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Flashcards in Glomerular Disease Deck (33)
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1
Q

What are podocytes?

A

Podocytes are cells in the Bowman’s capsule in the kidneys that wrap around capillaries of the glomerulus

2
Q

What proteins are filtered from te glomerulus?

A

All that are smaller than albumin

Immunoglobulins do not get filtered - they stay in the plasma

3
Q

What structural feature do podocytes contain?

A

They have interdigitating ‘fingers’ or foot processes

4
Q

What are the three layers of the filter barrier?

A

Endothelial cell

Basal lamina

Podocyte

5
Q

What are mesangial cells?

A

Tree like group of cells which support capilalries

6
Q

Where does filtrate travel after the glomerulus?

A

Goes into bowmans space and then into the proximal tubule

7
Q

What substances leave the efferent arteriole?

A

Blood cells someme fluid

abumin and larger proteins

Antibodies

8
Q

What is glomerulonephritis?

A

It is disease of the glomerulus

Either inflammatory or non-inflammatory

Primary - only affects the glomerulus or secondary other body parts are affected - SLE or Wegners

9
Q

What are the 4 comon presentations of glomerulonephritis?

A
  1. Haematuria (blood in urine)
  2. Heavy proteinuria (nephrotic syndrome)
  3. Slowly increasing proteinuria
  4. Acute renal failure
10
Q

What are the main causes of haematuria?

A

Urinary tract infection

Urinary tract stone

Urinary tract tumour

Glomerulonephritis

11
Q

What is the necessary test before taking a renal biopsy?

A

Clotting screen - risk of bleeding to death

12
Q

What is the pathogenesis of IgA nephropathy?

A

Excess IgA sometimes present in the serum (but this is true in some people who do not have glomerulonephritis)

IgA deposits are stuck in the mesangium and are not filtered in the urine - IgA – ‘irritates’ mesangial cells and causes them to proliferate and produce more matrix

Unknown why this causes RBC’s to escape

13
Q

What is the prognosis of IgA nephropathy?

A

Usually self-limiting - ie returns to normal

SMall % go onto chronic renal failure (via continued deposition of matrix)

14
Q

How is the clinical diagnosis of nephrotic syndrome made?

A

Must be abnormality of the glomerular filter - renal biopsy

15
Q

What is the hallmark feature of membranous glomerulonephritis?

A

Thickened glomerular basement membrane

Spikes of new basement membrane matrix material underneath podocytes - spikes try to surround and remove deposits of IgG

Deposits of IgG in the subendothelial site - between basal lamina and podocyte - cannot go further and is not filtered in the urine

16
Q

What is the issue associated with IgG in the subendothelial layer?

A

IgG is too big to be filtered into the urine, but IgG activates compliment (C3) which punches holes in the filter

17
Q

What is the consequence of complement punching holes in the filter?

A

Leaky filter allows albumin to be filtered into urine - nephrotic syndrome

18
Q

What is the prognosis of glomerulonephritis?

A

•1/4 in chronic renal failure within 10 years

This is not associated with inflamamtion– on wrong side of the basal lamina – inflammatory cells cannot reach

19
Q

What is the underlying cause of IgG production and accumulation in membranous glomerulonephritis?

A

Unknown but can have underlying malignancy

IN many patients antigen is phospholipase A2 receptor

Phospholipase A2 is present on podocytes – IgG is against this receptor

20
Q

Where does matrix deposition occur in diabetic nephropathy?

A

Matrix deposition in basal lamina underlying endothelium and in mesangial matrix

Kimmelsteil Wilson lesio - gross excess of mesangial matrix forming nodules

21
Q

Describe the basement membrane in diabetic nephropathy

A

Thickened and leaky

22
Q

Describe the messangial matrix in diabetic nephropathy

A

Compresses capillaries

23
Q

What are the histological features of diabetic nephropathy?

A

Small compressed capillary lumen (by messangial matrix)

Thickened capillary wall - leaks albumin

Thickened and narrowed arterioles reduce blood flow to glomerulus

Adhesions to bowmans capsule (glomerulus’s attempt to stop massive leakage of albumin into urine)

24
Q

What is the prognosis of diabetic nephropathy?

A

Inevitable decline if 1. established diabetic nephropathy and if 2. continued poor diabetic control

25
Q

What is rapidly rising creatinine associated with?

A

Acute renal failure

26
Q

What type of glomerulonephritis has cellular proliferation and influx of macrophages (crescent) within bowmans space?

A

Crescentic glomerulonephritis

27
Q

What are the main patterns of crescentic glomerulonephritis?

A
  • Granulomatosis with polyangiitis (also known as Wegener’s granulomatosis)
  • Microscopic polyarteritis (a disease very much like Wegeners)
  • Antiglomerular basement membrane disease
  • Many other forms of glomerulonephritis
28
Q

What does granulomatosis with polyangitis affect?

A

It is a form of vasculitis

Causes: Inflammation in the vessels which affects the vessels in the kidneys, nose and lungs

29
Q

What are further tests for granulomatosis with polyangitis?

A

Serum tests show presence of anti-neutrophil cytoplasmic antibodies

(ANCA)

30
Q

What are anti-neutrophil cytoplasmic antibodies?

A

•Antibodies directed against proteinase 3 and myeloperoxidase, 2 enzymes in primary granules of neutrophils

They are not deposited in the kidney

31
Q

How do ANCA produce tissue damage?

A

•Antibodies produce tissue damage via interactions with primed neutrophils and endothelial cells.

32
Q

What is the prognosis of wegners?

A

6 months if left untreated

Cyclophosphamide - 75% complete remission

33
Q
A