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Renal and urology > Glomerulonephritis > Flashcards

Glomerulonephritis Flashcards

1
Q

What are the main kinds of glomerular disease?

A

Diabetic Nephropathy

Glomerulonephritis (GN)

Amyloid/ Light Chain Nephropathy

Transplant Glomerulopathy

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2
Q

What are the two most common causes of end stage renal disease?

A
  1. Diabetes
  2. Chronic glomerulonephritis
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3
Q

What is glomerulonephritis?

A

An immune mediated disease of the kidneys affecting the glomeruli causing secondary tubulointerstitial damage

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4
Q

What are podocytes?

A

Cells that spread out around capillaries in branches, forming protein bridges (actin and myosin) between these branches to provide strong mechanical strength for the capillaries

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5
Q

What are mesangial cells?

A

Cells found between groups of capillaries that work in tandem with the glomerular basement membrane:

They act like smooth muscle cells and can cause vasoconstriction

They have immune function, releasing cytokines

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6
Q

What does the glomerular basement membrane consist of?

A

It is acellular and consists of collagen and protein

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7
Q

Which components of the glomerulus are injured in prolfierative glomerulonephritis?

A

Mesangial cells

Endothelial cells

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8
Q

Why does haematuria occur in proliferative GN?

A

Mesangial and endothelial cells are exposed to blood, so injury causes red cells in urine and a proliferative lesion and activation of the inflammatory cascade

This causes a nephritic syndrome

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9
Q

What does injury to podocytes result in?

A

Non-proliferative lesion and protein in urine

There is no activation of the inflammatory cascade since the podocytes are not exposed to blood

This causes nephrotic syndrome

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10
Q

What colour is urine typically in glomerulonephritis?

A

‘Smoky’, ‘rusty’ or coca-cola coloured

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11
Q

How should urine be examined if GN suspected and what would be expected?

A

Urinalysis: haematuria, proteinuria

Urine microsopy: RBC (dysmorphic), RBC & granular casts, lipiduria

Urine Protein: creatinine Ratio

24 hour urine - quantify proteinuria

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12
Q

How is haematuria normally picked up in glomerulonephritis?

A

Dipstick test - the haematuria is painless

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13
Q

How is proteinuria judged?

A

Microalbuminuria (30-300mg albuminuria/day)

Asymptomatic proteinuria (< 1 g/day)

Heavy proteinuria (1-3 g/day)

Nephrotic syndrome (> 3 g/day))

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14
Q

What is the usual diagnosis if red cell casts seen on microscopy of urine?

A

Indicates active, aggressive proliferative lesion

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15
Q

How does glomerulonephritis present?

A

Oedema

Hypoalbuminuria

Decresed renal function

Hypertension

Haematuria

Frothy urine

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16
Q

Why does hypertension occur in glomerulonephritis?

A

Fluid retention

Proliferative lesion causing increased renin secretion

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17
Q

What are the three indicators of nephrotic syndrome?

A

Oedema

Hypoalbuminuria

Proteinuria

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18
Q

Why does impaired immunity occur in nephrotic syndrome?

A

Opsonising antibodies are leaked out into urine

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19
Q

What is a complication of nephrotic syndrome that would make a patient present with unilateral loin pain and haematuria for the first time, and why?

A

Renal vein thrombosis

Hypoalbuminuria can change liver function, causing increased production of clotting and fibrotic factors

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20
Q

What are the features of nephrotic syndrome?

A

Proteinuria > 3 g/day (mostly albumin, also globulins)

Hypoalbuminaemia (<30)

Oedema

Hypercholesterolaemia

Usually normal renal function

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21
Q

What are the features of nephritic syndrome?

A

Acute Renal Failure

Oliguria

Oedema/ Fluid retention

Hypertension

Active urinary sediment: RBC’s, RBC and granular casts

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22
Q

What are the complications of nephrotic syndrome?

A

Infections

Renal vein thrombosis

Pulmonary emboli

Volume depletion: often due to overuse of ACEi, may lead to pre-renal AKI

Vit D deficiency

Subclinical hypothyroidism

23
Q

What are the four components of histological classification of glomerulonephritis?

A

Proliferative/non-proliferative

Focal/diffuse (< or > 50% glomeruli affected)

Global/segmental (all or part glomerulus affected)

Crescentic

24
Q

What does ‘crescentic’ mean on histological description of glomerulonephritis?

A

Presence of crescents: cells burst into Bowman’s space and form crescents around the glomerulus, causing ischaemia and death of the glomerulus

25
Q

What are the principles of treatment of glomerulonephritis?

A

Reduce degree of proteinuria

Induce remission of nephrotic syndrome

Preserve longterm renal function

26
Q

What are some of the non-immunosuppresive treatments of glomerulonephritis?

