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MBBS I CPRS > L76- Kidney diseases I > Flashcards

L76- Kidney diseases I Flashcards

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1
Q

Location of kidneys?

A

 Locate in retroperitoneum

 Vertebra: T12 - L3

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2
Q

Functions of Mesangium?

A

-Structural - hold capillary loops together
-produce ECM,
-analyze urine in distal
tubule,
-contract to reduce
perfusion

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3
Q

What is primary renal diseases?

A

kidney is the only/ predominant organ involved (no systemic manifestation)

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4
Q

What is secondary renal diseases?

A

kidney is injured in the

course of systemic diseases or infections

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5
Q

What is clinical-pathological diagnosis?

A

Combination of:
clinical hisotry and manifestations
+
Renal biopsy pathological diagnosis

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6
Q

3 methods to examine renal biopsy?

A
  • Light microscopy
  • Direct immunofluorescnce study
  • Electron microscopy
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7
Q

Explain how nephrotic syndrome can lead to hyperlipidemia?

A

Kidney glomeruli leak albumin:
> heavy proteinuria , hypoalbuminemia = reduced oncotic pressure
> Generalized edema
> Liver synthesizes proteins (e.g. lipoproteins) to compensate oncotic pressure
> hyperlipidemia

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8
Q

How does nephrotic syndrome affect drug levels?

A

Decrease in serum-binding protein > some drugs less able to be transported

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9
Q

How does nephrotic syndrome affect clotting and cause Deep vein thrombosis?

A

Hypercoagulability
» enhanced venous / arterial thromboembolism
» DVT

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10
Q

How does nephrotic syndrome affect immunity?

A

Loss of Ig, complements, impaired neutrophil phagocytic function&raquo_space; increase risk of infection

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11
Q

How does the kidney fail in nephrotic syndrome?

A

Progressively

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12
Q

Summarize all the complications of nephrotic syndrome?

A

Progressive renal failure

Increase risk of infection

Hypercoagulability

Decrease in serum-binding protein

Hyperlipidemia and lipiduria

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13
Q

Presentation of nephritic syndrome in urine?

A

Coke-colour Urine:

1) Mild to moderate proteinuria
2) Acute onset, gross visible hematuria or;
3) Microscopic hematuria with red cell casts

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14
Q

Presentation of nephritic syndrome in GFR and BP?

A

Hypertension

Decreased GFR

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15
Q

Which glomerular diseases are related to nephritic syndrome?

A

1) Acute poststreptococcal glomerulonephritis

2) Rapidly progressive glomerulonephritis

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16
Q

What is the presentation of acute kidney injury?

A
  • rapidly decline in GFR in hours/ days

- Severe form: oliguria (reduced urine) or anuria (no urine)

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17
Q

What is the definition of chronic kidney disease?

A

presence of kidney structural / functional abnormalities for
at least 3 months

or

Persistent declined GFR (< 60mL/min/1.73m^2) for at least 3 months

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18
Q

What type of disease is acute kidney injury associated with?

A

Glomerular, interstitium, tububles, blood vessel diseases

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19
Q

GFR in end stage renal disease?

A

GFR < 5% of normal

Final and irreversible

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20
Q

Treatment for end stage renal disease?

A

Renal replacement therapy:

1) Haemodialysis
2) Peritoneal dialysis
3) Kidney transplant

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21
Q

Define Azotemia?

A

Biochemical abnormality referring to elevation of blood urea, nitrogen and creatinine levels
+
Decrease in GFR

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22
Q

Define Uremia?

A

Toxic condition resulting from kidney disease

Retention of waste products (normally excreted) in bloodstream

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23
Q

What are the 3 categories of glomerular diseases? *

A

Primary glomerulonephritis

Systemic disease with glomerular involvement

Hereditary disorders

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24
Q

Which glomerular diseases are related to nephrotic syndrome?

Just rmb the top 4

A

1) Focal segmental glomerulonephritis
2) Membranoproliferative glomerulonephritis
3) Membranous neuropathy
4) Minimal change disease

(Amyloidosis, Diabetes mellitus, SLE)

