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Unit 3 Clin Med II > L17:Glomerulonephritis +PKD > Flashcards

L17:Glomerulonephritis +PKD Flashcards

1
Q

basic filtering unit of the kidney

A

glomerulus

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2
Q

Glomerular disease

A

damage to the major components of the glomerulus: podocyte, glomerular basement membrane, capillary endothelium, mesangium. Range in severity

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3
Q

Focal Glomerular disease

A

less than 50% of glomeruli

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4
Q

Diffuse Glomerular disease

A

all glomeruli

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5
Q

Primary Glomerular disease

A

glomerular injury is limited to kidney

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6
Q

Secondary Glomerular disease

A

systemic disease → renal abnormalities

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7
Q

Glomerulonephritis

A

Diseases of the nephritis spectrum

Inflammatory process→ renal dysfunction

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8
Q

Most common cause of glomerulonephritis

A

Deposition of immune complexes in the glomerulus

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9
Q

Glomerulonephritis can present

A

acutely: +/- resolution
-or-
chronically (indolent): progressive scarring

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10
Q

Etiologies of glomerulonephritis

A

IgA nephropathy

Poststreptococcal GN

Anti-GBM disease

Lupus Nephritis

IgA vasculitis (Henoch-Schonlein Purpura)

Pauce-immune GN

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11
Q

Nephritic syndrome findings

A

Edema, HTN

Smoky/cola colored urine

Proteinuria: subnephrotic <3.0 g/day

Elevated creatinine

Oliguria

Dysmorphic RBC in urine sediment

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12
Q

Rapidly progressive glomerulonephritis

A

most severe and urgent of nephritis spectrum: progressive loss of renal function over a short period of time

Extensive crescent formation

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13
Q

Crescents

A

nonspecific response to severe injury to glomerular capillary wall
Seen extensively in rapidly progressive glomerulonephritis

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14
Q

Hematuria:
Extraglomerular vs. Glomerular:
color

A

Extraglomerular: red/pink
Glomerular: cola-colored

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15
Q

Hematuria:
Extraglomerular vs. Glomerular:
Clots

A

Extraglomerular: +/- clots
Glomerular: no clots

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16
Q

Hematuria:
Extraglomerular vs. Glomerular:
Proteinuria

A

Extraglomerular: none
Glomerular: +/- proteinuria

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17
Q

Hematuria:
Extraglomerular vs. Glomerular:
RBC morphology

A

Extraglomerular: normal
Glomerular: dysmorphic

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18
Q

Hematuria:
Extraglomerular vs. Glomerular:
RBC casts

A

Extraglomerular: none
Glomerular: +/- RBC casts

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19
Q

Big thing on urine microscopy of glomerulonephritis

A

RBC casts

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20
Q

Serologic testing for glomerulonephritis should include

A 
ANA
Anti-DS DNA ab
 complement
C-ANCA, P-ANCA
Anti-GBM abs
 ASO titer
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21
Q

