Glomerulonephritis Flashcards

1
Q

What are the different types of glomerular diseases?

A

Diabetic nephropathy
Glomerulonephritis
Amyloid nephropathy
Transplant glomerulopathy

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2
Q

What is the commonest cause of end stage renal disease (after diabetes)?

A

Chronic glomerulonephritis

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3
Q

What is glomerulonephritis?

A

Immune-mediated disease of the kidneys affecting the glomeruli (with secondary tubulointerstitial damage)
Disruption of the glomerular capillary wall (endothelium, basement membrane and podocytes) leads to haematuria +/- proteinuria

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4
Q

What does damage to the endothelial or mesangial cells lead to?

A

PROLIFERATIVE LESION
RED CELLS IN URINE
NEPHRITIC SYNDROME

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5
Q

What does damage to the podocytes lead to?

A

NON-PROLIFERATIVE LESION
PROTEIN IN URINE
NEPHROTIC SYNDROME

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6
Q

How do podocytes respond to damage?

A

Atrophy

Loss of size/charge specific barrier

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7
Q

How do mesangial cells react to damage?

A

Proliferate
Release angiotensin 2 (hypertension)
Chemokine release
Attract inflammatory cells

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8
Q

How do endothelial cells react to damage?

A

Vasculitis

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9
Q

How is GN diagnosed?

A

Clinical presentation
Blood tests
Urine: haematuria, proteinuria, dysmorphic RBC, RBC and granular casts, lipiduria, urine protein:creatinine 24hr ratio
Kidney biopsy

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10
Q

What present in urine microscopy is pathognomonic of glomerulonephritis?

A

RBC and granular casts

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11
Q

How can haematuria present?

A

Asymptomatic microscopic haematuria

Episodes of painless macroscopic haematuria = GN should be painless

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12
Q

How can proteinuria present?

A
Microalbuminuria - 30-300 mg albuminaura/day  
Asymptomatic proteinuria (<1 g/day) 
Heavy proteinuria (1-3 g/day) 
Nephrotic syndrome (>3 g/day)
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13
Q

What do dysmorphic RBC in urine suggest?

A

They’ve been squished through the glomerulus

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14
Q

What are clinical renal presentations of GN?

A

Impaired renal function: AKI (rapidly progressive GN)
CKD/ESRD
Hypertension

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15
Q

What is nephritic syndrome?

A

AKI
Oliguria
Oedema/ fluid retention (due to lack of excretion)
Hypertension (fluid overload)
Active urinary sediment: RBC, RBC and granular cast

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16
Q

What is nephritis syndrome indicative of?

A

Proliferative process

Affecting endothelial cells

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17
Q

What is nephrotic syndrome?

A
Proteinuria >3 g/day (mostly albumin) 
Hypoalbuminemia (<30) 
Oedema (loss of oncotic pressure) 
Hypercholesterolaemia
Normal renal function
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18
Q

What is nephrotic syndrome indicative of?

A

Non-proliferative process

Affecting podocytes

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19
Q

What are complications of nephrotic syndrome?

A

Infections - you leak antibodies along with fluid
Renal vein thrombosis - polycythaemia
PE
Volume depletion - overaggressive diuretic use leading to pre-renal hypovolemia AKI
Vit D deficiency
Subclinical hypothyroidism

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20
Q

How will the presentation of GN differ from interstitial nephritis?

A

Presence of protein and blood in urine

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21
Q

What are the different types of GN?

A

Primary

Secondary: infections, drugs, malignancies, ANCA, SLE, goodpasture’s, HSP

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22
Q

How are the different types of GN differentiated histologically?

A

Renal biopsy
Light microscopy
Immunofluorescence (IgG deposits in GBM in goodpasture’s)
Electron micrograph (minimal change glomerulonephritis)

23
Q

What does proliferative and nonproliferative refer to?

A

Presence of absence of proliferation of mesangial cells

24
Q

What does focal or diffuse refer to?

A

More or less than 50% of glomeruli affected

25
Q

What does global or segmental refer to?

A

All or part of glomerulus affected

26
Q

What does crescentic refer to?

A

Presence of cresents - epithelial cell extracapillary proliferation e.g. RPGN in vasculitis

27
Q

What are the treatment principles of GN?

A

Reduce degree of proteinuria
Induce remission of nephrotic syndrome
Preserve long term renal function

28
Q

What are the non-immunosuppressive treatments of GN?

