Renal pathology Flashcards

1
Q

What is the functional unit of the kidney?

A

Nephron

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2
Q

What does the nephron consist of?

A

Renal corpuscle (glomerulus w/ Bowman’s capsule)
PCT
Loops of Henle
Distal tubules
Collecting ducts

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3
Q

Discuss the clinical presentation of patient’s with renal disease

A

Proteinuria (nephrotic syndrome)
Haematuria (nephritic syndrome)
Systemic hypertension
Renal failure
UTIs
Nephrolithiasis
Renal tubular defects

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4
Q

What is proteinuria?

A

> 30mg/24h (adults)
100mg/m2/24h (children)

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5
Q

What are features of nephrotic syndrome?

A

Heavy proteinuria (>3.5g/24h)
Generalised edema
Hypoalbuminemia
Hyperlipidemia

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6
Q

What are the types of haematuria?

A

Macroscopic vs microscopic
Intermittent vs persistent

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7
Q

What are non-haematuria causes of red urine?

A

Foods (beets, blackberries, rhubarb)
Medications (rifampicin, laxatives)
Poisons (lead, mercury)

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8
Q

What is the pathophysiology of haematuria?

A

Glomerular disease -> dysmorphic RBCs in urine

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9
Q

What are the features of nephritic syndrome

A

Acute onset haematuria
Oliguria
Systemic hypertension
+/- peripheral edema
+/- proteinuria

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10
Q

What are the pathogenetic mechanisms of glomerular inflammation?

A

Majority are immune mediated
- immune complex formation and deposition
- non immune complex mediated (lymphokines, cytokines)

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11
Q

What kinds of antigens are involved in antigen-antibody complex formation?

A

Planted antigens
Fixed antigens

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12
Q

Which primary renal diseases result in nephrotic syndrome?

A

Minimal change disease
Focal segmental glomerulosclerosis
Membranous glomerulosclerosis
Membranoproliferative glomerulosclerosis

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13
Q

Which primary renal diseases result in nephritis syndrome?

A

Diffuse proliferative
Mesangioproliferative
Thin basement membrane disease
Anti-GBM disease
Focal segmental proliferative

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14
Q

Which systemic diseases involve the renal system?

A

DM
SLE
Amyloidosis
Infections (HIV, malaria, hepatitis)
Drugs (heroin)

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15
Q

What is the most common cause of nephrotic syndrome in children?

A

Minimal change disease

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16
Q

What is minimal change disease associated with? (minority of cases)

A

Infections
Immunisation
Drugs
Neoplasia

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17
Q

Discuss the aetiology of minimal change disease

A

Immunologic (lymphokine/cytokine)
Not immune-complex mediated

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18
Q

Discuss clinical features of minimal change disease

A

Caucasian > black
M > F
Proteinuria
Responsive to steroids

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19
Q

How does minimal change disease appear on histology?

A

Light microscopy - normal
IF microscopy - normal
Epithelial cell foot process effacement on ultrastructural examination

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20
Q

What is the epidemiology of focal segmental glomerulosclerosis with hyalinosis?

A

Adult > children in NS
Black patients
Increasing with HIV

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21
Q

Discuss the aetiology of focal segmental glomerulosclerosis

A

Lymphokine/cytokine
Not immune-complex mediated

22
Q

How does focal segmental glomerulosclerosis appear on histology?

A

Focal lesions (<50% glomeruli involvement)
Segmental lesions
Loss of capillary loop patency
Glomerular tuft sclerosis
Epithelial cell foot process effacement

23
Q

What is the prognosis of focal segmental glomerulosclerosis?

