Nephritic syndrome, GN & vasculitis flashcards
20 high-yield MRCP Part 1 cards from the Intellect Medicos Nephrology course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.
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What urine finding distinguishes nephritic syndrome from nephrotic syndrome?
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Haematuria with red cell casts (dysmorphic red cells).
Why? Nephritic syndrome also features hypertension, oliguria, oedema and mild–moderate proteinuria (<3 g/day), from glomerular inflammation.
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How long after a streptococcal sore throat does post-streptococcal glomerulonephritis typically develop?
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1–3 weeks (3–6 weeks after impetigo).
Why? The latent period reflects immune complex formation. IgA nephropathy, by contrast, occurs within 1–2 days of an URTI.
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What is the complement pattern in post-streptococcal glomerulonephritis?
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Low C3 with normal C4.
Why? Immune complexes activate the alternative pathway. C3 usually returns to normal within about 8 weeks.
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What is the electron microscopy finding in post-streptococcal glomerulonephritis?
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Subepithelial 'humps' (lumpy immune complex deposits).
Why? Light microscopy shows diffuse endocapillary proliferative GN; immunofluorescence shows granular IgG and C3 ('starry sky').
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A 22-year-old man has visible haematuria starting 2 days after a sore throat. He had a similar episode last year. BP and complement are normal. What would renal biopsy immunofluorescence show?
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Mesangial IgA deposits (± C3).
Why? This is IgA nephropathy (Berger disease), the commonest primary GN worldwide. Episodes of frank haematuria occur within days of mucosal infection.
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Name two conditions associated with secondary IgA nephropathy.
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Coeliac disease, alcoholic liver disease and IgA vasculitis (HSP) — any two.
Why? These all involve abnormal IgA production or reduced hepatic clearance of IgA complexes.
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What is the first-line management of IgA nephropathy with proteinuria?
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Supportive care — ACE inhibitor or ARB at the maximum tolerated dose, with tight BP control.
Why? Reducing proteinuria slows progression. KDIGO 2025 aims for proteinuria below 0.5 g/day (ideally below 0.3) and BP ≤120/70. If proteinuria stays at 1 g/day or more, NICE allows targeted-release budesonide (TA1128) or sparsentan, a dual endothelin–angiotensin receptor antagonist that replaces the ACEi/ARB (TA1074); an SGLT2 inhibitor may also be added.
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Name the four classic features of IgA vasculitis (Henoch–Schönlein purpura).
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Palpable purpura (buttocks and legs), arthralgia, abdominal pain and nephritis.
Why? It is a small-vessel vasculitis with IgA immune complex deposition, mainly in children, often after an URTI. Treatment is usually supportive.
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In anti-GBM disease (Goodpasture's), what is the target antigen and the immunofluorescence pattern?
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The α3 chain of type IV collagen; linear IgG along the GBM.
Why? The same antigen is in alveolar basement membrane, so pulmonary haemorrhage (haemoptysis) accompanies rapidly progressive GN.
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What is the treatment of anti-GBM disease?
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Plasma exchange plus high-dose corticosteroids plus cyclophosphamide.
Why? Plasma exchange removes circulating anti-GBM antibody while immunosuppression stops further production.
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Type I membranoproliferative GN is classically associated with which infection, and what is its light microscopy appearance?
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Hepatitis C (with cryoglobulinaemia); 'tram-track' double-contoured GBM.
Why? Subendothelial immune complex deposits trigger mesangial interposition, splitting the GBM. Complement (C3 and C4) is low.
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Dense deposit disease (old type II MPGN) is associated with which autoantibody?
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C3 nephritic factor (stabilises C3 convertase of the alternative pathway).
Why? This causes persistent alternative-pathway activation: low C3, normal C4, C3-dominant deposits. It now falls under C3 glomerulopathy.
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Name three glomerular diseases that cause a LOW serum complement.
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Post-infectious GN, lupus nephritis, MPGN (including cryoglobulinaemia and endocarditis-associated GN).
Why? IgA nephropathy, anti-GBM disease and ANCA vasculitis usually have normal complement — useful in exam stems.
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The most common and severe class of lupus nephritis is class ______, whereas class V (membranous) typically presents with nephrotic syndrome.
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IV (diffuse proliferative)
Why? Class IV shows wire-loop lesions (subendothelial deposits) and 'full house' immunofluorescence (IgG, IgA, IgM, C3, C1q).
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The most common and severe class of lupus nephritis is class IV (diffuse proliferative), whereas class ______ typically presents with nephrotic syndrome.
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V (membranous)
Why? Class IV shows wire-loop lesions (subendothelial deposits) and 'full house' immunofluorescence (IgG, IgA, IgM, C3, C1q).
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What is the induction therapy for class III/IV lupus nephritis?
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Mycophenolate mofetil or IV cyclophosphamide, plus corticosteroids.
Why? KDIGO 2024 also allows belimumab added to MMF or cyclophosphamide, or MMF plus a calcineurin inhibitor (NICE TA882: voclosporin with MMF for active class III–V). Maintenance is with MMF or azathioprine. Everyone gets hydroxychloroquine unless contraindicated, plus ACEi/ARB for proteinuria.
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Granulomatosis with polyangiitis is associated with ______, whereas microscopic polyangiitis is associated with p-ANCA (anti-MPO).
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c-ANCA (anti-PR3)
Why? GPA has granulomas with sinus, lung (cavitating nodules) and kidney disease. MPA has no granulomas. EGPA (asthma + eosinophilia) is MPO-ANCA positive in a minority.
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Granulomatosis with polyangiitis is associated with c-ANCA (anti-PR3), whereas microscopic polyangiitis is associated with ______.
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p-ANCA (anti-MPO)
Why? GPA has granulomas with sinus, lung (cavitating nodules) and kidney disease. MPA has no granulomas. EGPA (asthma + eosinophilia) is MPO-ANCA positive in a minority.
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What is the induction treatment for ANCA-associated vasculitis with renal involvement?
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Glucocorticoids plus either rituximab or cyclophosphamide.
Why? Reduced-dose glucocorticoid regimens work as well as traditional high doses with less toxicity. Consider plasma exchange if creatinine is above 300 µmol/L, on dialysis or rising fast, or with alveolar haemorrhage and hypoxaemia. Maintenance is rituximab (preferred in relapsing or PR3 disease and frail older adults) or azathioprine, for 18 months to 4 years.
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What is the most common cause of rapidly progressive glomerulonephritis in adults?
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Pauci-immune (ANCA-associated) GN — type III RPGN.
Why? Biopsy shows crescents in Bowman's space with little or no immune deposit on immunofluorescence.
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- RTA & inherited tubular disorders
- Cystic, inherited & renal tumours
- Renal stones
- UTI, prostatitis & incontinence
- Prostate, testis & haematuria
- Sodium, potassium & calcium