Makindo Medical Notes

Related Subjects: |Metabolic acidosis |Lactic acidosis |Acute Kidney Injury (AKI) / Acute Renal Failure |Renal/Kidney Physiology |Chronic Kidney Disease (CKD) |Anaemia in Chronic Kidney Disease |Analgesic Nephropathy |Medullary Sponge kidney |IgA Nephropathy (Berger's disease) |HIV associated nephropathy (HIVAN) |Balkan endemic nephropathy (BEN) |Autosomal Dominant Polycystic kidney disease

About 🧾

• Mesangiocapillary Glomerulonephritis (MCGN) — also called Membranoproliferative GN (MPGN).
• Important cause of nephrotic syndrome but often shows a mixed picture of nephrotic + nephritic features.
• Hallmark = proliferation of mesangial cells + thickening of the glomerular basement membrane (GBM).
• Can progress to chronic renal failure if untreated.

Aetiology 🔬

• Thickened GBM due to immune deposits.
• Mesangial cell proliferation ➝ lobular distortion of glomeruli.
• Immune complex–mediated in most cases, though some are driven by complement dysregulation.

Classification & Causes 📚

• Type I MCGN 🧫
  • Subendothelial immune deposits (Ig + complement).
  • Causes: Hepatitis B, Hepatitis C, cryoglobulinaemia, bacterial endocarditis, autoimmune disease, monoclonal gammopathy.
• Type II MCGN (Dense Deposit Disease) 💡
  • Intramembranous dense deposits seen on EM.
  • Driven by acquired or inherited complement system abnormalities.
  • Associations: partial lipodystrophy, complement deficiencies, SLE.
  • Autoantibodies against C3 convertase (C3bBb) ➝ persistent complement activation.

Clinical Features 🤒

• 💧 Nephrotic syndrome: oedema, frothy urine, heavy proteinuria.
• 🔴 Nephritic features: haematuria, hypertension.
• 🩺 Often insidious but may present as acute nephritic syndrome.
• 📉 Progressive renal impairment common ➝ can lead to CKD/ESRD.

Investigations 🔍

• Renal Biopsy:
  • Light microscopy ➝ mesangial proliferation, thickened capillary loops (“tram-track” appearance).
  • Immunofluorescence ➝ deposits of IgM, IgG, C3, or C1q.
  • Electron microscopy ➝ dense deposits in Type II.
• Complement: Persistently low C3 (esp. Type II).
• Serology: Test for Hep B, Hep C, autoimmune screen, cryoglobulins.
• Type II: Look for anti–C3 convertase antibodies.

Management 🩺

• 🎯 Treat underlying cause: antiviral therapy (Hep B/C), immunosuppression for autoimmune disease.
• 💊 Immunosuppressants: corticosteroids, mycophenolate, cyclophosphamide in some cases.
• 🧬 Eculizumab: (anti-C5) for complement-mediated disease (esp. dense deposit disease).
• ⚖️ Strict BP control (ACEi/ARB) to reduce proteinuria + protect kidneys.
• 🩸 Renal replacement therapy (dialysis/transplant) in ESRF.

Prognosis 📈

• Often progressive ➝ many develop CKD within 10–15 years.
• Type II has worse prognosis than Type I.
• Recurrence after transplant is well-recognised, esp. dense deposit disease.

✨ Exam Pearl: Think of MCGN when a patient has nephrotic + nephritic features together (proteinuria + haematuria + low C3). 📌 “Tram-track” appearance on light microscopy = classic buzzword.

Cases — Mesangiocapillary Glomerulonephritis (MCGN / MPGN)

• Case 1 — Post-infectious type I 🦠: A 19-year-old man presents with haematuria, oedema, and hypertension 3 weeks after a streptococcal throat infection. Bloods: low C3 complement, normal C4. Biopsy: mesangial proliferation with subendothelial immune deposits. Diagnosis: immune-complex mediated MCGN (type I). Managed with supportive care and blood pressure control.
• Case 2 — Hepatitis C–associated 🌐: A 42-year-old woman with chronic hepatitis C presents with proteinuria, haematuria, and ankle swelling. Exam: purpuric rash on legs, mild hepatosplenomegaly. Bloods: cryoglobulins present, low complement. Biopsy: MPGN pattern with immune-complex deposition. Diagnosis: secondary MCGN due to HCV infection. Managed with antiviral therapy and immunosuppression if progressive.
• Case 3 — Complement-mediated (Dense Deposit Disease) 🔬: A 12-year-old girl presents with haematuria and proteinuria. Exam: periorbital oedema, hypertension. Bloods: persistently low C3 with normal C4. Biopsy: ribbon-like dense deposits within GBM on EM. Diagnosis: complement-mediated MCGN (type II / Dense Deposit Disease). Managed with ACE inhibitor, immunosuppression in severe cases, and nephrology follow-up.

Teaching Point 🩺: Mesangiocapillary GN is a rare cause of nephritic/nephrotic syndrome overlap. Classified as immune complex–mediated (e.g. post-infectious, hepatitis C, autoimmune) or complement-mediated (e.g. dense deposit disease, C3 glomerulopathy). Often presents with haematuria, proteinuria, low complement, and progressive renal impairment.