A

Poor response to steroids
50% progress to chronic renal failure
Disease recurs in renal transplants

24
Q

Discuss the aetiology of membranous glomerulnephritis

A

Immune-complex mediated
Ag-Ab complex deposition in relation to glomerular BM (sub-epithelial)

25
Q

Name causes of membranous glomerulonephritis

A

85% idiopathic (primary)
Infections
Drugs
Tumours
Auto-immune disease

26
Q

Name infectious causes of membranous glomerulonephritis

A

HBV
Malaria
Syphilis
Bilharzia

27
Q

Name toxin causes of membranous glomerulonephritis

A

Gold
Mercury
Heroin

28
Q

Name neoplastic causes of membranous glomerulonephritis

A

Carcinoma
Melanoma
Lymphoma

29
Q

Name auto-immune disease causes of membranous glomerulonephritis

A

SLE

30
Q

Discuss the features of membranous glomerulonephritis on histology

A

Glomerular BM changes
- diffuse spike formations
- subepithelial deposits
No cellular proliferation

31
Q

Discuss the prognosis of membranous glomerulonephritis

A

Adults - majority unresponsive to therapy and progress to chronic RF
Children - better prognosis, 10% to chronic RF

32
Q

Discuss the aetiology of membranoproliferative glomerulonephritis

A

Immune-complex mediated
Ag-Ab complex deposition in relation to glomurular BM (sub endothelial) and within the mesangium

33
Q

What is the difference in the Ag-Ab complexes in membranous glomerulonephritis and membranoproliferative glomerulonephritis

A

Membranous - subepithelial
Membranoproliferative - subendothelial

34
Q

Discuss the features of membranoproliferative glomerulonephritis on histology

A

Diffuse proliferative process
Crescentic
Distinctive glomerular BM changes
- increased mesangial cellularity
- double contour ‘tram tracks’

35
Q

Discuss the prognosis of membranoproliferative glomerulonephritis

A

Poor
Majority progress to CF

35
Q

Discuss the aetiology of post-infectious glomerulonephritis

A

Diffuse proliferative glomerulonephritis
Ag-Ab complex deposition following a transient infection

36
Q

Which organisms can result in post-infectious glomerulonephritis?

A

Bacteria
- BHS
- staph
- meningo
- pneumo
Viruses
Malaria
Bilharzia
Toxoplasmosis

37
Q

Discuss the features of post-infectious glomerulonephritis on histology

A

Diffuse proliferative glomerulonephritis
Large subepithelial humps

38
Q

What is the prognosis of post-infectious glomerulonephritis?

A

Generally good

39
Q

What is mesangioproliferative glomerulonephritis?

A

A heterogeneous group of diseases including SLE and IgA nephropathy

40
Q

Discuss the causes of mesangioproliferative glomerulonephritis

A

Majority = idiopathic
Autoimmune (SLE)
Infectious (HBV, bilharzia)
Drugs
Neoplasm (carcinoma, malignant, lymphoma)

41
Q

What are the 3 main kidney lesions in HIV renal disease?

A

HIV associated nephropathy (HIVAN)
HIV immune complex kidney disease (HIVICKD)
Thrombotic microangiopathy

42
Q

What are the histological features of thrombotic microangiopathy?

A

Intimal swelling
Arteriolar thrombi
Fibrinoid material in vascular lumina

43
Q

Which genes are implicated in HIVAN?

A

APOL1
MYH9
(African descent)

44
Q

Discuss the clinical presentation of HIVAN

A

Acute onset proteinuria
Progressive renal insufficiency
Hypoalbuminemia
Minimal peripheral edema
BP normal
Enlarged kidneys

45
Q

Discuss the histological features of HIVAN

A

Pan-nephropathy (collapsing variant of FSGS)
Microcystically dilated tubules
Interstitial inflammation and fibrosis

46
Q

What is the prognosis of HIVAN?

A

Poor

47
Q

In which amyloidosis types is renal involvement common?

A

AL
AA

48
Q

Discuss the histological features of amyloidosis

A

Extracellular deposits within the glomerulus, around blood vessels and within interstitial

49
Q

Discuss the pathogenesis of diabetic glomerulopathy

A

Increased GMB permeability -> excess collagen IV deposition -> protein glycosylation -> hyperinfiltration

50
Q

Discuss the histological features of diabetic glomerulopathy

A

Capillary wall thickening
Mesangial expansion
Kimmelstiel Wilson lesion

51
Q
A