A
Anti-hypertensives (target BP <130/80 - <120/75 if proteinuria) 
ACEi/ARB
Diuretics
Statins
Anticoagulants/aspirin/ antiplatelets
29
Q

What immunosuppressive drugs are used in GN?

A

Corticosteroids (prednisolone)
Azathioprine
Alkylating agents (cyclophosphamide)
Calcineurin inhibitors (cyclosporin /tacrolimus)

30
Q

What can be used for immunosuppression in GN?

A

Drugs
Plasmapheresis
Antibodies: IV immunoglobulin (monoclonal T or B cells)

31
Q

What is the general treatment of a nephrotic patient?

A
Fluid restriction
Salt restriction 
Diuretics
ACEi/ARB
Anticoagulation 
IV albumin if volume deplete
Immunosuppression
32
Q

What are the main types of primary GN?

A
Minimal change
FSGS
Membranous
Membranoproliferative 
IgA nephropathy
33
Q

What is the commonest cause of nephrotic syndrome in children?

A

Minimal change nephropathy

34
Q

What can be seen histologically in minimal change nephropathy?

A

Normal renal biopsy on light microscopy and immunofluorescence with foot process fusion on EM

35
Q

How is minimal change nephropathy treated?

A

Oral steroids

Does NOT cause progressive renal failure

36
Q

What is the commonest cause of nephrotic syndrome in adults?

A

Focal segmental glomerulosclerosis (FSGS)

37
Q

What can cause FSGS?

A

Primary

Secondary: HIV/heroin use/obesity/reflux nephropathy

38
Q

What will FSGS look like histologically?

A

Light microscopy: focal segmental glomerulosclerosis

Minimal Ig/complement deposition on IF

39
Q

How is FSGS treated?

A

Prolonged steroids

50% will progress to end stage renal failure after 10 years

40
Q

What is the 2nd commonest cause of nephrotic syndrome in adults?

A

Membranous nephropathy

Thickened basement membrane

41
Q

What causes membranous nephropathy?

A

Primary
Secondary: infections (hep B/ parasites), connective tissue disease (SLE), malignancies (carcinomas/ lymphomas), drugs (gold, penicillamine)

42
Q

What will renal biopsy show in membranous nephropathy?

A

Subepithelial immune complex deposition in the basement membrane

43
Q

How is membranous nephropathy treated?

A

Steroids
Alkylating agents
B cell monoclonal Ab
30% progress to end stage renal failure within 10 years

44
Q

What is the commonest glomerulonephritis in the world?

A

IgA nephropathy

45
Q

How will IgA nephropathy present?

A

Asymptomatic microhaematuria +/- non-nephrotic range proteinuria
Macroscopic haematuria after resp/GI infection
AKI/ CKD

46
Q

What condition is IgA nephropathy associated with?

A

Henoch-schonlein purpura: arthritis, colitis, purpuric skin rash, renal involvement

47
Q

What will renal biopsy show in IgA nephropathy?

A

Mesangial cell proliferation and expansion on light microscopy with IgA deposits in mesangium on IF

48
Q

How is IgA nephropathy treated?

A

BP control - ACEi/ ARB

25% progress to end stage renal failure within 10-30 years

49
Q

What is rapidly progressive glomerulonephritis?

A

Treatable cause of acute renal failure

Rapid deterioration in renal function over days/weeks

50
Q

What will RPGN show on biopsy?

A

Glomerular crescents

51
Q

What ANCA-positive conditions can cause RPGN?

A

GPA - c-ANCA

MPA - p-ANCA

52
Q

What ANCA-negative conditions can cause RPGN?

A

Goodpasture’s disease - anti-GBM
Henoch Schonlein Purpura IgA
SLE

53
Q

Describe what occurs in ANCA associated vasculitis?

A

Neutrophils primed inducing PR3 and MPO to cell surface where they interact with ANCA in blood stream
Neutrophils adhere to endothelial cells
Release of proteolytic enzymes and reactive oxygen species
ANCA activated neutrophils promote inflammatory process and perpetuate vasculitis

54
Q

What is the treatment of RPGN?

A

Strong immunosuppression with supportive care including dialysis
Immunosuppression with IV steroids or cytotoxics (cyclophosphamide/ azathioprine)
Plasmapheresis