Glomerulonephritis Flashcards
4 features of GN
haematuria
proteinuria
renal insufficiency
hypertension
Haematuria in GN
persistent microscopic
dysmorphic RBC on microscopy
Proteinuria in GN
persistent, proteinuria >1gram/mmol creatinine
Values of hypertension
> 140/80mmHg
How is renal insufficiency described?
rising creatinine
mild or severe
slow or rapid deterioration
nephritic>nephrotic
Nephritic state
hypertension, renal impairment, haematuria, dysmorphic RBC, cellular casts, active urine sediment
Nephrotic syndrome
oedema proteinuria hypoalbuminaemia hyperlipidaemia primary or secondary glomerular disease
Differential diagnosis of nephrotic syndrome
congestive heart failure - JVP raised, normal albumin, minimal proteinuria
hepatic disease - no proteinuria, LFT abnormal
Aetiology of GN
autoimmune, infection, malignancy, drugs, others
2 types of GN
proliferative and non-proliferative
proliferative GN
excessive numbers of cells in glomeruli
Include infiltrating leucocytes
Non-proliferative GN
Glomeruli look normal or have areas of scarring
normal numbers of cells
Diffuse GN
> 50% glomeruli affected
Focal GN
<50% glomeruli affected
Global GN
All of the glomeruli are affected
Segmental GN
part of the glomerulus is affected
4 types of proliferative GN
Diffuse proliferative = post infective nephritis
focal proliferative = mesangial IgA
focal necrotising crescentic nephritis
membrano-proliferative nephritis
What is the usual cause of post infective GN?
10-21 days after throat or skin streptococcal infection
Causative organisms of post strep GN
Lancefield group A strep
Presentation of post infective GN
dark urine - haematuria
10-21 days after infection
Treatment of post strep GN
antibiotics?
diuretics eg furosemide
vasodilator drug for hypertension eg amlodipine
IgA nephropathy
IgA deposition in mesangium and mesangial proliferation is the most common cause of GN worldwide
Presentation of IgA nephropathy
Microscopic haematuria and proteinuria
nephrotic syndrome
IgA crescentic GN
3 broad causes of crescentic GN
ANCA eg polyangiitis
Anti GBM nephritis
other eg vasculitis, SLE
Presentation findings of ANCA crescentic GN
ANCA +ve
rash, proteinuria, haematuria, high creatinine
Treatments of ANCA crescentic GN
high dose steroids
plasma exchange
cyclophosphamide
What does anti-GBM crescentic GN present as?
nephritis
nephritis and lung haemorrhage
Diagnosis of anti GBM GN
Anti GBM antibodies in serum AND kidney
Treatments of anti GBM GN
aggressive immunosuppressions
steroid, cyclophosphamide, plasma exchange
Crescentic GN management
immunosuppression
- CCS
- plasma exchange
- cytotoxic eg cyclophosphamide
- B cell therapy eg Rituximab
- complement inhibitors
3 types of non proliferative GN
minimal change disease
focal and segmental GN
membranous nephropathy
Treatments of nephrotic syndrome
loop diuretics and salt restriction for oedema
renin-angiotensin-aldosterone blockade for hypertension
reduce thrombosis risk eg warfarin or heparin
reduce risk of infection - pneumococcal vaccine
treat dyslipidaemia - statins
Minimal change nephrotic syndrome description
commonest form In children
rapid oedema
complete loss of proteinuria with steroids
2/3 patients relapse
Treatment of minimal change nephropathy
Prednisolone (first relapse aswell) - cyclophosphamide - ciclosporin - Tacrolimus - Rituximab And general nephrotic syndrome treatments
How does focal and segmental GN present?
nephrotic syndrome
focal and segmental sclerosis
Problem with focal and segmental glomerulosclerosis
resistant to steroids
Treatment of focal and segmental glomerulosclerosis
general measures
steroids?
ciclosporin, cyclophosphamide, rituximab
How is membranous nephropathy diagnosed?
histology
2 serum positive enzymes
Secondary causes of membranous nephropathy
malignancy
SLE
rheumatoid arthritis
Drugs eg NSAIDs
Treatment of membranous nephropathy
general measures for 6 months
immunosuppression if not improving
cyclophosphamide and steroids
cyclosporin and rituximab
