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X Clin Med II Exam 3 > Glomerulonephritis and PKD > Flashcards

Glomerulonephritis and PKD Flashcards

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1
Q

What can cause glomerulonephritis?

A 
IgA nephropathy
Poststreptococcal GN
Anti-GBM antibody disease
Lupus nephritis
IgA vasculitis (HSP)
Pauci-immune GN
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2
Q

What is an early sign of kidney disease?

A

Proteinuria (due to increased permeability and the filtration not working right)

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3
Q

What is glomerular disease?

A

Damage to the major components of the glomerulus (podocyte, glomerular basement membrane, capillary endothelium or mesangium)

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4
Q

Primary vs secondary glomerular disease

A

Primary: glomerular injury limited to kidney
Secondary: renal abnormalities result from a systemic disease

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5
Q

What is glomerulonephritis?

A

Group of diseases that present in nephritic spectrum and usually signifies inflammatory process in glomerulus causing renal dysfunction

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6
Q

Cause of glomerulonephritis

A

Deposition of immune complexes of glomerulus

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7
Q

Major clinical findings of nephritic syndrome

A 
Hematuria (dysmorphic RBCs and RBCs casts)-cola urine
Proteinuria (subnephrotic <3 g/day)
Elevated creatinine (or decrease in GFR)
Oliguria
Edema (periorbital, peripheral)
HTN
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8
Q

What is rapidly progressive glomerulonephritis?

A

Most severe and urgent end of nephritic spectrum

Progressive loss of renal function over short period of time

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9
Q

What characterizes rapidly progressive glomerulonephritis on a biopsy?

A

Crescent formation

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10
Q

What is the crescent formation?

A

Nonspecific response to severe injury to glomerular capillary wall

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11
Q

Common causes of hematuria

A

UTI, stones, cancer, BPH

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12
Q

How do you distinguish extraglomerular from glomerular hematuria?

A

Extraglomerular: red/pink, may have clots!, normal RBCs
Glomerular: cola-colored, no clots, may have proteinuria, dysmorphic RBCs, maybe RBC casts

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13
Q

Serologic testing for GN

A

Creatinine, ANA, anti-ds DNA, complement, ANCA, anti-GBM antibodies, antistreptolysin O titer

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14
Q

Antiproteinuric therapy of GN

A

ACE-I or ARB

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15
Q

What warrants immediate hospitalization in GN?

A

Acute nephritic syndrome or RPGN

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16
Q

Most common cause of primary GN in world

A

IgA nephropathy (Berger’s disease)

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17
Q

Which type of IgA nephropathy is most common?

A

Primary (renal-limited)

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18
Q

When is IgA nephropathy seen in the most?

A

2nd and 3rd decades of life

Males more

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19
Q

Pathogenesis of IgA nephropathy

A

IgA deposition in the glomerular mesangium due to an inflammatory response

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20
Q

Most common presentation of IgA nephropathy

A

An episode of gross hematuria usually following a URI (often 1-2 days after illness)
On nephritis spectrum

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21
Q

How do you confirm IgA nephropathy

A

Kidney biopsy (more severe or progressive disease)

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22
Q

Tx of IgA nephropathy

A

1/3 is spontaneous clinical remission
Tailor to risk of progression-ACE-I or ARB
Glucocorticoids +/- immunosuppressive agents

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23
Q

Who is at higher risk of progressing to end stage renal disease?

A

Proteinuria > 1 g/d
Decreased GFR
HTN

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24
Q

Cause of poststreptococcal GN

A

Infection with group A beta-hemolytic strep infections (usually pharyngitis or impetigo)

