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Nephrology > Glomerular Nephritis > Flashcards

Glomerular Nephritis Flashcards

1
Q

What are the most common causes of Secondary Nephrotic Syndrome

A 
Diabetic Nephropathy
Renal Amyloidosis
Multiple Myeloma
HIV associated Nephropathy
Hepatitis B associated kidney disease
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2
Q

What are clinical features of Diabetic Nephropathy

A

Decline in kidney fxn
HTN
retinopathy
peripheral neuropathy

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3
Q

What is the pathophysiology of Renal Amyloidosis

A

Deposition of abnormal fibrillary structures of proteins

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4
Q

What is the epidemiology of Renal Amyloidosis

A

Dx in 60s

slight predominance in males

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5
Q

describe AL Amyloidosis

A

Most common systemic amyloidosis in USA

deposition of Ig LIGHT CHAIN

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6
Q

describe AA Amyloid

A
  1. more common in developed countries
  2. deposition of AMYLOID A PROTEIN
  3. develops secondary to chronic inflammatory states (RA, TB, IBD, FMF, Lymphoma)
  4. multiorgan failure
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7
Q

Describe AF Amyloid

A
  1. Autosomal dominant disorder (deformities of TRANSTHYRETIN)
  2. Disorders of fibrinogen A alpha chain
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8
Q

AB2m

A

Hemodialysis associated amyloidosis

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9
Q

What are the most common features of Renal Amyloidosis

A 
Fatigue
Weight loss
purpura
Hepatosplenomegaly
Lymphadenopathy
Macroglossia
Urine LIGHT CHAIN
Increased Plasma cells
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10
Q

What is Dx of Renal Amyloidosis

A

SERUM & URINE FREE LIGHT CHAINS

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11
Q

What is the Light microscopy appearance of Renal Amyloidosis

A

CONGO RED positivity

crystal violet stains amyloid deposits in glomeruli and vessels

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12
Q

What is the Immunostaining difference between amyloid AL and AA?

A

Amyloid AL: Anti-Ig Light chains (kappa, lambda)

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13
Q

What is the electronmicroscopy of Renal amyloidosis

A

nonbranching irregular fibrils deposited in glomeruli, vessel walls, and extracellular spaces

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14
Q

What is the treatment for AL Amyloid?

A

Chemo: high dose MELPHALAN, peripheral stem cell transplantation

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15
Q

What is the treatment for AA Amyloid?

A

control chronic infections
Colchicine
Liver transplant

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16
Q

What is the pathophysiology of Multiple Myeloma?

A

proliferation of plasma cells:

  1. Coppt of IG LIGHT CHAINS + TAMM-HORSFALL Proteins = cast formation in DCT
  2. tubularreabsorption of light chaings = INFLAMMATION + FIBROSIS
17
Q

How does MM cause renal injury?

A 
Nephrotic syndrome (Cast, Ig, FSGS nephropathy)
ATN
18
Q

What are the clinical manifestation of MM?

A

Pain in lower back, Generalized malaise, Bruising

-minimal proteinuria

19
Q

What is the Dx of MM?

A

(need 1 major and 1 minor or 3 minor)
major:
Bx: plasmacytoma; Bone marrow: 30% PLASMA CELLS; elevated monoclonal Ig in blood/urine
minor:
marrow - 10%-30%, minor Ig, Osteopenia/lytic lesions, Abnormally low Ab levels

20
Q

What is the most important determinant of survival in MM?

A

kidney fxn

21
Q

What are the clinical manifestions of HIV associated nephropathy?

A

Nephrotic Syndrome
Kidney failure (ESRD)
No HTN - Sodium wasting in PCT
Severity of HIVAN correlates with CD4 cell count

22
Q

What is the Bx of HIVAN?

A

Collapsing glomerulopathy (prominent visceral epithelial cells/podocytes)

Microscystic dilation of tubules (PATHOGNOMONIC)
Tubulo-reticular bodies on EM

23
Q

What are 4 common causes for Nephritis

A
  1. Lupus nephritis
  2. MembranoProliferative GN
  3. IgA Nephropathy/HSP
  4. Pulmonary-Renal Syndromes
24
Q

What are some Sx for SLE?

A
  1. Constitutional
  2. Arthralgia, arthropathy
  3. Dermatologic (malar rash)
  4. AKI, CKD, Nephritic disease, Nephrotic syndrome
  5. Seizure, psychosis
25
Q

What happens to the glomerulus in Membranoproliferative GN?

A
  1. Mesangial hypercellularity

2. Endocapillary proliferation

26
Q

What are the clinical features of Membranoproliferative?

A
  1. Nephrotic Syndrome
  2. Acute Nephritic syndrome
  3. Asymptomatic proteinuria
  4. Hematuria
  5. ESRD in 10 years
27
Q

What is the histological difference between Type I, II, III MPGN?

A

Type I: Immunocomplexes in subendothelial space, mesangium

Type II: Dense Deposit Disease, deposits ain the mesangium, GBM, TBM and Bowman’s capsule

Type III: marked disruption of GBM w/ subendothelial and subepithelial electro-dense deposits

28
Q

What are the two categories of MPGN based on etiology/pathogenesis?

A
  1. Immune Complex-associated MPGN (ICM-MPGN)
  2. Complement mediated MPGN-C3N, DDD
    - –2 = complement dysregulation
29
Q

What are characteristics of CM-MPGN?

A
  • LOW C3, Normal C4
  • Acquired cause: circulating Auto-antibodies
  • Genetic cause: abnormalities in activating/regulating factors in CM
30
Q

What are the autobodies directed against in CM-MPGN?

A

complement regulating factors:
Factor H, Factor I, Factor B, convertase
auto-Ab: C3NeF

31
Q

What auto-Ab is predominantly found in patients affected by DDD (80%)

A

C3NeF (less frequently in C3GN, absent in CFHR5)

32
Q

What is the activity of C3NeF

A

binds to C3 convertase prolonging its survival

C3NeF can stabilize C5 convertase

33
Q

What does renal Bx look like in MPGN patients?

A

clear C3 staining with few/no immunoglobulin deposition

34
Q

what cause C3 GN?

A

dysregulation and excessive activation of the ALT complement (low C3 and positive serum C3NeF)

35
Q

What is the main cause of MPGN in the Middle East, South America, and Africa?

A

Chronic bacterial, viral, parasitic infections

36
Q

What are are serum characteristics of ICM-MPGN?

A

circulating immune complexes
seen in chronic infections (Hep B, C, parasites)
Automimmune disease (SLE, RA)

37
Q

What enzyme activity is decreased in patients with IgAN?

A

Leukocyte-b-1,3-galactosyl transferase

38
Q

What is the clinical triad of Goodpasture’s syndrome

A

(ANCA-negative vasculitis)

  1. Pulmonary hemorrhage
  2. glomerulonephritis
  3. circulating Anti-GBM Abs

Nephrology (13 decks)

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