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Renal > Glomerular Disease 1 > Flashcards

Glomerular Disease 1 Flashcards

1
Q
  1. What is a diffuse process?
  2. What is a focal process
  3. What is a global disease?
  4. What is a segmental disease?
A
  1. All of the glomeruli
  2. Some of the glomeruli
  3. The entirety of a glomeruli
  4. Only part of a glomeruli
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2
Q

How does glomerular disease present? (3)

A

Loss of GFR - Temporal change
Hematuria - Quality
Proteinuria - Quantity

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3
Q

What is a nephrotic syndrome?

A

Proteinuria > 3.5 g/day
Hypoalbuminemia
Edema
Hyperlipidemia
Lipiduria
Hypercoaguability (Loss proteins C and S)

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4
Q

What is nephritis?

A

Mild proteinuria
Hematuria
Hypertension
Edema

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5
Q

What are causes of acute glomerulonephritis?

A
  • IgA nephropathy
  • Post-infectious GN
  • Anti-GBM dz/Goodpasture’s
  • Small vessel vasculitis
  • Lupus nephritis
  • Membranoproliferative GN
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6
Q

What are mainly nephrotic: dz?

\What are mainly nephritic dz?

Which ones have crossover?

A

Nephrotic: Minimal change, focal segmental glomerulosclerosis, membranous nephropathy, IgA nephropathy

Nephritic: Crescentic (ANCA), Acute post-infectious,, Membranoproliferative GNs

Crossover: Membranoproliferative GN, IgA nephropathy

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7
Q

What is IgA nephropathy?
What is the common age range for patients?
What is the most prominent feature?
Is proteinuria present?

A

Most common GN worldwide
Most patients between age of 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

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8
Q

What are other complications that accompany IgA nephropathy?

A

Dysuria and loin pain with hematuria
Hematuria frequently occurs in conjunction with a URI (synpharyngitic hematuria)
HTN may be present in patients with more advanced dz

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9
Q

How does IgA nephropathy appear on LM, IF, and EM?

A

LM: Variable mesangial hypercellularity
IF: Mesangial IgA deposition
EM: Mesangial ectrone dense deposits

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10
Q

What is IgA nephropathy’s prognosis?
What are treatment’ options?

A

Prognosis: Based on serum creatinine, BP, proteinuria
40% will slowly develop CKD

Tx: Fish oil can slow progression
ACEi to control BP
Corticosteroids/immunosuppressants used in progressive dz

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11
Q

What is Henoch-Schonlein Purprua?
How can it manifest?

A

Systemic disorder haracterized by IgA deposition in multiple organs

Manifestations:
Skin - Characteristic non-blanching purpura or legs and buttocks
Joints - Transient arthralgias
GI - Abdominal pain, vomiting, melena, hematochezia
Kidney - Hematuria, proteinuria, rarely with progressive renal dz

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12
Q

What is post-infectious GN and its standard course?

A

Often post-streptooccal GN

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13
Q

What are the symptoms of post-strep GN?

What are the laboratory studies for post-strep GN?

A

Sudden onset HTN, azotemia, oliguria, edema and cola- or tea-colored urine

Low C3 level, ASO elevated, urinalysis reveals RBC casts, mild proteinuria

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14
Q

Morphologic features of post-infectious GN (LM, IF, EM)

A

LM: Enlarged, hypercellular, glomeruli, diffuse mesangial and endocapillary proliferation with neutrophils. May see crescents
IF: Granular capillary wall and mesangial IgG and C3
EM: Mesangial and large subepithelial “hump-like” deposits

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15
Q

What is the prognosis of post-strep GN

A

95% of children will recover with conservative management (1% progress to renal failure)
60% of adults will recover promptly

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16
Q

What is rapidly progressive GN?
What are the causes?
What are the characteristics on LM?

A

“Crescentic CN”
Classic nephritic syndrome with rapid progression (days to weeks) to renal failure

Causes: Anti-GBM/Goodpasture’s, immune complex GN (lupus, post-infectious, cryoglobulinemia), ANCA associated (Pauci immune)

Segmental necrosis and cellular crescent

17
Q

What is Anti-GBM/Goodpasture’s syndrome gender predisposition?

How does it present

What is the cause?

A

More often in males than females

Presents as a pulmonary-renal failure syndrome: hemoptysis, pulmonary infiltrates, glomerulonephritis

Due to circulating anti-GBM Ab
Antigen is alpha-3-chain of type IV collagen

18
Q

What is the diagnostic criteria for Anti-GBM/Goodpasture’s Syndrome?

What is treatment?

A
  1. Anti-GBM antibody in blood, linear IgG and C3 on kidney biopsy IF
  2. Treatment with plasmapheresis, prednisone, cytoxan
19
Q

What is pauci-immune GN?
What causes it?

A

Crescenteric GN with little deposition of immune reactants

Idiopathic or ANCA

20
Q

What small vessel vasculitis are associated with nephritis?

A

Microscopic polyangiitis - No granulomatous inflammation and no asthma

Wegner’s granulomatosis - Necrotizing granulomatous inflammation; no asthma

  • c-ANCA in 80%
  • URT symptoms, mononeuritis multiplex, purpura, nephritis
  • Renal biopsy: cresenteric GN without immune deposits

Curg-Strauss syndrome: Necrotizing granulomatous, inflammation, asthma, eosinophilia

21
Q

What are secondary causes of nephrotic syndrome?

