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This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
The Bottom Line
- Nephritic syndrome = haematuria (macro or micro with red cell casts), hypertension, oliguria, oedema, and modest proteinuria (<3.5 g/day)
- Caused by glomerulonephritis (GN). Commonest in UK: IgA nephropathy (most common GN worldwide), post-infectious GN, ANCA-associated vasculitis
- Red cell casts on urine microscopy are PATHOGNOMONIC for glomerular disease
- Rapidly progressive GN (RPGN): crescent formation → rapid loss of renal function over days-weeks. Treat urgently with immunosuppression ± plasma exchange
- Key investigations: urine microscopy (red cell casts), immunology (ANCA, anti-GBM, ANA, complement, anti-streptolysin O), renal biopsy (definitive)
Overview
Nephritic syndrome results from glomerular inflammation (glomerulonephritis) that damages capillary walls, allowing red blood cells and protein to leak into urine. The key causes are classified by mechanism: IgA nephropathy (IgA deposition in mesangium — commonest GN worldwide), post-streptococcal/post-infectious GN (immune complex deposition after group A strep infection), ANCA-associated vasculitis (granulomatosis with polyangiitis [GPA], microscopic polyangiitis [MPA], eosinophilic GPA [EGPA]), anti-GBM disease (Goodpasture syndrome — anti-glomerular basement membrane antibodies, often with pulmonary haemorrhage), and lupus nephritis (SLE). Rapidly progressive glomerulonephritis (RPGN) is a clinical emergency characterised by crescent formation on biopsy and rapid deterioration in renal function over days to weeks.
Epidemiology
IgA nephropathy is the commonest primary glomerulonephritis worldwide, typically presenting in young males with visible haematuria during or immediately after an upper respiratory tract infection (synpharyngitic haematuria). Post-streptococcal GN typically affects children 1–3 weeks after a throat or skin infection. ANCA-associated vasculitis has a peak incidence at age 65–75 years. Anti-GBM disease is rare (~1 per million/year) but devastating. Overall, glomerulonephritis accounts for approximately 10–15% of end-stage renal disease.
Clinical Features
Symptoms
Visible (macroscopic) haematuria — "tea-coloured" or "cola-coloured" urine
Reduced urine output (oliguria)
Peripheral oedema (less severe than nephrotic syndrome)
Headache and visual disturbance (hypertension)
Malaise, myalgia, arthralgia (systemic vasculitis)
Haemoptysis (pulmonary-renal syndrome: anti-GBM disease or ANCA vasculitis)
Recent sore throat or skin infection (post-streptococcal GN — 1–3 weeks prior)
Signs
Hypertension (often moderate-severe, may be acute onset)
Peripheral oedema
Signs of fluid overload (raised JVP, pulmonary crackles)
Skin rash (vasculitis: palpable purpura; HSP in children; SLE: butterfly rash)
Nasal crusting, epistaxis, saddle-nose deformity (GPA — granulomatosis with polyangiitis)
Pulmonary haemorrhage signs (crackles, haemoptysis, dropping Hb)
Investigations
First-line
UrinalysisHaematuria (dipstick positive blood + protein). Microscopy: dysmorphic red blood cells and red cell casts (pathognomonic for glomerular bleeding)
U&Es and eGFRRising creatinine, falling eGFR — assess rate of decline (rapidly progressive = emergency)
FBC, CRP, albuminAnaemia (chronic disease or pulmonary haemorrhage), raised inflammatory markers, albumin may be low but usually >25 g/L
Second-line
Immunology panelANCA (p-ANCA/c-ANCA or MPO/PR3), anti-GBM antibodies, ANA + dsDNA + complement C3/C4 (lupus), anti-streptolysin O titre / anti-DNase B (post-streptococcal)
Serum complement levelsLow C3: post-infectious GN, MPGN, lupus nephritis, cryoglobulinaemia. Normal C3: IgA nephropathy, ANCA vasculitis, anti-GBM
Serum immunoglobulins and electrophoresisRaised IgA: IgA nephropathy. Paraprotein: myeloma-associated kidney disease
Specialist
Renal biopsyDefinitive investigation in most cases — determines histological diagnosis, activity/chronicity, and guides treatment (e.g. crescents in RPGN)
Chest X-ray / CT chestIf pulmonary-renal syndrome suspected — assess for pulmonary haemorrhage (bilateral infiltrates)
Management
KDIGO Glomerulonephritis Guidelines 20211
General measures
- Control hypertension: ACEi/ARB preferred (also reduce proteinuria)
- Fluid and salt restriction if oedematous/oliguric
- Monitor renal function closely — rapid deterioration requires emergency intervention
- Dialysis if severe AKI with refractory hyperkalaemia, acidosis, or fluid overload
2
Cause-specific treatment
- IgA nephropathy: ACEi/ARB for proteinuria reduction. Immunosuppression (corticosteroids) if persistent proteinuria >1 g/day despite ACEi/ARB
- Post-streptococcal GN: supportive (self-limiting in most cases). Treat streptococcal infection. Resolve usually within 2–4 weeks
- ANCA vasculitis: induction with cyclophosphamide or rituximab + high-dose steroids. Plasma exchange if severe/dialysis-dependent. Maintenance with rituximab or azathioprine for ≥2 years
- Anti-GBM disease (Goodpasture): plasma exchange (remove pathogenic antibodies) + cyclophosphamide + steroids. Poor prognosis if dialysis-dependent at presentation
- Lupus nephritis: steroids + mycophenolate mofetil (induction and maintenance) or cyclophosphamide (induction)
3
Rapidly progressive GN (RPGN)
- Clinical emergency — rapid creatinine rise over days to weeks
- Urgent renal biopsy to confirm crescentic GN
- Immediate high-dose IV methylprednisolone (500 mg–1 g daily for 3 days)
- Definitive immunosuppression based on cause (as above)
- Plasma exchange for anti-GBM disease and severe ANCA vasculitis
Complications
- Rapidly progressive GN: Without treatment, progresses to ESRD within weeks-months. Crescents on biopsy = poor prognosis
- Pulmonary haemorrhage: In anti-GBM disease (Goodpasture) and ANCA vasculitis — life-threatening
- Hypertensive emergency: Acute severe hypertension with end-organ damage
- CKD/ESRD: IgA nephropathy progresses to ESRD in ~25% over 20 years. ANCA vasculitis — relapse rate ~50%
- Immunosuppression complications: Infection, bone marrow suppression, secondary malignancy
UKMLA Exam Tips
- 1Red cell casts = glomerulonephritis (pathognomonic). White cell casts = pyelonephritis/interstitial nephritis. Granular "muddy brown" casts = ATN
- 2IgA nephropathy: haematuria DURING/immediately after URTI (synpharyngitic). Post-streptococcal: haematuria 1–3 WEEKS after infection (latent period)
- 3Low complement: post-infectious GN, lupus nephritis, MPGN, cryoglobulinaemia. Normal complement: IgA, ANCA, anti-GBM
- 4c-ANCA (PR3): granulomatosis with polyangiitis (GPA, formerly Wegener). p-ANCA (MPO): microscopic polyangiitis
- 5Goodpasture = anti-GBM disease + pulmonary haemorrhage. Often young male smoker with haemoptysis + rapidly declining renal function
- 6RPGN = crescents on biopsy → emergency. Three causes: anti-GBM (type I), immune complex (type II), pauci-immune/ANCA (type III)
practicetest your knowledge on nephritic syndromeApply what you've learnt with UKMLA-style questions from the iatroX Q-Bank — renal and beyond.
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