Glomerulonephritis Flashcards
Outline the function and the structure of the glomerulus?
A semi-permeable membrane used as a filter between the blood in capillaries and the the inter-tubular fluid.
Capillaries –> Basement Membrane –> Podocytes
Define the term glomerulonephritis?
Glomerulonephritis includes a range of immune-mediated disorders that cause inflammation within the glomerulus.
Describe the following terms with regard to glomerulonephritis: diffuse, focal and segmental?
Diffuse: affecting all glomeruli
Focal: affecting some of the glomeruli
Segmental: only affects part of an affected glomeruli
Describe the basic pathology of glomerulonephritis?
Immunological attack by antibodies or T cells.
The glomerulus responds to the attack in one of 3 ways:
Capillary
a) endothelial proliferation
b) proliferation of mesangial cells
c) capillary wall necrosis
BM thickening
Deposition of podocytes in the bowman’s capsule
Describe the different causes of antigens being present on the glomerulus?
Neoplasm SLE Goodpasture's Amyloid Infection Diabetes
Henoch Schnolein Purpura
What are the causes of glomerulonephritis and which are most common in children and adults?
- IgA Nephropathy (including HSP)
- SLE
- Anti Glomerular basement membrane disease (Goodpastures)
- Proliferative (post infective)
- Rapidly Progressing
In children: Minimal Change Disease
In adults: IgA nephropathy
Describe the clinical presentation of glomerulonephritis?
Spectrum of disease from asymptomatic to nephrotic/nephritic syndrome.
Often asymptomatic and found on urinalysis: microscopic haematuria and proteinuria
Can present with:
- Frank haematuria
- Progressive HTN
- Renal failure
- Oedema
How does IgA nephropathy present?
Post URTI
- Micro/macro haematuria
- Progressive hypertension
Pathophysiology: mesangial cell proliferation caused by IgA deposition.
In HSP:
- Rash
- Arthralgia
- Abdominal pain
How does anti-GBM/Goodpasture’s disease present?
Macroscopic haematuria followed by oliguria
Respiratory symptoms:
- Dyspnoea
- Cough
- Haemoptysis
What is the pathophysiology in Goodpasture’s diseaseand how is it treated?
It is an autoimmune disease driven by anti glomerular basement membrane autoantiboidies (anti GBM).
These attack the basement membrane in both the kidneys and lungs.
Urgent treatment is needed with:
- Steroids
- Plasma exchange (to remove circulating anti GBM)
- Dialysis may be needed
Describe the clinical presentation of proliferative glomerulonephritis?
Infection related (often post streptococcal)
Renal:
Haematuria
HTN
Systemic:
Acute oedema
Respiratory distress
It is more common in the developing world
How should proliferative glomerulonephritis be managed?
Supportive measures:
- Diuretics
- Anti-hypertensives
Treat underlying cause.
Outline the investigations which should be done in suspected glomerulonephritis?
Bedside:
- Urinalysis: (haematuria/proteinuria)
- Urine protein quantification
Bloods:
- FBC, LFTs, CRP, U/E’s
- Serum immunoglobulins, serum and urine protein electrophoresis: to exclude myeloma.
- Autoantibodies: if connective tissue disease suspected
Imaging:
- Renal US
- CXR
Renal biopsy: except in the mildest cases or in nephrotic syndrome in children. (needed for diagnosis)
How do you manage glomerulonephritis generally?
Symptomatic:
- Control oedema with diuretics
- BP control with ACEi or angiotensin II receptor antagonists.
Depending on type and degree of histological finding:
Immunosupressants: (except in proliferative)
- Corticosteroids
- Cyclophosphosphamide
IV Ig
What is rapidly progressive glomerulonephritis?
A glomerulonephritis which progresses to renal failure within days to weeks.
It is usually in the context of a nephritic syndrome*
On renal biopsy it is often associated with extensive glomerular crescent formation.
(if the question asks about cresenteric glomerulonphritis thing of rapidly progressive)
*Haematuria
Proteinuria (not as high as nephrotic)
HTN
Oliguria
