence pauci)
  • Pathogenesis of pauci-immune GN/vasculitis
    • ~80-90% have a circulating (ANCA) which is etiologically active in the production of vasculitis
    • Infection, drug exposure, or other inflammatory processes activate polymorphonuclear leukocytes and endothelial cells –>
      • Local generation of cytokines
      • Translocation of ANCA lysosomal antigens, PR3 or MPO to the cell membrane
      • Specific anti PR3 and anti MPO antibodies bind and further activate target neutrophils to secrete damaging ROS & other mediators of inflammation –> production of a necrotizing vasculitis
  • Treatment
    • Aggressiveness –> high dose steroids and cyclophosphamide
    • Long-term: trimethoprim/sulphamethoxazole
      • Maintain remission in granulomatosis with polyangiitis (GPA), esp respiratory disease
    • Rituximab + glucocorticoids is as effective as CYC to induce remission of severe GPA/MPA
    • Closely monitored for signs of toxicity from the immunosuppressant therapy
    • Serial measurement of ANCA level determines disease activity or predict relapse (controversial).
19
Q

Chronic glomerulonephritis

  • General
  • Characterized by…
  • Associated w/…
  • Diagnosis
  • Clinical findings
  • Cause
A
  • General
    • End-stage glomerular disease secondary to any form of glomerular disease
  • Characterized by…
    • Diffuse glomerulosclerosis
    • Advanced tubulointerstitial and vascular chronic injury
  • Associated w/…
    • Broad casts, variable hematuria and proteinuria, HTN, & small kidneys (< 9 cm w/ increased echogenicity)
  • Diagnosis
    • No specific diagnosis can be established when the disease is end-stage
    • Biopsy is generally not useful + risk of bleeding w/ small kidneys
  • Clinical findings
    • Kidneys are contracted (small)
    • Proteinuria may be reduced to non-nephrotic range
    • Urinary sediment has RBCs, broad casts
    • In final stages accompanied by “uremic state”
    • HTN may dominate clinical picture
  • Cause
    • All previously mentioned glomerular syndromes may –> chronic GN
20
Q

Key features

  • Treatment in all diseases
  • Acute post-infectious
    • IF
    • EM
  • Ig A nephropathy
    • IF
  • MPGN
    • General
  • Lupus
    • IF
  • Goodpasture syndrome
    • IF
  • Type III – Pauci immune
    • IF
A
  • Treatment in all diseases
    • Slow the progression of renal damage
    • Control HTN & hyperlipidemia
    • ACE-Is
    • Smoking cessation
    • Treat the sequelae of renal disease ( anemia, hyperparathyroidism, etc.)
  • Acute post-infectious
    • IF: Lumpy Bumpy
    • EM: Subepi, Hump, flame like,
  • Ig A nephropathy
    • IF: mesangial Ig A deposits
  • MPGN
    • Double contour of BM, Tram Tracks, Subendothelial deposits
  • Lupus
    • IF: “Full house,” different classes of histology
  • Goodpasture syndrome
    • IF: Linear deposits
  • Type III – Pauci immune
    • IF: Minimal immune deposits
21
Q

St. Andrew’s Flag

  • Think of glomerular disease as…
  • On one end
  • On the other end
  • Diseases in b/n will have varying degrees of…
A
  • Think of glomerular disease as a continuum
  • On one end
    • Diseases that are primarily “nephrotic” (ex. minimal change)
  • On the other end
    • Diseases that are primarily “nephritic” (ex. rapidly progressive GN)
  • Diseases in b/n will have varying degrees of…
    • Proteinuria (nephrosis)
    • Aggressive inflammatory change (nephritis)

Renal (24 decks)

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