13-TMA & VIRAL NEPHRIDITES

• Thrombotic micro-angiopathic anemia (TMA)


  Syndromes with multiple etiologies that have a characteristic microvascular pathology causing microangiopathic hemolytic anemia (MAHA) and thrombocytopenia
• Types of TMA


  • Primary TMA
  • Secondary TMA
• Primary TMA


  • Atypical HUS
  • TTP
• Secondary TMA


  • Shiga toxin HUS (typical HUS)
  • Autoimmune dis: SLE, scleroderma
  • Malignant hypertension
  • Preeclampsia/ HELLP syndrome
  • Systemic infection
  • Malignancy
  • Hemopoietic stem cell transplant
  • Drugs
• Clinical features of TMA


  • Thrombocytopenia: (consumptive: ↑D-dimer > 2 (NR<0.5))
  • Hemolytic anemia: peripheral schistocytes, ↑LDH, ↓ haptoglobin)
  • Target organ damage: renal, CNS, cardiac
  • Blood film: schistocytes (helmet cells) due to fragmentation of RBCs
• Management of TMA


  1. Plasma exchange: 14 – 21 sessions (4-liter exchange /session)

  2. Immunosuppression: steroids
• Viruses that may cause nephritides


  • HIV
  • Hepatitis C
  • Hepatitis B
  • BK virus (polymyoma)
  • CMV
  • EBV
  • Varicella – Zoster
  • Adenovirus
  • Coxachie B
  • Mumps
  • Rubella
  • ECHO virus
  • Influenza
• Types of renal injury caused by viruses


  • Glomerulonephritis
  • Vasculopathy (vasculitis)
  • Tubulointerstitial disease (interstitial nephritis)
• Hepatitis B Virus


  • Membranous GN (long-term exposure 5 to 10 years)
  • HbeAg +ve (infective, non-immune, persistent antigenemia à renal involvement)
  • Low C3 C4
• Hepatitis C Virus


  • Membranoproliferative GN
  • Cryoglobulinemia
• Treatment for Hepatitis B


  1. Hepatitis B drugs (lamivudine / tenofovir) à not as effective

  2. Best way to prevent is by vaccination
• Treatment for Hepatitis C


  1. Interferon (old treatment)

  2. Newer hep C drugs are very effective, clear the virus in 95-97% of cases

  3. Plasmapheresis if cryoglobulinemia
• HIV Nephropathy


  • Collapsing focal segmental GS
  • Kidneys are echogenic and large (due to dilation of tubules à cysts)
  • Almost exclusively in African Americans with profound proteinuria
  • African Americans have a gene called apolipoprotein I which it protects them from Trypanosoma pallidum (sleeping sickness) but makes them susceptible to renal involvement
  • Respond to treatment with HAART and ACEI, corticosteroids (controversial), dialysis
• BKV (polyoma virus)


  • Doesn't affect normal individuals but commonly affects immunocompromised
  • Home of the virus is the kidney, normally secreted in the urine with no problem
  • Problems start with renal transplant and intensive immunosuppression à virus reactivatedà affects the kidney tubules and glomerulus à acute kidney injury
  • Impaired renal function ± constitutional symptoms
  • Creatinine suddenly increases 6 months to1 year after transplant, but no rejection
  • Renal biopsy: viral tubular lesion but no evidence of rejection (polyoma viral inclusions in renal tubular cells)
  • Clue cells with viral inclusions are shed into urine
  • Diagnosis: BKV PCR
  • Treatment: decrease the immunosuppression