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Glomerular Disease Flashcards

1
Q

What are the 3 mechanisms of glomerular disease?

A
  • Immunocomplex deposition
    • circulate the deposit in glomerulus
      • Eg DNA-anti-DNA complexes in Lupus
    • activates complement resulting in neutrophil chemotaxis
  • antibodies against GBM or glomerular antigens
  • cytokine production by inflammatory cells
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2
Q

What are the 3 ways by which glomerular disease presents?

A

Hematuria (quality)

Loss of GFR (temporal change)

Proteinuria (quantitity)

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3
Q

How do we name glomerular disease? diffuse vs focal

glocal vs segmental

A

How many glomeruli?

Diffuse (all), focal (some)

How much of a glomerulus

glocal (entire glomerulus), segmental (part of)

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4
Q

Nephrotic syndrome

A
  • proteinuria > 3.5 g/day
  • hypoalbuminemia
  • edema
    • loss of plasma oncotic pressure vs Na/H20 retention
  • hyperlipidemia
    • increased hepatic protein production
  • lipiduria
  • hypercoagulability
    • loss of proteins C and S
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5
Q

Nephritis

A
  • mild proteinuria
  • hematuria
    • RBCs, RBC casts, dysmorphic RBCs
  • hypertension
  • edema
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6
Q

What are the 3 main primary nephrotic syndromes?

A

minimal change disease

focal segmental glomerulosclerosis

membranous nephropathy

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7
Q

What are the causes of acute glomerulonephritis

A

IgA nephropathy

post-infectious GN

Anti GBM disease/ Goodpasture’s

small vessel vasculitis

lupus neprhitis

membranoproliferative GN

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8
Q

What is IgA Nephropathy

who gets it, what is the most prominent feature, when does it occur? what symptoms occur with it?

A
  • Most common GN worldwide
  • most patients begtween age 10-50
  • hematuria is most prominent feature
    • 50-60% episodic gross hematuria
    • 30% persistent microhematuria
    • 10% acute GN or nephrotic syndrome
  • Proteinuria, if present, is generally mild
  • many cases are subclinical
  • dysuria and loid pain may accompany hematuria
  • hematuria frequently occurs in conjunction with an upper respiratory infection (synpharyngitic hematuria)
  • HTN may be present in patients iwth more advanced disease
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9
Q

What is seen on Light microscopy(LM), electron microscopy (EM) and immunoflouresence (IF)?

A
  • LM: Variable mesangial hypercellularity
    • may see segmental proliferation, segmental sclerosis and necrosis with crescents
  • IF: Mesangial IgA deposition
  • EM: Mesangial electron dense deopsits (paramesangial)
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10
Q

What is the prognosis of IgA nephropathy? What kind of treatment is it?

A
  • serum creatinine, BP, and degree of proteinuria
    • 40% of patients will slowly develop chronic kidney disease
  • fish oil may slow progression of disease
  • ACE inhibitors used to control blood pressure
  • Corticosteroids, other immunosuppressants also may be used in progressive disease
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11
Q

What is henoch-schonlein purpura?

A
  • Nephritic
  • Systemic disorder characterized by IgA deposition in multiple organs
  • multiple manifestations
    • skin: characteristic non-blanching purpura on legs and buttocks
    • joints: transient arthralgias
    • GI tract: abdominal pain, vomiting, melena, hematochezia
    • kidney: hematuria, proteinuria. rarely progressive renal failure
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12
Q

What is Post infectious GN? What is the prognosis?

A

post-streptococcal GN-classic example

follows infection in nephritogenic strain of group A beta hemolytic streptococcus

occurs 7-14 days after pharyngitis; 14-28 days after skin infection (note this is not synpharyngetic which means simultaneous and is seen with IgA nephropathy)

95% of children will recover with conservatice management, 1% progress to renal failure

60% of adults will recover promptly

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13
Q

What are the causes of rapidly progressive GNs

A

classic nephritic syndrome with rapid progression (days to weeks) to renal failure

sometimes referred to as crescentic GN

causes:

  • Anti-GBM/Goodpasture’s
  • Immune complex GN
    • lupus nephritis
    • post-infectious
    • cryoglobulinemeia
  • ANCA associated GN (Pauci immune)
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14
Q

WHo gets Anti-GBM/ Goodpastures syndrome? How does it present?

