Renal pathology Flashcards

1
Q

What is the difference between focal, diffuse, segmental and global glomerular lesions?

A

Focal=Less than 50% of all glomeruli involved
Diffuse=More than 50% of all glomeruli involved
Segmental= Less than 50% of each individual glom involved
Global= More than 50% of each individual glom involved

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2
Q

What are the common pathogeneses of primary glomerular disease?

A

Autoimmune conditions such as Good-Pasture syndrome directed against the glom itself.
Antibody against something has been deposited in the glomerulus.
Deposition of a circulating Ag-Ab immune complex

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3
Q

What are some common causes of secondary glomerular disease?

A
SLE
HTN
DM
vasculitis
sarcoidosis
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4
Q

What histological changes can occur within the glomerulus to indicate damage?

A

Hypercellularity- Proliferation of mesangial, endothelial and epithelial cells. Leukocyte infiltration. Formation of crescents indicating accumulation of cells in Bowman’s space.
Basement membrane thickening-accumulation of immune complexes
Hyalinisation and sclerosis

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5
Q

What are the signs and symptoms of glomerulonephritis?

A

Haematuria, increase creatinine, increase urea, oliguria

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6
Q

What are the two main types of acute glomerulonephritis?

A

Post-infectious and necrotising

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7
Q

What is the most common age age group and causative agent of post-infectious acute glomerulonephritis?

A

Children mostly.

Anti-strep antibodies

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8
Q

What are the 3 main types of necrotising acute glomerulonephritis?

A

1) anti-GBM
2) Immune complex mediated
3) ANCA associated

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9
Q

What is nephrotic syndrome?

A

Nephrotic syndrome is characterized by a massive renal loss of protein (> 3.5 g/day) resulting in edema, hypercoagulability (antithrombin III deficiency), and an increased risk of infection (loss of immunoglobulins). Typical laboratory findings of nephrotic syndrome include hyperlipidemia and fatty casts on urinalysis.

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10
Q

What are the 3 most common causes?

A

Membranous nephropathy
Minimal change disease
Focal segmental glomerular sclerosis

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11
Q

What is membranous nephropathy? Who does it affect? What are it’s causes? How doe sit present on microscopy? How is it managed?

A

The most common cause in white adults leading to diffuse thickening of the GBM.
Primary- anti-phospholipase a2 antibodies can lead to primary membranous nephropathy. Secondary can be due to SLE, hepatitis B and C and medications.
LM: glomerular capillary loops and basement membrane appear thickened
IM: subepithelial deposits
EM: subepithelial dense deposits (“spike and dome appearance”)
Corticosteroids

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12
Q

What is minimal change disease? Who does it affect? What are it’s causes? How does it present on microscopy? How is it managed?

A
Most common in children. 
Can be associated with Hodgkin lymphoma.
LM: no changes
EM: effacement of the foot processes
Corticostroids
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13
Q

What is focal segmental glomerular sclerosis? Who does it affect? What are it’s causes? How does it present on microscopy? How is it managed?

A

Most common cause of nephrotic syndrome in black populations. Potentially due to high prevalence of APOL1 gene which protects from trypanosomiasis. Can be associated with heroin abuse, HIV infection, obesity, and sickle cell disease.
LM: segmental sclerosis
IM: IgM and C3 inside the sclerotic regions
EM: effacement of the foot processes
Poor response to corticosteroids

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14
Q

What is IgA nephropathy?

A

A condition in which mesangial IgA immune complex deposits lead to glomerulonephritis. Typically presents in patients in their 2nd to 3rd decade of life with microhematuria and episodic gross hematuria during/directly after upper respiratory tract/gastrointestinal infections or strenuous exercise.

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15
Q

What is Alport syndrome?

A

A genetic disorder that is characterized by glomerulonephritis, often in combination with sensorineural hearing loss and, in some cases, eye abnormalities. It is caused by a genetic defect of type IV collagen, which is usually inherited in an X-linked dominant pattern. The disorder, therefore, usually affects boys.

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16
Q

What is thin GBM disease?

A

Histologically normal glomeruli.

EM marked thinning of GBM.

17
Q

What is the leading cause of CKD?

A

Diabetic nephropathy

18
Q

What is the causative agent of amyloidosis chronic glomerulonephropathy?

A

Abnormal proteinaceous material deposited in tissues

19
Q

What stain and microscopic finding are associated with amyloidosis?

A

Positive congo red and birefringence under polarised light

20
Q

What are the causes of primary and secondary amyloidosis?

A

Primary- Multiple myeloma

Secondary- TB, Crohn’s

21
Q

What patterns of disorder are seen in SLE?

A

Mesangial increase.
Necrosis is variable, segmental or global, diffuse or focal.
Membranous pattern.
Deposition of all immunoproteins.

22
Q

What renal changes are associated with hypertension?

A

Intimal thickening with narrowing of the lumen.
Hyalinosis.
Leads to ischaemic changes in the kidney: glomerular sclerosis, tubular atrophy, interstitial fibrosis

23
Q

What cells are most present in the kidney during pyelonephritis?

A

Neutrophils

24
Q

What are the main causative agents of tubulointerstitial nephritis?

A

NSAIDs.

25
Q

What is the pathology in multiple myeloma kidney?

A

Light chain casts in the kidney which leads to an inflammatory process

26
Q

How does polycystic kidney disease differ in adults and children?

A

Children- Autosomal recessive

Adults- Autosomal dominant. Associated with cell membrane protein polycystin

27
Q

What is acute tubular necrosis?

A

Clinicopathological term.
Necrosis of the tubular epithelium in association with acute renal impairment.
The proximal tubule is prone to ischaemia and shows vacuolation of the tubular epithelial cells.