A

Anti-hypertensives

ACE inhibitors/ ARBs

Diuretics

Statins

27
Q

What are some of the immunosuppressive drugs used to treat glomerulonephritis?

A

Corticosteroids (Prednisolone po/MethylPred IV)

Azathioprine

Alkylating agents (Cyclophosphamide/ Chlorambucil)

Calcineurin inhibitors (Cyclosporin/Tacrolimus)

Mycophenolate Mofetil (MMF)

28
Q

Why is plasmapheresis used in immunosuppresive treatment of GN?

A

Used to remove antibodies causing the GN from the circulation

29
Q

Why are antibodies used in immunosuppressive treatment of glomerulonephritis?

A

Monoclonal T or B cell antibodies can be used to switch off B cell production to stop production of antibodies causing GN

30
Q

How are nephrotic patients managed?

A

Fluid restriction

Salt restriction

Diuretics

ACE Inhibitors/ ARBs

IV Albumin (only if volume depleted)

Immunosuppression

31
Q

What values of proteinuria indicate remission from nephrotic syndrome?

A

Complete remission: proteinuria < 300 mg/day
Partial remission: proteinuria < 3g/day

32
Q

What is the commonest cause of nephrotic syndrome in children?

A

Minimal change nephropathy

33
Q

What is the pathology in minimal change nephropathy?

A

Podocyte foot process fusion

34
Q

What is the first line treatment for minimal change nephropathy?

A

Oral steroids - 94% go into remission

35
Q

What is the second-line treatment for minimal change nephropathy?

A

Cyclophosphamide

36
Q

Does minimal change nephropathy cause progressive renal failure?

A

No

37
Q

What is the commonest cause of nephrotic syndrome in adults?

A

Focal segmental glomerulosclerosis

38
Q

What is the pathology in focal segmental glomerulosclerosis?

A

Affects small parts of the glomerulus in segments causing scarring and sclerosis

Stops formation of protein bridges between podocytes

39
Q

Does focal segmental glomerulosclerosis cause renal damage?

A

50% progress to end stage renal failure after 10 years

40
Q

What can cause focal segmental glomerulosclerosis?

A

HIV

Heroin use

Obesity

Reflux nephropathy

41
Q

What is the second commonest cause of nephrotic syndrome in adults?

A

Membranous nephropathy: most common cause in the UK

42
Q

What are some secondary causes of membranous nephropathy?

A

Infections (hepatitis B/ parasites)

Connective tissue diseases (lupus)

Malignancies (carcinomas/ lymphoma)

Drugs (gold/penicillamine)

43
Q

What can be seen on renal biopsy with membranous nephropathy?

A

Subepithelial immune complex deposition in the basement membrane

44
Q

What is the treatment for membranous nephropathy?

A

Steroids

Alkylating agents

B cell monoclonal Ab

45
Q

What is the commonest glomerulonephritis in the world?

A

IgA nephropathy

46
Q

How does IgA nephropathy present?

A

Asymptomatic microhaematuria ± non-nephrotic range proteinuria

Macroscopic haematuria after resp/GI infection

AKI/ CKD

47
Q

What is IgA nephropathy associated with?

A

Associated with Henoch-Schonlein Purpura (HSP)

(arthritis/colitis/purpuric skin rash)

48
Q

What is seen on renal biopsy?

A

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

49
Q

How is IgA nephropathy treated?

A

BP control

ACE inhibitors & ARBs

Fish oil

50
Q

What is the disease process in IgA nephropathy?

A

Slight genetic abnormality in IgA causes it to become stuck in the kidney: tends to lodge in mesangial cell, stimulating proliferation

Endothelial depositon causes cytokine aggregation and an inflammatory cascade occurs

51
Q

What may cause rapidly progressive glomerulonephritis in an ANCA positive patient?

A

Systemic Vasculitis

Wegener’s granulomatosis (Granulomatosis with polyangitis)

Microscopic polyangiitis

52
Q

What are some of the ANCA negative causes of rapid progressive glomerulonephritis?

A

Goodpasture’s disease: Anti-GBM

Henoch Scholein Purpura HSP/IgA

Systemic Lupus Erythematosus

53
Q

What is rapidly progressive glomerulonephritis?

A

A treatable cause of acute renal failure with rapid deterioration in renal function over days/weeks

There is active urinary sediment (RBC’s, RBC & Granular Casts) causing haematuria

54
Q

What is the treatment for rapidly progressive glomerulonephritis?

A

Immediate immunosuppression and treatment of systemic cause:

Steroids (IV Methylprednisolone /oral prednisolone)

Cytotoxics (Cyclophosphamide/Mycophenolate/ Azathioprine

Plasmapheresis

Renal and urology (11 decks)

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