A
  • males> females
  • may present as pulmonary-renal syndrome
    • hemoptysis
    • pulmonary ifiltrates
    • glomerulonephritis
      • GN alone in anti-GBM disease
  • due to circulating anti-GBM antibody
    • antigen is a3 chain of type V collagen
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15
Q

How do we diagnose and treat Anti-GBM/ Goodpasture syndrome?

A

diagnosis:

+ anti-GBM antibody in blood

Linear IgG and C3 on kidey biopsy IF

treatement:

plasmapheresis

prednisone

cytoxan

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16
Q

What is Pauci immune GN?

A

cresenteric GN with litte deposition of immune reactants

“pauci immune”

idiopathic or associated with antineutrophil cytoplasmic antibody (ANCA) vasculitis

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17
Q

What are 3 small vessel vasculitis?

A
  • microscopic polyangiitis
    • no granulomatous inflammation and no asthma
  • granulomatosis with polyangiitis (wegners)
    • necrotizing granulomatous inflammation; no asthma
  • eosinophilic granulomatosis with polyangiitis
    • necrotizing granulomatous inflammation, asthma, eosinophilia
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18
Q

What is granulomatosis with polyangiitis (GPA)? How does it present and what is seen on renal biopsy?

A
  • granulomatous vasculitis of medium to small arterioles
  • c-ANCA + in 80%
  • presentation
    • upper respiratory tract symptoms (sinusitis, nasal lesions, hemoptysis)
    • mononeuritis mulitplex
    • purpura
    • nephritis
  • renal biopsy: cresenteric GN without immune deposits
    *
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19
Q

Fill this in

20
Q

what are the 3 primary nephrotic renal diseases? in children 80% will have which one?

A

membranous nephropathy

focal segmental glomerulosclerosis (FSGS)

minimal change

21
Q

What are secondary causes of nephrotic syndrome?

A

systemic diseases:DM, SLE, amyloidosis

infections: HIV, Hepatitis B, Hepatitis C, syphyllis
drugs: classical examples include NSAIDs, gold, penicillamine

22
Q

what laboratory studies/techniqes are used to dignose nephrotic syndrome?

A
  • ANA, anti-ds-DNA, complement levels
  • serum and urine protein electrophoreses
  • HBV and HCV serologies
  • cryoglobulins
  • syphillis serology

renal biopsy is generally indicated

23
Q

what are teh treatments for all causes of nephrotic syndrome?

A

ACE inhibitor or Angiotensin II receptor blocker to lower intraglomerular pressure and reduce proteinuria

lipid lowering statin

diuretic, salt restriction to improve edema

24
Q

What is the most common cause of nephrotic syndrome in children?