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25
What are the primary glomerulonephritis/ glomerulopathy diseases?
Membranous nephropathy Minimal change Focal segmental glomerulonephritis IgA neuropathy Rapidly progressive (crescentic) Glomerulonephritis Membranousproliferative glomerulonephritis Acute post-infectious glomerulonephritis Chronic glomerulonephritis
26
What are the systemic diseases with glomerular involvement?
``` SLE Goodpasture syndrome Diabetes Amyloidosis Bacterial endocarditis ``` (Microscopic polyangiitis, Wengener granulomatosis, Henoh- Scholein purpura)
27
Name 3 hereditary syndromes that causes kidney damage? *
Alport syndrome Fabry disease Thin basement membrane disease
28
What is the most common mechanism of glomerular injury pathogenesis?
Immune, Ag-Ab reactions
29
3 ways that immune mechanism causes glomerular injury? *
1) Ab react in-situ within glomerulus 2) Deposition of circulating Ag-Ab complexes in glomeruli 3) Ab directed against normal components of GBM 4) Cell-mediated or alternative complement immune injury
30
Apart from immune damage, what are the 2 other ways glomerular injury occurs?
Metabolic alterations of GBM Genetic defect of GBM synthesis and cellular protein
31
3 locations for Ag-Ab complexes to deposit to cause glomerular injury?
From circulation: 1) Subendothelial deposit In-situ: 1) Within GBM 2) SubEPITHELIAL deposit (outside capillary)
32
2 things that lead to uremia?
Decrease GFR Decrease glomerular blood flow
33
What causes primary membranous nephropathy? *
binding of autoantibodies to M-type phospholipase A2 receptor (PLA2R) expressed on podocytes
34
What causes secondary membranous nephropathy? | *
- Infection (Hepatitic B or C) - Malignancy - Autoimmune disease (SLE, Rhuematoid arthritis) - Sarcoidosis - Drugs
35
Pathogenesis of membranous nephropathy?
 Chronic in situ deposit of Ig containing immune complex in subepithelial space along GBM
36
light microscopy appearance of membranous nephropathy? Give stains
* Holey, frothy, bubble, spiked appearance on GBM in Silver stain * Diffuse thickening of capillary wall in H&E stain
37
Immunofluorescence appearance of membranous nephropathy?
Granular deposition in Subepithelial space | in-situ deposition, not circulation
38
Electron microscopy appearance of membranous nephropathy?
Electron-dense deposits | In subepithelial space
39
Main clinical manifestations of nephrotic syndrome?
Proteinuria (3.5 g or more in adults/day) Hypoalbuminemia Generalized oedema Hyperlipidaemia and lipiduria
40
What is the marker for Primary membranous nephropathy?
PLA2R
41
What is the treatment of primary and secondary membranous nephropathy?
Primary = steroids Secondary = Treat underlying cause
42
What are the outcomes of membranous nephropathy?
60% pateints have persistent proteinuria 10% progress to renal failure in 10 years
43
Age group affected by membranoproliferative glomerulonephritis ?
Children and young adults
44
Presentation of membranoproliferative glomerulonephritis?
Nephrotic syndromes (e.g. generalized edema, hyperlipiduria...etc) Haematuria
45
What are the 4 types of membranoproliferative glomerulonephritis?
Idiopathic Secondary C3 glomerulonephritis Dense Deposit disease
46
Light microscopy of membranoproliferative glomerulonephritis?
Hypercellularity: Cellular proliferation of mesangial cells + Leukocyte infiltration Capillary wall thickening Basement membrane splitting
47
Immunofluorescence appearance of membranoproliferative glomerulonephritis?
dense deposits at capillary walls subendothelium
48
Explain electron microscopy of membranoproliferative glomerulonephritis
Splitting of glomerular basement membrane immune deposition at subendothelium causes formation of new GBM under original GBM
49
Treatment of membranoproliferative glomerulonephritis?
Treat underlying cause Drugs targeting C3 glomerulonephritis
50
Outcome of membranoproliferative glomerulonephritis?
50% develop chronic renal failure within 10 years
51
Pathology of Minimal change disease?
injure podocytes and cause proteinuria with effacement of foot processes Exact cause unknown
52
Age groups affected by minimal change disease?
Most common (90%) nephrotic syndrome in children Peak incidence at 2-6 years old
53
Associated factors that can lead to minimal change disease?
Drugs (e.g. NSAID and Interferons) Lymphoma Infection and recent vaccination
54
Light microscopy of minimal change disease?
glomeruli that have a normal appearance
55
Immunofluorescence of minimal change disease?
No staining
56
Electron microscopy of minimal change disease?
Diffuse (more than 50%) effacement of foot processes of podocytes >> loss of filtration slit
57
Treatment of minimal change disease>?
Steroid | little steroid-dependence or resistance
58
Outcome of minimal change disease?
Prognosis is excellent
59
Given the exact cause of minimal change is unknown, what are some possible etiologies?
 Circulating factor  Abnormality in cell-mediated immunity  Cytokines
60
Complication of minimal change disease? Explain