What is used for diagnosis?

Treatment?

A

Systemic diseases, Diabetes mellitus, SLE, amyloidosis, infections (HIV, HBV, HCV, syphilis), drugs (NSAIDs, gold penicillamine)

2ndary causes: ANA, anti-dsDNA, complement, serum and urine protein electrophoreses, HBV/HCV serologies, cryoglobulins, syphilis serology
Also renal biopsy generally indicated

ACEi/ARB (reduce intraglomerular pressure and proteinuria), statins (lipids), diuretics, salt restriction (edema)

22
Q

What is minimal change disease?

What is the course with children?

What are the causes with adults?

A

Most common cause of nephrotic syndrome in children

Peak incidence ages 2-6, 5% progress to ESRD, spontaneous remissions can occur, treatment with steroids often induces remission although relapses occur in about 75%, fewer relapses after puberty

In adults can be idiopathic or associated with drugs (NSAIDs), neoplasms (Hodgkin’s lymphoma, other cancers), infections (syphilis, HIV)

23
Q

What is observed for Minimal Change Disease on LM, IF, EM?

What is treatment?

A

LM: Glomeruli, interstitium and tubules appear normal
IF: Negative or mesangial IgM
EM: Podocyte foot process effacement

Children respond well to corticosteroids, majority of adults also respond to steroid (longer than in children, partial remissions)

24
Q

What is membranous nephropathy?

What are the secondary causes?

A

Most common cause of nephrotic syndrome in Caucasian adults

Secondary causes account for 15-20% of cases
Infections - HBV
Connective tissue diseases - SLE
Neoplasms - Carcinoma of lung, colon, stomach, breast, non-Hodgkin’s lymphoma
Drugs - Gold, penicillamine, Hg, NSAIDs, captopril

25
Q

What is the course of membranous nephropathy?

What is the prognosis?

A

Onset is generally insidious
Patients usually present with heavy proteinuria & nephrotic syndrome
HTN & Azotemia later
Occult malignancies and infections may become evident later
Renal vein thrombosis occurs in 20%

Rule of thirds
1/3rd spontaneous remission
1/3rd partial remission with stable function
1/3rd slowly progressive loss of renal function

26
Q

What is Membranous Nephropathy appearance on LM, IF, EM?

What is the treatment?

A

LM: Diffuse thickening of GBM, GBM “spikes” on silver stain
IF: Granular GBM deposits of IgG
EM: Subepithelial deposits

Treatment: ACEi/ARB for those without poor prognostic factors, otherwise steroids/immunosupressants

27
Q

What is focal segmental glomerulosclerosis?

What are the sequelae?

What are the types of FSGS?

A

Most common cause of idiopathic nephrotic syndrome in African-Americans

More agressive than minimal change disease: HTN, hematuria more common, renal dysfunction is commonly progressive, ESRD occurs 5-20 years after presentation

Primary - Usually presents with acute onset of nephrotic syndrome
Secondary - Usually manifests with slow increasing renal insufficiency and proteinuria
Hereditary - Mutations in proteins that make up the glomerular slit diaphragm

28
Q

What are secondary causes of FSGS?

A

Drugs - NSAIDs, heroin
Infections - HIV
Massive obesity
Healed previous glomerular injury
Loss of functioning renal mass - unilateral agenesis, reflux nephropathy

29
Q

How does FSGS appear on LM, IF, EM?

What is prognosis?

What is treatment?

A

LM: **Focal and segmental glomerular sclerosis **with capillary collapse, hyaline and lipid deposition and adhesion to Bowman’s capsule
IF: Negative or IgM and C3 in mesangium or in segmental scars
EM: Podocyte foot prcess effacement, may see segmental sclerosis

Prognosis correlates with degree of proteinuria, progression in 50% at 10 years, trreatment for steroid-resistant/relapsing patients is problematic

Treat with ACEi to reduce proteinuria, corticosteroids or other immunosuppressive

30
Q

What is the sequelae of Membranoproliferative Glomerulo-nephritis (MPGN)?

What are the causes of MPGN?

A

Proteinuria & hematuria commonly coexisting with HTN in 1/3
Low C3 complement is a prominent feature
Variable presentation: 50% nephrotic syndrome, 30% asymptomatic proteinuria w/w/o hematuria, 20% acute GN

Primary or Secondary (SLE, connective tissue diseases, cryoglobulinemia, infections - HCV, HBV, endocarditis, abscesses, neoplasms)

31
Q

What is MPGN findings in LM, IF, EM?

A

LM: Hypercellular glomeruli, endocapillary cell proliferation, lobular appearing glomeruli
IF: Granular C3 deposition
EM: Subendothelial deposits

32
Q

What is SLE?

What is lupus nephritis?

What iare the sequelae?

What is treatment for SLE?

A

Multi-system auto-immune disorder (abnormal autoantibody production, immune complex deposition, inflammatory cell infiltration)

Common cause of diffuse proliferative GN with many of the different clinical syndromes of renal disease can occur in the setting of SLE (renal biopsy needed to clarify lesion)

40% of the patients develop overt nephritis (follow U/A in SLE patients, HTN suggests the presence of renal disease)

General principles: Aggressive BP control, lipid control, appropriate treatment of extrarenal involvement
Classes III-V: Usually treated with corticosteroids + cytotoxic therapy; Class IV: Renal failure rate 25% by 5-10 years

Renal (17 decks)

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