Glomerulonephritis Flashcards
What part of glomerulus is damaged in nephrotic syndrome?
State the triad of symptoms seen in nephrotic syndrome and explain why they occur
- Podocyte damage which leads to abnormal size of filtration slits
Triad of symptoms:
- Proteinuria >350mg/mmol (or 3.5g in 24hr)
- Hypoalbuminaemia <30g/L
- Oedema
- Usually accompanied by hypercholesteraemia
Proteins can leak out of glomerulus due to abnoral/increased size of filtration slits (caused by podocyte damage) which leads to protein in urine and a lack of albumin in blood which then decreases oncotic force in capillaries leading to oedema
Nephrotic syndrome can be caused by primary or secondary renal diseases; state some examples of each
Primary
- Minimal change disease
- Membranous glomerulonephropathy
- Focal segmental glomerulosclerosis
Secondary
- Diabetes
- SLE
- Amyloidosis
State at least 4 potential complications of nephrotic syndrome
- Venous thromboembolism
- Higher risk of infection
- Progression of CKD
- Hyperlipidaemia
- Hypertension
Explain why those with nephrotic syndrome are at increased risk of VTE
What do we do if albumin <20g/L?
Hypercoagulable due to:
- Increased clotting factors
- Decreased antithrombin III
- Platelet abnormalities
Albumin <20g/L give LMWH
Discuss the management of nephrotic syndrome
- Oedema: diuretics, salt & fluid restriction
- Proteinuria: ACE inhibitor
- Hypercholesterolaemia: monitor & consider statin
- Treat underlying cuse e.g. steroids
Which part of glomerular filtration barrier is damaged in neprhitic syndrome?
What is the triad of symptoms?
Inflammation in glomerulus which causes damage to endothelium (leading to heamaturia)
Triad of symptoms:
- Haematuria
- Reduction in GFR
- Hypertension
Discuss the management of nephritic syndrome
- Involve renal team
- Hypertension: ACEinhibitors, salt & fluid restriction
- Dialysis if GFR reduced
- Treat underlying disease
State some causes of nephritic syndrome
- Post-infectious glomerulonephritis
- IgA nephropathy
- Small vessel/ANCA associated vasculitis
- Anti-GBM disease/Goodpasture syndrome
- Thin basement membrane disease
- Alport syndrome
- Lupus nephritis
For post-infectious glomerulonephritis, discuss:
- When it occurs
- Who it usually affects
- Investigation findings
- Treatment specific to the disease (i.e. is there any specific treatment, alongside generic treatment, for post infectious glomerulonephritis)
- Weeks after group A beta haemolytic streptococcal infection
- 1-2 weeks after tonsilitis
- 3-4 weeks after impetigo/cellulitis
- Children 3-12yrs
- Investigation findings:
- +ve anti-streptococcal antibodies (ASO titre)
- Low serum C3
- Biopsy: immune complex deposition, IgG, IgM, C3
- Usually self-limiting. Can lead to rapidly progressive glomerulonephritis.
For IgA nephropathy causing glomerulonephritis, discuss:
- How it presents
- What age usually presents in
- Investigation findings- including urine, bloods & biopsy
- Progression to ESRF
- Any specific treament (i.e. is there any specific treatment alongside generic treatment for nephritis)
- Episodic gross haematuria during or directly after URT, GI infection or strenous exercise
- More common in males, peak incidence 20-30yrs
- Investigation findings:
- Microhaematuria with intermittent gross haematuria
- High IgA
- Normal C3 and C4
- Biopsy: mesangial immune complexes in glomeruli
- No specific treatment just usually support therapy
For small vessel/ANCA associated vasculitis, discuss:
- 3 types that can cause nephritis
- How they present
- Investigation findings inlcuding ANCA results & biopsy
- Specific treatment (i.e. is there any specific treatment, alongside generic treatment, for post infectious glomerulonephritis)
For anti-GBM disease, discuss:
- How it usually presents
- Who it commonly presents in
- Investigation results- bloods, CXR & biopsy
- Specific treatment (i.e. is there any specific treatment, alongside generic treatment, for post infectious glomerulonephritis)
- Glomerulonephritis and may have haemoptysis
- More common males, peak incidence in 30’s and >60s
- Investigation results:
- Anti-GBM antibodies
- Pulmonary infiltrates CXR
- Biopsy: IgG deposition along basement membrane
- Treatment:
- Plasma exchange
- Immunosupression
For thin basement membrane disease, state:
- Whether it is herediatary?
- What the defect is
- What urine & biopsy investigations show
- Specific treatment (i.e. is there any specific treatment, alongside generic treatment, for post infectious glomerulonephritis)
- Hereditary
- Defect in type IV collagen
- Investigation results:
- Persistent microscopic haematuria
- Biopsy: diffuse thinning GBM membrane
- Treatment: just monitor renal func. Has good prognosis
For alport sydnrome, discuss:
- Inheritence pattern
- Mutation
- Other associated problems
- Whether it leads to ESRF
- Investigation results: inlcuding urine & biopsy
- Specific treatment (i.e. is there any specific treatment, alongside generic treatment, for post infectious glomerulonephritis)
- X-linked recessive
- Mutation in type V collage
- Hearing loss, eye abnormalities
- Often leads to ESRF
- Investigation findings
- Micrscopic haematuria with intermittent visible haematuria
- Biopsy: splitting of GBM and alternating thickening & thinning of GBM
- Renal transplant
For lupus nephritis, discuss:
- Who it occurs in
- Nephritic or nephrotic
- Investigation results: include bloods & biopsy
- Specific treatment
- Pts with SLE
- Can be nephritic or nephrotic
- Investigation results:
- ANA
- Anti ds-DNA
- Biopsy: 6 different classes of lupus nephritis with different biopsy findings and different treatments
- Immunosupressive therapy based on classification/presentation
