Nephritic and nephrotic syndromes Flashcards

1
Q

What is the pathophysiology of Berger’s disease?

A

Due to IgA immune complex deposits in the mesangium of the nephrons. These complexes form elsewhere in the body and travel to the kidneys where they deposit.

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2
Q

What type of hypersensitivity is Berger’s disease? Why?

A

Type 3

As the immune complexes form elsewhere and travel to where they deposit (the kidneys) and cause destruction there.

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3
Q

Common presentations and features of a patient with IgA nephropathy?

A

Young male

Recurrent episodes of macroscopic (frank) haematuria

Is typically associated with URTI (a few days, a few weeks would be associated with post-streptococcal nephritis)

Often occurs in childhood

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4
Q

What would you see under a microscope when a patient has IgA nephropathy?
Immunofluorescence?

A

Mesangial proliferation (IgA immune complexes).

You would get a positive immunofluorescence for IgA and C3 (part of the complement system)

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5
Q

What is the difference between IgA nephropathy and post-streptococcal glomerulonephritis?

A

n1. Post-streptococcal glomerulonephritis is associated with LOW complement levels (In Berger’s –> these are elevated due to immune complex activation)

  1. The main symptom in post-streptococcal glomerulonephritis is PROTEINURIA (haematuria may also occur) but in IgA nephropathy, you have haematuria (and lower levels of proteinuria compared to Post-strep glomerulonephritis)

3.URTI usually triggers both but IgA —> develops after 1-2 days after URTI

Post streptococcal glomerulonephritis —> develops 1-2 weeks after URTI

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6
Q

What is the difference between nephritic and nephrotic syndrome?

A

Nephritic
Describes inflammation of the GBM (glomerular basement membrane)

Haematuria
Cola coloured urine
Oliguria
Proteinuria (less than 3g per 24 hours)–> not as much as in nephrotic syndrome
Fluid retention (oedema in peri-oribtal region,face and hands)
Pt may also have hypertension (either a history of it or currently has it)

Nephrotic
The basement membrane of the glomerulus becomes highly permeable. Allows proteins to pass through.

SIGNIFICANT proteinuria ( more than 3g per day/24hrs)
HYPOalbuminemia (<25g per litre)
Peripheral oedema
HYPERcholesterolaemia

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7
Q

What are the top causes of nephrotic syndrome in adults?

A

Membranous nephropathy

Focal segmental glomerulosclerosis

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8
Q

Most common cause of nephrotic syndrome in children?

A

Minimal change disease

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9
Q

What causes minimal change disease?

A

Most cases are idiopathic but a few minor cases can be due to DRUGS (rifampicin,NSAIDs) HODGKIN’S LYMPHOMA or THYMOMA, INFECTIOUS MONONUCLEOSIS

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10
Q

What is the pathophysiology of Minimal change disease?

A

T-cells in the blood reach the glomerulus and release cytokines that specifically destroy the foot processes of the podocytes (podocytes are found over the GBM(glomerular basement membrane))——> This process is called effacement.

So negatively charged proteins like albumin can pass through. But larger ones like immunoglobulins can’t. This is why there is highly selective proteinuria in minimal change disease.

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11
Q

Upon conducting a renal biopsy, what would be seen in a patient who has minimal change disease? light and electron microscopy

A

Light microscopy —> nothing

Electron microscopy —> fusion of podocytes and effacement of the foot processes (which are found at the bottom/foot of the podocytes)

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12
Q

What can cause membranous nephropathy and how serious is it?

A

Causes may be idiopathic (majority of cases) or secondary (e.g. due to SLE/hep B)

If this nephrotic syndrome is not managed medically, it can develop into end stage renal disease (ESRD)

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13
Q

Upon histologic view, what would you see if someone has membranous nephropathy?

A

IgG and complement deposits in the subepithelial space

THICKENED GBM

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14
Q

Upon electron micrsocopy, what would be seen in a person who has membranous nephropathy?

A

Spike and dome shape of the GBM matrix and effacement of the foot processes of the podocytes

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15
Q

What is seen on light microscopy when a pt has focal segmental glomerulosclerosis?

A

Focal and segmental sclerosis and hyalinosis

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16
Q

What is seen on electron microscopy if a pt has FSGS?

A

Effacement of the foot processes

17
Q

Patients with diabetic nepropathy should aim blood pressure readings less than……

A

130/80mmHg

18
Q

If a patient has a urinary ACR above 3mg/mmol and has suspected diabetic nephropathy, what medication should they be started on?

A

ACE inhibitor/ARB antagonist (dual therpay with both should NOT be started)

19
Q

How would you diagnose alport’s syndrome?

A

molecular genetic testing
renal biopsy
electron microscopy: characteristic finding is of the longitudinal splitting of the lamina densa of the glomerular basement membrane, resulting in a ‘basket-weave’ appearance

20
Q

What is Alport syndrome caused by?

A

It is due to a defect in type 4 collagen which affect the eyes, cochlea and the glomerulus.

21
Q

What are some causes of rapidly progressive glomerulonephritis?

A

-Goodpasture’s syndrome

-Wegener’s granulomatosis

-Others; SLE, microscopic polyarteritis

22
Q

What would you see under microscopic view if a patient has rapidly progressive glomerulonephritis?

A

Epithelial cresents in the majority of the glomeruli

23
Q

What does Goodpastures syndrome cause? Why?

A

Glomerulonephritis and pulmonary haemorrhage.

This is because of the anti-GBM antibodies binding to type 4 collagen fibres in the basement membrane of the glomerulus and lungs.When they do, it activates the complement system which results in these presentations. It is a type 2 hypersensitivity reaction.

24
Q

What is the management for a patient who has GoodPastures syndrome?

A

-Plasmapheresis
-Steroids
-Immunosuppressive agents
-Cyclophosphamide