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Renal Module > lecture 11 - autoimmune kidney diseases > Flashcards

lecture 11 - autoimmune kidney diseases Flashcards

1
Q

how much of cardiac output does the kidney receive?

A

25%

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2
Q

what is the filtration fraction (plasma that filters into the nephron)?

A

20%

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3
Q

what can’t get through the filtration barrier?

A

red blood cells and serum albumin

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4
Q

what does it mean if you see red blood cells in the urine?

A

something wrong with the normal physiology of the filtration barrier

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5
Q

what is chronic kidney disease?

A

structural or functional abnormalities of the kidney with or without decreased GFR

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6
Q

what are the markers for kidney disease?

A

abnormalities in the composition of blood or urine

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7
Q

how long do you need to have kidney disease before it can be chronic?

A

more than or equal to 3 months

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8
Q

what can be used to tests for kidney disease?

A

a dipstick urinalysis

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9
Q

how many stages of chronic kidney disease are there?

A

5

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10
Q

what is the eGFR like in stage 5 of kidney disease?

A

less than 15

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11
Q

what are some examples of autoimmune kidney diseases?

A

Membranoproliferative Glomerulus (MPGN), Atypical haemolytic uraemic syndrome (aHUS), SLE - lupus nephritis, IgA nephropathy and Goodpastures syndrome

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12
Q

what is the most common autoimmune kidney disease?

A

IgA nephropathy

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13
Q

what is the MPGN pathophysiology?

A

get proliferations which eat up the space in the glomerulus which means can’t get the function

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14
Q

how can proliferations eat up the space in the glomerulus?

A

immune activators, chemokines and cytokines

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15
Q

what would you see in MPGN?

A

dense deposits disease - electron dense glomerulus

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16
Q

how do you diagnose MPGN?

A

by doing a kidney biopsy

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17
Q

what would you see from the biopsy of MPGN?

A

hypercellularity, thickening of the glomerular basement membrane and proliferation

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18
Q

what are classical pathways activated by?

A

they are activated by antibodies

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19
Q

What is the lectin pathway involved in?

A

It is involved with dealing with apoptotic and damaged cells

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20
Q

What does the activation of lectin and classical pathway lead to?

A

The C3 activation which passes the alternative pathway which acts on the right side of the complement pathway and acts on the amplification route

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21
Q

What regulators are important in stoping the activation complement?

A

Factor H and DAF

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22
Q

What is the membrane attack complex important for?

A

It is important in MPGN

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23
Q

What type of anaphylatoxins can activate the complement system?

A

C5a and C3a

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24
Q

What do C3a and C5a interact with?

A

Molecules that lead to vasodilation and vasoconstriction - modulating the blood flow into the kidney

25
Q

Where are C3 and C4 made?

A

They are made mostly in the liver - the kidney generates about 20% of the total levels of the complement in the blood

26
Q

What is one of the most abundant proteins?

A

C3 - has the potential to cause damage

27
Q

What works together to inactivate C3?

A

Factor H and factor I

28
Q

What does CR1 do?

A

It is a really important natural regulator the regulates the complement, lectin and the alternative pathways on the cell surface, endothelial cells and the podocytes

29
Q

What protect against C3?

A

MCP and DAF they are ubiquitous

30
Q

What prevents MAC?

A

CD59

31
Q

What does the C4 binding protein do?

A

Stops the lectin and the classical pathway

32
Q

What are complement regulators involved in?

A

In the removal of immune complexes, the liver is a major source of clearance

33
Q

What organ do you want to get rid of immune complexes?

A

The kidney

34
Q

What allows the removal of immune complexes?

A

CR1 - complement receptor 1, it is expressed at high levels of erythrocytes and allows immune complexes to bind and be carried to the liver

35
Q

What is another type of cell that is important in complement and waste disposal?

A

Apoptotic cells - they self compact and maintain of all of the DNA and important mitochondrial antigens

36
Q

What are anaphyltoxins important for?

A

Bone regeneration

37
Q

What system is importantly for self tissue renwal?

A

The complement system

38
Q

What can C3a signalling help?

A

Can help dampen down the response

39
Q

What is C3 glomerulopathy (C3G)?

A

It is a new name for the spectrum of disorders with glomerular pathology associated with C3 desposition

40
Q

What is the dominant thing you see in C3 glomerulopathy?

A

The dysregulation of the alternative pathway in the kidney and deposition of C3 on the glomerular endothelial cells and the mesangial

41
Q

Where was Factor H deficiency discovered?

A

In pigs - led to the finding that 1 or 2 people had this. The loss of Factor H leads to dense deposit disease of C3G

42
Q

What does C3 nephritic factor (C3NeF) do?

A

It stabilises the C3 convertase and stops it from being broken down by the regulators like Factor H and I - will lead to CB3 action

43
Q

What has recently been identified?

A

Anti-Fb - don’t know where they come from

44
Q

What do anti factor H do?

A

Interact with regulators and stops the alternative pathway from being over active

45
Q

What is the haemolytic uraemic syndrome (HUS) triad known as? - biomarkers for HUS

A

Acute renal failure, thrombocytopenia, microangiopathic hemolytic anemia

46
Q

What are the triad of HUS caused by?

A

Shiga toxin producing E.Coli e.g. food poisoning - it is an acute disease

47
Q

Who does HUS affect?

A

Infants and young children it has a relatively good prognosis

48
Q

What does shiga toxin bind to?

A

GABA3 in the glomerular endothelial cells and activate the cells.

49
Q

What happens when GABA3 cells in endothelial cells are activated?

A

They turn inflamed and allow thrombosis. The coagulation system interacts with the complement where clots form - takes out the kidney very quickly

50
Q

Where does secondary HUS come from?

A

Clinical or autoimmune disorders even cancer - which can lead to TMA in the kidney

51
Q

What is Atypical HUS?

A

It’s a genetic form and leads to TMA

52
Q

What makes the process go from non thrombotic to thrombotic?

A

P-Selectin - resulting in TMA

53
Q

What gene is frequently mutated in aHUS?

A

CFH - 40% familiar mutations, 25% sporadic

54
Q

What is taken away to get aHUS?

A

Factor H, you end up with lysis and deposits of MAC

55
Q

What is systemic lupus Erythematosus?

A

A chronic inflammatory systemic autoimmune disease, characterised by polyclonal B-cell activation and abnormal autoantibodies

56
Q

What does lupus patients not have?

A

C1Q

57
Q

What happens in wound healing if you deposit collagen and fibronectin?

A

Kidney will become unfunctional

58
Q

What is IgA nephropathy?

A

An immune complex disease - it has genetic disorder, starts seeing natural antibodies as foreign

59
Q

what are the 4 stages of wound healing?

A

haemostasis - clot formation, inflammation, proliferation, regeneration

Renal Module (11 decks)

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