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|Acute Kidney Injury (AKI) / Acute Renal Failure
|Renal/Kidney Physiology
|Chronic Kidney Disease (CKD)
|Anaemia in Chronic Kidney Disease
|Analgesic Nephropathy
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|IgA Nephropathy (Berger's disease)
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⚡ Rapid diagnosis, especially in rapidly progressive GN, is crucial.
🧪 Measuring ANCA and Anti-GBM antibodies allows early detection and improves outcomes.
About 📖
- Glomerulonephritis (GN): Inflammation of the glomerulus due to immune-mediated injury.
- Involves changes to the basement membrane, mesangium, or capillary endothelium.
- Mechanisms: antibody-mediated, complement activation, or cell-mediated injury.
Classifications 🧩
- Clinical: Nephritic ⚠️ vs. Nephrotic 💧 syndrome.
- Treatment Response: Steroid-responsive vs. Non-responsive.
- Aetiology: e.g., Post-streptococcal GN.
- Histology: Focal, diffuse, segmental, or with basement membrane changes/sclerosis.
Primary GN 🔬
- Minimal Change Disease (MCD)
- Focal Segmental Glomerulosclerosis (FSGS)
- Membranous Nephropathy
- IgA Nephropathy (Berger’s disease)
- Rapidly Progressive GN (Anti-GBM, pauci-immune GN)
- Post-Streptococcal GN
- Membranoproliferative GN (MPGN)
Secondary GN 🌍
- Lupus Nephritis (SLE-associated)
Clinical Features 🚨
- Acute haematuria (tea-coloured urine), proteinuria, red cell casts.
- Hypertension + oedema.
- Impaired renal function (AKI features).
- ⚠️ Severe hypertension with headache / neuro signs = poor prognostic marker.
Investigations 🔍
- FBC: Anaemia.
- Urinalysis: Haematuria, proteinuria, RBC casts.
- U&E: Check creatinine, urea, K⁺, calcium.
- ESR/CRP: Raised in inflammation.
- Blood gases: Look for metabolic acidosis.
- Immunology: ANA, ENA, ANCA, Anti-GBM, cryoglobulins, complement (C3/C4), ASOT.
- SPEP: For plasma cell disorders.
- 24-hr proteinuria: Quantify protein loss.
- USS + Biopsy: Assess kidney size, histology confirms diagnosis.
Complement Levels 🧬
- Low: Cryoglobulinaemia, SLE, endocarditis, shunt nephritis, MPGN, post-strep GN.
- Normal: Polyarteritis nodosa, Goodpasture’s, IgA nephropathy, HSP, idiopathic RPGN.
Management 🛠️
- 🏥 Admit if: anuria, nephrotic syndrome, massive proteinuria, severe hypertension, pulmonary features.
- 💧 Fluid restriction if overloaded.
- 💊 Loop diuretics for oedema / proteinuria.
- ⚡ Severe hypertension + neuro signs → urgent therapy (CCBs, IV nitroprusside).
Indications for Steroids 💊
- Vasculitis: Steroids = mainstay.
- SLE: High-dose steroids.
- HSP: May help renal involvement.
- Granulomatosis with Polyangiitis: Steroids + cyclophosphamide.
- Idiopathic RPGN: IV methylprednisolone pulses.
- Goodpasture’s: Steroids + cyclophosphamide + plasmapheresis (esp. pulmonary haemorrhage).
Exam Pearl ✨
🔑 Complement levels guide diagnosis:
- Low C3 = post-strep GN, MPGN, SLE.
- Normal C3 = IgA nephropathy, Goodpasture’s.
👉 Always ask for a renal biopsy if diagnosis uncertain or rapidly progressive GN suspected.
Cases — Glomerulonephritis
- Case 1 — Post-infectious GN 🦠: A 9-year-old boy presents with cola-coloured urine, periorbital oedema, and hypertension 2 weeks after a sore throat. Urine: proteinuria and red cell casts. Bloods: low C3 complement, raised ASO titre. Diagnosis: post-streptococcal glomerulonephritis. Managed with supportive care and BP control.
- Case 2 — IgA nephropathy (Berger’s disease) 🩸: A 22-year-old man develops visible haematuria 24 hours after an upper respiratory infection. Exam: mild ankle oedema. Urine: haematuria, proteinuria. Renal biopsy: mesangial IgA deposition. Diagnosis: IgA nephropathy. Managed with ACE inhibitor for proteinuria and nephrology follow-up.
- Case 3 — Rapidly progressive GN (crescentic) ⚡: A 35-year-old woman presents with oedema, hypertension, and oliguria progressing over days. Urine: haematuria, proteinuria. Bloods: creatinine rapidly rising. Biopsy: crescentic GN. Serology: ANCA positive. Diagnosis: RPGN secondary to ANCA-associated vasculitis. Managed with high-dose corticosteroids, cyclophosphamide, and plasma exchange if severe.
Teaching Point 🩺: Glomerulonephritis is a spectrum ranging from post-infectious nephritic syndromes to immune-mediated diseases like IgA nephropathy and rapidly progressive crescentic GN. Key features: haematuria, proteinuria, oedema, and hypertension. Biopsy is often needed for definitive diagnosis and guiding therapy.