Antiproteinuric therapy of glomerulonephritis

A

ACE-I or ARB

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22
Q

immediately hospitalize

A

Acute nephritic syndrome

Rapidly progressive glomerulonephritis

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23
Q

IgA nephropathy aka

A

Berger Disease

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24
Q

most common cause of primary glomerulonephritis

A

IgA nephropathy

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25
Primary IgA nephropathy is
renal-limited | more common
26
Secondary IgA nephropathy is due to
cirrhosis celiac HIV CMV
27
Who is most likely to get IgA nephropathy
2nd/3rd decades of life Males Asians and Caucasians Inheritable
28
Pathogenesis of IgA nephropathy
inciting cause unknown→ IgA deposition in mesangium→ inflammatory response
29
Presentation of IgA nephropathy
URI→ gross hematuria 1-2 days later→ presentation along nephritic spectrum (nephrotic rare)
30
IgA nephropathy vs. Postinfetious GN: | Timing
IgA nephropathy: 1-2 days after URI | Postinfetious GN: 1-3 weeks after infection
31
How to confirm IgA nephropathy diagnosis
Kidney biopsy | *usually for severe/progressive*
32
3 options for disease course of IgA nephropathy
1. Spontaneous clinical remission (⅓) 2. Progression to end stage renal disease (ESRD) (20-40%) 3. Chronic microscopic hematuria and stable creatinine
33
Higher risk for progression of IgA Nephropathy
Proteinuria >1g/d Decreased GFR HTN
34
If at higher risk for progression of IgA nephropathy, treat with
ACE-I or ARB
35
Other tx for IgA nephropathy
Glucocorticoids +/- immunosuppressants
36
Postinfectious glomerulonephritis aka
Poststreptococcal glomerulonephritis
37
Postinfectious glomerulonephritis is preceded by
pharyngitis or impetigo | group A beta-hemolytic strep
38
Who gets Postinfectious glomerulonephritis
Male children most commonly
39
Serology of Postinfectious glomerulonephritis
Elevated ASO titers | Low complement
40
Anti-GBM disease
circulating antibodies against GBM=glomerular basement membrane -nephritic spectrum, can be RPGN also against alveolar basement membrane -cough, dyspnea, +/- hemoptysis
41
Bimodal distribution of Anti-GBM disease
First peak ~30 years, male, more lungs | Second peak ~60 years, female
42
Goodpasture syndrome referes to
glomerulonephritis + pulmonary hemorrhage
43
Anti-GBM disease cause
idiopathic HLA gene Associated with pulmonary infection, tobacco use, hydrocarbon exposure
44
Serology of Anti-GBM disease
Anti-GBM antibodies in in serum (or kidney biopsy) | ANCA
45
ANCA stands for
anti-neutrophil cytoplasmic antibodies
46
Treatment for anti-GBM disease
plasmapheresis | immunosuppressants
47
Lupus antibodies
anti-ds DNA antibodies
48
higher incidence of lupus in
nonwhites
49
Suspect lupus when
Abnormal urinalysis -and/or- Elevated serum creatinine confirm with biospy
50
IgA vasculitis aka
Henoch-Schonlein Purpura
51
Classic tetrad of IgA vasculitis
palpable purpura (rash) arthralgia abdominal pain renal disease
52
IgA vasculitis presentation
rash followed by renal involvement | nephritis OR nephrotic
53
Pauci-Immune Glomerulonephritis aka
ANCA associated vasculitis
54
3 Pauci-Immune Glomerulonephritises
1. Granulomatosis with polyangiitis 2. Microscopic polyangiitis 3. Eosinophilic granulomatosis with Polyangiitis
55
Pauci-Immune Glomerulonephritis more likely to have C-ANCA
Granulomatosis with Polyangiitis
56
Pauci-immune glomerulonephritis more likely to have P-ANCA
Microscopic polyangiitis | Eosinophilic granulomatosis with Polyangiitis
57
Renal histology of Pauci-Immune Glomerulonephritises
NO immune deposits!
58
Granulomatosis with Polyangiitis features
Necrotizing granulomatous inflammation Vasculitis of small-medium vessels Upper and lower respiratory tracts + kidneys
59
Granulomatosis with Polyangiitis respiratory presentation
``` chronic sinusitis saddle nose otitis media ocular cough dyspnea hemoptysis ```
60
Granulomatosis with Polyangiitis renal manifestations
Crescentic necrotizing glomerulonephritis
61
Other Granulomatosis with Polyangiitis symptoms
``` Fever weight loss arthritis skin polyneuropathy ```
62
Micrscopic polyangiitis vs GPA
Micrscopic polyangiitis doesn't have granuloma formation and spares upper respiratory tract
63
Granulomatosis with Polyangiitis aka
Wegener granulomatosis
64
Eosinophilic Gralumonatosis with Polyangiitis aka
Churg-Strauss syndrome
65
Eosinophilic Gralumonatosis with Polyangiitis affects the systems
Lung, skin, heart, renal, GI, neuro (peripheral neuropathy)
66
asthma + eosinophilia =
Eosinophilic Gralumonatosis with Polyangiitis
67
3 phases of Eosinophilic Gralumonatosis with Polyangiitis
1. Prodrome: asthma/allergies 2. Eosinophilic/tissue infiltrative phase 3. Necrotizing vasculitis of small-medium vessels
68
Treatment of Pauci-immune glomerulonephritis
Corticosteroids + cytotoxic agents (immunosuppressants) *prognosis poor without treatment*
69
65-70% of all renal masses are
simple cysts
70
simple cysts presentation
asymptomatic | incidentally found on ultrasound
71
a benign cyst appears
smooth, thin, sharply demarcated walls, does not enhance with contrast→ treat with follow ups
72
How do you get polycystic kidney disease
Inherited→ irreversible decline in kidney function | All races, ethnicities, genders
73
PKD inheritnace
autosomal dominant or recessive
74
genes for autosomal dominant PKD
PKD1 or PKD2
75
what percent of PKD patients get end stage renal disease
50% by 60 years
76
most common genetic cause of chronic kidney disease
autosomal dominant PKD
77
autosomal dominant PKD features
Massive, bilateral kidney enlargement | Progressive decline in renal function
78
mechanism of autosomal dominant PKD
Cysts accumulate fluid→ enlarge → compress neighboring renal parenchyma→ compromise renal function
79
decline in GFR of autosomal dominant PKD correlates with
with kidney size/cyst volume AND reduction in renal blood flow
80
extrarenal manifestations of autosomal dominant PKD
intracranial aneurysms hepatic/pancreatic/splenic cysts valvular disease
81
renal manifestations of autosomal dominant PKD
``` HTN abdominal/flank pain palpable kidneys hematuria UTIs nephrolithiasis +/- proteinuria ```
82
Diagnosis of autosomal dominant PKD
Ultrasound initially US unclear→ CT/MRI Findings: Large kidneys + extensive cysts Genetic testing for definitive diagnosis
83
treatment of autosomal dominant PKD
Blood pressure control: low salt, statins Tolvaptan Supportive therapy Dialysis or kidney transplant
84
Tolvaptan
meds for autosomal dominant PKD
85
Autosomal recessive PKD gene
PKHD1
86
autosomal recessive PKD presents in
infants and children | neonates can get ESRD if severe
87
2 organ systems affected by autosomal recessive PKD
Kidneys + hepatobiliary tract
88
autosomal recessive PKD is characterized by
bilateral, markedly enlarged kidneys → progressive renal impairment. HTN congenital hepatic fibrosis, portal HTN feeding difficulties and growth impairment
89
detection of autosomal recessive PKD
routine antenatal ultrasound after 24 weeks of gestation

Unit 3 Clin Med II (8 decks)

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