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25
When is poststreptococcal GN seen more?
In kids | Seen more in males
26
Pathophysiology of post-streptococcal GN
Immune complex with antigen deposited into glomerulus and triggers complement activation and inflammation
27
Presentation of post-streptococcal GN
Varies across nephritic spectrum | Sxs 1-2 wks after infection!
28
Lab findings of post-streptococcal GN
Elevated streptococcal antibodies (ASO titers) | Low complement
29
Tx of post-streptococcal GN
Usually see resolution within first 2 wks Supportive Children more likely to recover
30
What is anti-GBM disease?
Circulating antibodies directed against glomerular basement membrane
31
Where else is target antigen seen in anti-GBM disease?
Alveolar basement membrane (acute renal pulmonary glomerulonephritis)
32
Who tends to have anti-GBM disease?
First is about 30 (male predominance and lung involvement) | Second about 60 (with female predominance)
33
Difference between anti-GBM disease and goodpasture syndrome
Anti-GBM: anti-GBM and GN (just kidney) | Goodpasture: GN and pulmonary hemorrage
34
Presentation of anti-GBM disease
Usually idiopathic (HLA predisposition)--pulm infection, tobacco use, hydrocarbon exposure Renal involvement: nephritic spectrum (RPGN) Pulm involvement: cough, dyspnea, overt hemoptysis
35
How to diagnose anti-GBM disease
See anti-GBM antibodies in serum or kidney biopsy | Test for ANCA
36
Tx of anti-GBM disease
Plasmapheresis (remove antibodies from circulation) | Immunosuppressive agents
37
What is lupus nephritis?
Immune complex mediated glomerular disease due to anti-ds DNA antibodies Many patterns of injury (usually nephritis spectrum) Nonwhites
38
When do you usually suspect lupus nephritis?
By abnormal urinalysis and/or elevation of serum creatinine | Confirm with renal biopsy
39
What is IgA vasculitis (HSP) caused by?
Immune mediated vasculitis with tissue deposition of IgA containing immune complexes
40
When is HSP usually seen?
Mostly in kids (more males) Unknown cause Often post-URI
41
Classic tetrad of HSP
Rash (palpable purpura), arthralgias, abdominal pain and renal disease
42
Renal disease associated with HSP
Adults have increased risk of progressive renal disease | Involvement usually after rash (nephritis or nephrotic)
43
Tx of HSP
Usually self limited | Support, symptomatic care and targeted therapy for complications
44
What causes Pauci-immune GN?
Systemic ANCA-associated vasculitides: - granulomatosis with polyangiitis (GPA) - microscopic polyangiitis (MPA) - eosinophilic granulomatosis with polyangiitis (EGPA)
45
What is ANCA?
Antibodies that produce vascular and tissue damage (P-ANCA and C-ANCA)
46
What is seen on renal biopsy in pauci-immune GN?
Absence/paucity of immune deposits
47
How does pauci-immune GN present?
RPGN
48
What is granulomatosis with polyangiitis?
ANCA-associated vasculitis Rare, complex multisystem autoimmune disease -C-ANCA
49
Hallmark feature of GPA
Necrotizing granulomatous inflammation (pauci-iimune vasculitis of small-medium vessels)
50
Where does GPA usually occur?
Upper and lower respiratory tracts or kidneys
51
Presentation of GPA
Upper and lower airway: sinusitis, saddle nose, otitis media, ocular involvement, cough, dyspnea Renal: GN (crescent necrotizing GN-cap wall collapses in on self) Fever, malaise, weight loss, arthritis, skin, polyneuropathy
52
What is microscopic polyangiitis?
ANCA-associated vasculitis of small-medium vessels | -P-ANCA
53
MPA and GPA
Present similarly with GN and lung involvement | but in MPA there is absence of granuloma formation and sparing of upper respiratory tract (no sinusitis etc)
54
What is eosinophilic granulomatosis with polyangiitis?
Churg-strauss syndrome ANCA associated vasculitis (lung, skin, heart, renal, GI, neuro-peripheral neuropathy) -P-ANCA
55
What is EGPA associated with?
Asthma and eosinophilia
56
3 phases of EGPA
Prodrome: allergic disease (asthma or allergic rhinitis) Eosinophilic/tissue infiltrative phase Vasculitis: necrotizing vasculitis of small-medium vessels
57
Tx for pauci-immune GN
Immunosuppressants (corticosteroids and cytotoxic agents) | Without tx, poor prognosis
58
When are simple cysts usually found?
Incidentally on ultrasound
59
What are the benign features associated with a simple cyst?
Smooth thin walls that are sharply demarcated and do not enhance with contrast
60
Standard of care for benign cyst
Periodic reevaluation
61
What is polycystic kidney disease?
Inherited disease that causes irreversible decline in kidney function (dominant or recessive)
62
What do pts with PKD usually need?
Renal replacement therapy (dialysis or kidney transplant)
63
Most common genetic cause of CKD
Autosomal dominant PKD | +FH in most
64
Genes associated with most cases of ADPKD
PKD1 or PKD2
65
What characterizes ADPKD?
Massive kidney enlargement (bilateral) | Progressive decline in renal function (GFR)--renal function remains intact until 4th decade (usually ESRD by 60)
66
Pathogenesis of ADPKD
Cysts accumulate fluid Enlarge Compress neighboring renal parenchyma Progressively compromising renal function
67
What is hyperfiltration of the kidneys?
When some nephrons lose function, others will begin to compensate
68
Why is decreased GFR seen in ADPKD?
Increasing kidney size and cyst volume and reduction in renal blood flow
69
Manifestations of ADPKD
Renal: HTN and abdominal/flank pain (palpable kidneys, hematuria, proteinuria, UTIs and nephrolithiasis) Extrarenal: hepatic cysts (intracranial aneurysms, CV disease, other cysts)
70
Initial modality to diagnose ADPKD
U/s
71
Typical findings on diagnostics of ADPKD
Large kidneys and extensive cysts scattered throughout both kidneys
72
Definitive diagnosis of ADPKD
Genetic testing
73
Tx of ADPKD
Strict BP control, low salt diet, statins Avoid caffeine Supportive therapy Complications (infected renal cyst, cyst hemorrhage, stones) Meds: Tolvaptan (vasopressin receptor antagonist) Dialysis or kidney transplant
74
When is autosomal recessive PKD seen more?
Infants and kids (due to mutation of PKHD1 gene)
75
2 primary systems affected in ARPKD
Kidneys and hepatobiliary tract (so more limited)
76
What characterizes ARPKD?
Bilateral markedly enlarged kidneys and congenital hepatic fibrosis (if neonates have ESRD then maybe respiratory distress)
77
Manifestations of ARPKD
Varies Progressive renal impairment or HTN Portal HTN May see feeding difficulties and growth impairment (b/c they compress diaphragm and cause satiety)
78
How to detect ARPKD
Routine antenatal u/s after 24 wks gestation
79
Tx of ARPKD
Supportive therapy with multidisciplinary team

X Clin Med II Exam 3 (6 decks)

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