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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
Q

Primary IgA nephropathy is

A

renal-limited

more common

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26
Q

Secondary IgA nephropathy is due to

A

cirrhosis
celiac
HIV
CMV

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27
Q

Who is most likely to get IgA nephropathy

A

2nd/3rd decades of life
Males
Asians and Caucasians
Inheritable

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28
Q

Pathogenesis of IgA nephropathy

A

inciting cause unknown→ IgA deposition in mesangium→ inflammatory response

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29
Q

Presentation of IgA nephropathy

A

URI→ gross hematuria 1-2 days later→ presentation along nephritic spectrum (nephrotic rare)

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30
Q

IgA nephropathy vs. Postinfetious GN:

Timing

A

IgA nephropathy: 1-2 days after URI

Postinfetious GN: 1-3 weeks after infection

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31
Q

How to confirm IgA nephropathy diagnosis

A

Kidney biopsy

usually for severe/progressive

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32
Q

3 options for disease course of IgA nephropathy

A
  1. Spontaneous clinical remission (⅓)
  2. Progression to end stage renal disease (ESRD) (20-40%)
  3. Chronic microscopic hematuria and stable creatinine
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33
Q

Higher risk for progression of IgA Nephropathy

A

Proteinuria >1g/d
Decreased GFR
HTN

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34
Q

If at higher risk for progression of IgA nephropathy, treat with

A

ACE-I or ARB

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35
Q

Other tx for IgA nephropathy

A

Glucocorticoids +/- immunosuppressants

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36
Q

Postinfectious glomerulonephritis aka

A

Poststreptococcal glomerulonephritis

37
Q

Postinfectious glomerulonephritis is preceded by

A

pharyngitis or impetigo

group A beta-hemolytic strep

38
Q

Who gets Postinfectious glomerulonephritis

A

Male children most commonly

39
Q

Serology of Postinfectious glomerulonephritis

A

Elevated ASO titers

Low complement

40
Q

Anti-GBM disease

A

circulating antibodies against GBM=glomerular basement membrane
-nephritic spectrum, can be RPGN
also against alveolar basement membrane
-cough, dyspnea, +/- hemoptysis

41
Q

Bimodal distribution of Anti-GBM disease

A

First peak ~30 years, male, more lungs

Second peak ~60 years, female

42
Q

Goodpasture syndrome referes to

A

glomerulonephritis + pulmonary hemorrhage

43
Q

Anti-GBM disease cause

A

idiopathic
HLA gene
Associated with pulmonary infection, tobacco use, hydrocarbon exposure

44
Q

Serology of Anti-GBM disease

A

Anti-GBM antibodies in in serum (or kidney biopsy)

ANCA

45
Q

ANCA stands for

A

anti-neutrophil cytoplasmic antibodies

46
Q

Treatment for anti-GBM disease

A

plasmapheresis

immunosuppressants

47
Q

Lupus antibodies

A

anti-ds DNA antibodies

48
Q

higher incidence of lupus in

49
Q

Suspect lupus when

A

Abnormal urinalysis
-and/or-
Elevated serum creatinine

confirm with biospy

50
Q

IgA vasculitis aka

A

Henoch-Schonlein Purpura

51
Q

Classic tetrad of IgA vasculitis

A

palpable purpura (rash)
arthralgia
abdominal pain
renal disease

52
Q

IgA vasculitis presentation

A

rash followed by renal involvement

nephritis OR nephrotic

53
Q

Pauci-Immune Glomerulonephritis aka

A

ANCA associated vasculitis

54
Q

3 Pauci-Immune Glomerulonephritises

A
  1. Granulomatosis with polyangiitis
  2. Microscopic polyangiitis
  3. Eosinophilic granulomatosis with Polyangiitis
55
Q

Pauci-Immune Glomerulonephritis more likely to have C-ANCA

A

Granulomatosis with Polyangiitis

56
Q

Pauci-immune glomerulonephritis more likely to have P-ANCA

A

Microscopic polyangiitis

Eosinophilic granulomatosis with Polyangiitis

57
Q

Renal histology of Pauci-Immune Glomerulonephritises

A

NO immune deposits!

