Glomerulonephritis Flashcards
What is nephrotic syndrome?
Triad of:
1. Proteinuria (>3g/24h)
2. Hypoalbuminaemia (<30g/L)
3. Oedema
Other: hypercholesterolaemia, hypercoagulopathy,
What are the basic/non basic investigations for suspected glomerulonephritis?
Basic - U+Es, Urinalysis, quantify proteinuria, check albumin and ultrasound.
Non basic - GN screen, myeloma screen and kidney biopsy
What is seen in a GN screen?
ANCA,
ANA,
C3/4,
Anti-GBM,
Rh factor
What are some causes of pure nephrotic syndrome?
Minimal change disease,
Membranous GN,
Focal segmental GN,
Amyloidosis,
Diabetic nephropathy
What can a kidney biopsy show?
Light microscopy,
Immunofluorescence,
Electron microscopy (looks at ultrastructure)
It is the gold standard for diagnosis of GN
What are features of Minimal Change disease?
Most commonly occurs in children.
T cell and cytokine mediated damage to glomerular BM
Presentation: Nephrotic syndrome, normotensive
Biopsy: Normal glomeruli on LM. Electron microscopy shows fusion of podocytes.
What is the management of minimal change disease?
1st line: Oral corticosteroids
2nd line if resistant to steroids: Cyclophosphamide
Describe the presentation and causes of membranous glomerulonephritis
Causes: Idiopathic: Anti-phospholipase A2 antibodies, infection (hep B, malaria or syphilis), malignancy, drugs (penicillamine, NSAIDs), autoimmune diseases.
Presents with nephrotic syndrome or proteinuria. Biopsy shows thickened basement membrane with spike and dome appearence.
What is the management of membranous glomerulonephritis
All patient’s given an ACEi or ARB.
Most resolve spontaneously and don’t need immunosupression but if needed then give steroids AND cyclophosphamide as steroids alone are not effective.
What are the complications of nephrotic syndrome?
Increased risk of thrombosis due to loss of antithrombin III and plasminogen in urine,
Hyperlipiaemia,
CKD,
Increased risk of infection,
Hypocalcaemia (vitamin D lost in urine)
What is membranoproliferative GN?
GN more likely to cause nephritic syndrome but can overlap. Can be caused by Hep C. Typically affects patients under age 30.
Describe features and investigations of anti-GBM disease
Caused by anti GBM antibodies. Presents with Haemoptysis, pulmonary haemorrhage, AKI rapidly progressive.
Investigations: Unrinalysis, urine microscopy and culture, U&Es, CXR, GN screen, and renal biopsy
What is the treatment of goodpasture’s syndrome?
Plasma exchange,
Steroids and cyclophosphamide.
What is nephritic syndrome?
Syndrome with: Haematuria (microscopic or macroscopic), oliguria, hypertension, proteinuria (<3g in 24h)
What disease can cause nephritic syndrome?
SHARP AIM
SLE
HSP,
Anti-GBM disease,
RPGN,
Post-infectious GN,
Alport syndrome,
IgA nephropathy,
Membranoproliferative glomerulonephritis
WHat are the investigations for nephritic syndrome
Urine dipstick,
Urine microscopy (looking for casts),
Urine PCR,
FBC, U&Es, LFTs, bone profile,
GN screen,
Ultrasound of kidneys,
Kidney biopsy
Describe features of IgA nephropathy
Caused by excess IgA which deposits in the mesangium. On biopsy there is hypercellularity.
Presents 1-2 days after URTI with nephritic syndrome
What is the management of IgA nephropathy?
- If only isolated haemturia, protienuria < 500-1000mg/day and normal eGFR then no treatment needed.
- Persistent proteinuria (>500-1000mg/day) or slightly reduced eGFR then ACEi.
- Falling eGFR or failure to respond to ACEi then steroids
What are the causes of rapidly progressive glomerulonephritis?
Type 1 - Anti-GBM antibody disease,
Type 2 - Immune complex deposition eg, lupus nephritis, IgA nephropathy, HSP
Type 3 - Pauci immune disease (absence of anti GMB antibodies or immune complexes), ANCA vasculitis
What are the signs and symptoms of rapidly progressive glomerulonephritis?
Nephritic syndrome, peripheral oedema, fatigue, loss of appetitie, nausea and vomiting, persistent hiccups
What are the investigations for RPGN?
ANCA,
Anti-GBM,
Renal biopsy
What is the general management of nephrotic syndrome?
Furosemide with care,
ACE inhibitor/ARB (not in minimal change),
Statin (not in minimal change),
SGLT2 (not in vasculitis)
What are features of amyloidosis?
Deposition of abnormal proteins.
AA amyloidosis -(occurs when increased serum amyloid A) malignancy or chronic microbial infection.
AL amyloidosis (L=light chain) - myeloma or waldenstrom’s macroglobulinaemia.
It can present with nephrotic syndrome, neuropathy, periorbital purpura, malabsorption, joint inflammation
What is the investigation for amyloidosis?
Congo red staining shows apple green bifringence.
What are the causes of membranoproliferative GN?
Type 1 - cryoglobinaemia, hepatitis C. Tram track appearance of immune deposits
Type 2 - Partial lipodystrophy, factor H deficiency. Results in persistant activation of complement pathway so low levels of c3.
Type 3 - Hepatitis B and C
What is cryoglobinaemia?
Abnormal blood proteins call cryoglobulins clump together in cold temperature causing reduced blood flow. Presents with purpura, arthralgia and weakness