GBM lose protein filter function Lose albumin > blood oncotic pressure decrease > increase filtration into tissue and hypovolemic shock > Pre-renal damage and acute tubular necrosis > Acute renal failure
61
Pathology of Focal segmental glomerulosclerosis (FSGS)?
<50%, partial glomerulosclerosis: Replacement of capillary loops of glomerulus by ACELLULAR, AMORPHOUS material* *derived from plasma protein, collagen, basement membrane materials
62
Primary FSGS presentation and features are similar to which nephrotic disease?
Minimal change
63
Differential diagnosis between minimal change and FSGS?
FSGS has no response to steroids (but minimal change has excellent response) FSGS = more likely to progress to chronic renal failure and recurrence after transplant
64
Is Acute proliferative / post-infectious glomerulonephritis nephrotic or nephritic?
Nephritic syndrome
65
Pathology of Acute proliferative / post-infectious glomerulonephritis?
Immune complex glomerulonephritis usually preceded by Group A, B-haemolytic streptococci infection of pharynx (1-4 weeks before)
66
Age group most affected by Acute proliferative / post-infectious glomerulonephritis?
Children
67
What other infections can precede Acute proliferative / post-infectious glomerulonephritis?
Staphylococcal Pneumococcal Virus (HBV/ HIV/ HCV) Parasites (malaria/ toxoplasmosis)
68
Light microscopy of Acute proliferative / post-infectious glomerulonephritis?
Hypercellular glomeruli with neutrophils
69
Explain where the immune complex deposition occurs in Acute proliferative / post-infectious glomerulonephritis?
Immune-complexes formed by antibodies and circulating or planted antigens >> depositing in the subepithelial space, forming lumps (from circulation)
70
Immunofluorescence appearance of Acute proliferative / post-infectious glomerulonephritis?
Spotty immune deposits "Starry sky" appearance due to deposits of IgG (and complement 3)
71
Electron microscopy appearance of Acute proliferative / post-infectious glomerulonephritis?
Electron dense deposits forming subepithelial humps at GBM
72
Outcome of appearance of Acute proliferative / post-infectious glomerulonephritis?
95% recover with conservative therapy
73
Explain Hypercellular glomeruli | in Acute proliferative / post-infectious glomerulonephritis?
Injury to glomerular tufts > leakage of plasma protein stimulates Bowman’s capsule >> parietal epithelium proliferates >> enlarged, hypercellular glomeruli
74
What is rapidly progressive (crescentic) glomerulonephritis associated with?
Severe glomerular injury with multiple possible causes: Type I,II, III
75
Name a type I rapidly progressive (crescentic) glomerulonephritis?
Goodpasture syndrome = Anti-GBM antibody mediated glomeruplonephritis
76
Name 4 type II rapidly progressive (crescentic) glomerulonephritis?
Immune complex mediated: Lupus nephritis IgA nephropathy Acute poststreptococcal glomerulonephritis (Henoch- Schonlein purpura)
77
Name a type III rapidly progressive (crescentic) glomerulonephritis?
Pauci- immune mediated: ANCA-associated (Wegener granulomatosis, microscopic polyangiitis)
78
Goodpasture syndrome pathology in kidney?
Autoantibody attack noncollagenous C terminal (NC1) domain of alpha 3 chain of collagen type IV at GBM
79
Goodpasture syndrome pathology in lungs?
Autoantibodies cross-react with pulmonary alveolar basement membranes>> cause pulmonary haemorrhage and death
80
What precedes goodpasture syndrome?
Flu-like illness | Hydrocarbon or solvent exposure
81
Light microscopy appearance of Goodpasture? *
Focal necrotizing lesions Cellular crescent at Bowman's capsule Diffuse parietal epithelium proliferation Fibrin deposition
82
immunofluorescence appearance of Goodpasture?
" Linear ribbon deposition" of IgG along GBM
83
Electron microscopy appearance of Goodpasture?
No deposit by usual electron microscopy >> antibodies too small to be detected
84
Treatment of goodpasture syndrome?
Plasmapheresis/ plasma exchange High dose steroid and Cyclophosphamide
85
Outcome of good pastures syndrome?
Chronic renal replacement therapy or kidney transplant
86
What type of disease in IgA nephropathy?
Immune complex glomerulonephritis
87
What is the most common cause of Glomerulonephritis worldwide?
IgA nephropathy
88
What are the presentations of IgA nephropathy?
Microscopic/ macroscopic haematuria Proteinuria (10% nephrotic range) Chronic or acute kidney failure
89
Light microscopy appearance of IgA nephropthy? *PAS stain*
Mesangial hypercellularity with increased matrix Capillary loop not much affected
90
immunofluorescence appearance of IgA nephropthy?
Dominant or co-dominant deposits of IgA at mesangial cells
91
Electron microscopy appearance of IgA nephropthy?
Mesangial electron dense deposits (immune complexes)
92
Treatment of IgA nephropathy?
Depends on clinical setting Corticosteroid if significant proteinuria or rapidly progressive kidney injury
93
Outcome of IgA nephropathy?
Slow progression to chronic renal failure in 15-40% patients in 20 years Recurrence after kidney transplant

MBBS I CPRS (78 decks)

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