58
Q

Granulomatosis with Polyangiitis features

A

Necrotizing granulomatous inflammation
Vasculitis of small-medium vessels
Upper and lower respiratory tracts + kidneys

59
Q

Granulomatosis with Polyangiitis respiratory presentation

A 
chronic sinusitis
saddle nose
otitis media
ocular
cough
dyspnea
hemoptysis
60
Q

Granulomatosis with Polyangiitis renal manifestations

A

Crescentic necrotizing glomerulonephritis

61
Q

Other Granulomatosis with Polyangiitis symptoms

A 
Fever
weight loss
arthritis
skin
polyneuropathy
62
Q

Micrscopic polyangiitis vs GPA

A

Micrscopic polyangiitis doesn’t have granuloma formation and spares upper respiratory tract

63
Q

Granulomatosis with Polyangiitis aka

A

Wegener granulomatosis

64
Q

Eosinophilic Gralumonatosis with Polyangiitis aka

A

Churg-Strauss syndrome

65
Q

Eosinophilic Gralumonatosis with Polyangiitis affects the systems

A

Lung, skin, heart, renal, GI, neuro (peripheral neuropathy)

66
Q

asthma + eosinophilia =

A

Eosinophilic Gralumonatosis with Polyangiitis

67
Q

3 phases of Eosinophilic Gralumonatosis with Polyangiitis

A
  1. Prodrome: asthma/allergies
  2. Eosinophilic/tissue infiltrative phase
  3. Necrotizing vasculitis of small-medium vessels
68
Q

Treatment of Pauci-immune glomerulonephritis

A

Corticosteroids + cytotoxic agents
(immunosuppressants)
prognosis poor without treatment

69
Q

65-70% of all renal masses are

A

simple cysts

70
Q

simple cysts presentation

A

asymptomatic

incidentally found on ultrasound

71
Q

a benign cyst appears

A

smooth, thin, sharply demarcated walls, does not enhance with contrast→ treat with follow ups

72
Q

How do you get polycystic kidney disease

A

Inherited→ irreversible decline in kidney function

All races, ethnicities, genders

73
Q

PKD inheritnace

A

autosomal dominant or recessive

74
Q

genes for autosomal dominant PKD

A

PKD1 or PKD2

75
Q

what percent of PKD patients get end stage renal disease

A

50% by 60 years

76
Q

most common genetic cause of chronic kidney disease

A

autosomal dominant PKD

77
Q

autosomal dominant PKD features

A

Massive, bilateral kidney enlargement

Progressive decline in renal function

78
Q

mechanism of autosomal dominant PKD

A

Cysts accumulate fluid→ enlarge → compress neighboring renal parenchyma→ compromise renal function

79
Q

decline in GFR of autosomal dominant PKD correlates with

A

with kidney size/cyst volume
AND
reduction in renal blood flow

80
Q

extrarenal manifestations of autosomal dominant PKD

A

intracranial aneurysms
hepatic/pancreatic/splenic cysts
valvular disease

81
Q

renal manifestations of autosomal dominant PKD

A 
HTN
abdominal/flank pain
palpable kidneys
hematuria
UTIs
nephrolithiasis
\+/- proteinuria
82
Q

Diagnosis of autosomal dominant PKD

A

Ultrasound initially
US unclear→ CT/MRI

Findings: Large kidneys + extensive cysts

Genetic testing for definitive diagnosis

83
Q

treatment of autosomal dominant PKD

A

Blood pressure control: low salt, statins

Tolvaptan

Supportive therapy

Dialysis or kidney transplant

84
Q

Tolvaptan

A

meds for autosomal dominant PKD

85
Q

Autosomal recessive PKD gene

86
Q

autosomal recessive PKD presents in

A

infants and children

neonates can get ESRD if severe

87
Q

2 organ systems affected by autosomal recessive PKD

A

Kidneys + hepatobiliary tract

88
Q

autosomal recessive PKD is characterized by

A

bilateral, markedly enlarged kidneys → progressive renal impairment. HTN

congenital hepatic fibrosis, portal HTN

feeding difficulties and growth impairment

89
Q

detection of autosomal recessive PKD

A

routine antenatal ultrasound after 24 weeks of gestation

Unit 3 Clin Med II (8 decks)

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