Lecture 14: Glomerulonephritis Flashcards

1
Q

glomerulonephritis clinical features

A
  • haematuria (non-visible or visible)
  • proteinuria (low grade or nephrotic)
  • hypertension
  • renal impairment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

nephrotic syndrome definition

A
  • a clinical syndrome that arises secondary to increased permeability of serum proteins through a damaged basement membrane in the renal glomerulus.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

nephrotic disease is characterised by which signs and symptoms?

A
  • proteinuria (> 3.5g/day or 350mg/mmol creatinine)
  • oedema (particularly periorbital and peripheral)
  • hypoalbuminaemia: < 35g/L
  • hyperlipidaemia
  • lipiduria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

nephritic syndrome definition

A
  • A group of kidney disorders that result in the presence of red blood cells in urine (haematuria), non-nephrotic range proteinuria, and often hypertension.
  • typically characterised by inflammation and damage to the glomeruli.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

nephritic syndrome typically presents with:

A
  • haematuria, often microscopic but can be macroscopic
  • hypertension
  • non-nephrotic range proteinuria
  • oedema (less severe than in nephrotic syndrome
  • in severe cases, symptoms of AKI like oliguria and anuria.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

describe the two types of glomerulonephritis

A

Proliferative:
- excessive numbers of cells in glomeruli, including infiltrating leucocytes.

Non-proliferative:
- glomeruli look normal or have areas of scarring, they have normal numbers of cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the most common cause of glomerulonephritis world-wide?

A

IgA nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

IgA nephropathy presentation

A
  • Recurrent gross or microscopic haematuria, generally occurring 12–72 hours after an upper respiratory tract or gastrointestinal infection.
  • Mild proteinuria.
  • Hypertension.
  • Less commonly, presentations can include nephrotic syndrome or a rapidly progressive GN, resulting in acute renal failure.
  • Associations with Henoch-Schönlein purpura (HSP)/IgA vasculitis, chronic liver disease, inflammatory bowel disease (IBD), and skin and joint disorders, such as psoriasis, have been observed.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

features of post-streptococcal (infectious) glomerulonephritis

incubation period, genetic predisposition

A
  • follows 10-21 days after infection typically of throat or skin
  • most commonly with lancefield group A streptococci
  • genetic predispostion: HLA-DR,-DP.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how can IgA nephropathy be differentiated from post-streptococcal glomerulonephritis?

A
  • IgAN occurs 1-2 days post-infection vs 1-3 weeks post infection in PSGN.
  • renal biopsy in IgAN shows IgA immune-complec deposits vs IgG immune complex deposits in PSGN.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

clinical features of anti-GBM glomerulonephritis

used to be known as goodpasture syndrome

A
  • haemoptysis and pulmonary haemorrhage
  • AKI, often severe and rapidly progressive, leading to renal failure.
  • more common in males
  • two peaks in age of presentation: 20-30 years and 60-70 years
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

anti-GBM disease treatment

A

aggressive immunosuppression:
- steroid
- plasma exchange and cyclophosphamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

nephrotic syndrome non-specific management

A
  • treat oedema: salt and fluid restriction and loop diuretics
  • hypertension: use renin-angiotensin-aldosterone blockade
  • reduce risk of thrombosis: heparin or warfarin
  • reduce risk of infection e.g. pneumococcal vaccine
  • treat dyslipidaemia e.g. statins
  • specific therapy towards cause of the non-proliferative glomerulonephritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

minimal change disease features

A
  • commonest cause of GN in children.
  • sudden onset of oedema - days
  • remission with steroids (often)
  • relapse occurs in 2/3 patients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

minimal change disease treatment

A
  • prednisolone 1mg/kg for up to 16 weeks
  • once remission achieved, slow taper over 6 months
  • initial relapse treated with further steroid course
  • subsequent relapses treated with: cyclophosphamide, cyclosporin, tacrolimus, mycophenolate mofetil, rituximab
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

treatment of focal and segmental glomerulonephritis

A
  • general measures, as previously described
  • trail of steroids, positive response, even partial remission, carries better prognosis
  • alternative options: cyclosporin, cyclophosphamid, and rituximab
17
Q

membranous nephropathy treatment

most common cause of nephrotic syndrome in adults

A
  • general measures for at least 6 months
  • immunosuppression if symptomatic nephrotic syndrome, rising proteinuria or deteriorating renal function.
  • cyclophosphamide and steroids (alternate months) for 6 months
  • tacrolimus
  • rituximab
18
Q

membranous nephropathy causes

A
  • idiopathic (majority)
  • malignancies
  • SLE
  • rheumatoid arthritis
  • drugs: NSAIDs, gold, penicillamine