A

Minimal change disease

25
what is the peak incidence of mininmal change disease?
2-6 5% progress to rend stage renal disease spontanneous remissions can occur treatment with steroids often includes remission although relapses occur in about 75% fewer relapses after puberty
26
what causes Minimal change disease?
in adults, can be idiopathic or associated with: * drugs-NSAIDs * neoplasms-Hodgkin's lymphoma, pancreatic, prostate, lung, colon and renal cell carcinomas, mesothelioma, oncocytoma * infections-syphyllis, HIV
27
What do you see on LM, IF, EM for minimal change disease?
LM: Glomeruli, interstitium and tubules appear normal IF: negative or mesangial IgM EM: Podocyte foot process effacement (fusion)
28
How do we treat minimal change disease?
* children respond well to corticosteroids * majority of adults with minimal change disease respond to steroids * usually takes longer than in children * partial remissions may occur
29
Who gets membranous nephropathy?
* most common cause of nephrotic syndrome in caucasian adults * caused by antibodies to the podocyte antigens phospholipiase A2 receptor (70%) or thrombospondin type 1 domain containing 7A (10%)
30
what are secondary causes of membranous nephropathy?
* infections: HBV * connectivetissue diseases: SLE * Neoplasms-carcinoma of lung, colon, stomach, breast; non-Hodgkin's lymphoma * consider age appropriate cancer screening * drugs-gold, penicillamine, mercury, NSAIDs, captopril
31
What is the onset of membranous nephropathy like? how do patients present?
* onset is insidious * patients usually present with heavy proteinuria and nephrotic syndorme * HTN and azotemia occur later * occult malignancies and infections may become evident later * renal vein thrombosis occurs in 20%
32
What is seen on LM, IF, EM in membranous nephropathy?
LM: diffuse thickening of GBM, GBM "spike" on silver stain IF: granular GBM deposits of IgG EM: subepithelial deposits \*\*spikes are seen bc staning for the basement membreane so the complexes dont get stained
33
where do immune deposits deposit in membranous nephropathy?
immune deposits form on the subepithelial aspect of glomerula basement membrane
34
What is the rule of thirds for membranous nephropathy?
1/3 apontaneous remission 1/3 partial remission with stable function 1/3 slowly progressive loss of renal function
35
How do we treat people with membranous nephropathy?
patients with poor prognostic factors might be managed conservatively with ACE and/or ARB and followed closely otherwise steroids and or immunosuppressive drugs
36
Who gets Focal Segmental glomerulosclerosis? What is seen with it?
* most common cause of idiopathic nephrotic syndrome in African Americans * more aggressive than minimal change disease * HTN, hematuria more common * renal dysfunction is commonly progressive * ESRD occurs 5-20 yrs after presentation
37
How does primary FSGS present? Secondary? Heriditary?
Primary: usually presents with acute onset of nephrotic syndrome secondary FSGS: usualyl manifests with slowly increasing renal insufficiency and proteinuria herditary FSGS: mutations in proteins that make up the glomerular slit diaphragm
38
what are the causes of secondary FSGS?
drugs-NSAIDs, heroin infections- HIV Massive obesity healed previous glomerular injury loss of functioning renal mass-unilateral agenesis, reflux nephropathy, etc.
39
What is seen on LM, IF and EM for Focal Segmental Glomeruloscleosis?
LM: focal and segmental glomerular sclerosis with capillary collapse, hyaline and lipid deposition and adhesion to Bowman's capsule IF: negative of IGM and C3 in mesangium or in segmental scars EM: podocyte foot process effacement; may see segmental sclerosis \*\*global sclerosis
40
how do we treat FSGS?
* prognosis correlates with degree of proteinuria-ACE inhibitors decrease proteinuria * corticosteroid can induce remission in some patients patients * treatment for steroid resistant patients and patients who relapse is problematic * immunosuppressives * progression to ESRD in 50% at 10 years \*\*\*black, HIV, obesity
41
what is seen in membranoproliferative glomerulo-nephritis (MPGN)
* proteinuria and hematuria commonly coexist * HTN occurs in 1/3 * low C3 complement is a prominent feature * variable clinical presentation * 50% nephrtoic syndrome * 30% asymptomatic proteinuria +- hematuria * 20% acute Gn
42
What are the 2 types of MPGN and what is seen?
* Primary MPGN * Secondary MPGN * connective tissue diseases- SLE cryoglobulinemia * infections- Hepatitis C virus, HBV, endocarditis abscesses * neoplasms
43
what is seen on LM, IF, EM for MPGN?
LM: hypercellular glomeruli, endocapillary cell proliferation, lobular appearing glomeruli IF: granular C3 deposition EM: subendothelial deposits
44
what 3 things happen with systemic lupus erythematous (SLE)
* a multisystem auto-immune disorder * abnormal autoantibody production * immune complex deposition * inflammatory cell infiltration
45
What is lupus nephritis?
* common cause of diffuse proliferative GN * 40% of patients develop overt nephritis * follow U/A in SLE patients * HTN suggests the presence of renal disease * man of the different clinical syndromes of renal disease can occur in the setting of SLE * renal biopsy is important to order considering the lesion in SLE
46
treatment for lupus nephritis
* general principles of management of any class of lupus nephritis * aggressive BP control * control of lipid levels * appropriate treatment od extrarenal involvement * classes III-V usually treated with corticosteroids + cytotoxic therapy * class IV: renal failure rate 25% by 5-10 yrs

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