Infection Related Glomerulopathies
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Infection Related Glomerulopathies
- 1. Infection Related Glomerulopathy Introduction – Rapid Overview Mohammed Abdel Gawad Nephrology Specialist Alexandria – EGY drgawad@gmail.com Mansoura University – September 2014
- 3. At the beginning of the last century: Postulated that the disease resulted from antibodies that instead of having beneficial effects were pathogenic, an insight that constitutes a landmark that opened the field of immune-mediated renal disease.1 Clemens von Pirquet
- 5. • Post-streptococal GN • Endocarditis associated GN • Shunt nephritis
- 6. • Post-streptococal GN • Endocarditis associated GN • Shunt nephritis
- 7. Post-streptococcal Glomerulonephritis Nephritogenic strains of group A Streptococcus pyogenes Streptococcal impetigo of M types 47, 49, 55, and 57 Throat infections with streptococcus types 1, 2, 4, and 12 4–6 weeks 7–15 days Nephritis Poynard T, Yuen MF, Ratziu V et al. Viral hepatitis C. Lancet 2003; 362:2095–2100.
- 8. Post-streptococcal Glomerulonephritis Nephritogenic strains of group A Streptococcus pyogenes Streptococcal impetigo of M types 47, 49, 55, and 57 Throat infections with streptococcus types 1, 2, 4, and 12 4–6 weeks 7–15 days Nephritis Poynard T, Yuen MF, Ratziu V et al. Viral hepatitis C. Lancet 2003; 362:2095–2100.
- 9. Post-streptococcal Glomerulonephritis Pathogenesis Streptococcal Infection Streptococcal proteinase exotoxin B (SPEB) Development of circulating immune complexes Deposited subendothelial and mesangial locations Initiate an inflammation (local complement activation and the recruitment of neutrophils and monocytes macrophages) Cationic antigens or dissociation of immune complexes into the outer aspect of the glomerular basement membrane
- 10. Post-streptococcal Glomerulonephritis Pathogenesis Streptococcal Infection Streptococcal proteinase exotoxin B (SPEB) Nephritis-associated plasmin receptor (NAPLr) A local direct mechanism of glomerular inflammatory damage it is not co-localized with complement or immunoglobulin Development of circulating immune complexes
- 11. Post-streptococcal Glomerulonephritis Complement Activation Low C3 / Normal or slightly low C4 NAPLr C3Nef IgG antibodies in sera
- 12. Post-streptococcal Glomerulonephritis Pathology Diffuse endocapillary GN with proliferation of mesangial and endothelial cells
- 13. Post-streptococcal Glomerulonephritis Pathology Glomerular immune deposits of C3 (100% of the cases), IgG (62%), IgM (76%)
- 16. Post-streptococcal Glomerulonephritis Important Clinical Points If decreased C3 levels lasted for more than a month (suggests lupus or hypocomplementemic MPGN) Mild proteinuria (<500 mg/day) and microscopic hematuria may persist for up to 1 year
- 17. • Post-streptococal GN • Endocarditis associated GN • Shunt nephritis
- 18. Endocarditis-Associated Glomerulonephritis Pathogenesis Deposition of immune complexes containing bacterial antigens in glomeruli, a mechanism similar to that proposed for PSGN.
- 19. Endocarditis-Associated Glomerulonephritis Complement Activation Low C3 / low C4
- 20. Endocarditis-Associated Glomerulonephritis Pathology Less commonly: focal GN, MN, and MPGN type I may be found.
- 21. Endocarditis Renal Presentation (other than GN) Infective Endocarditis High Cr at presentation, which improves on antibiotics Proteinuria/Hematuria Low complement +ve RF and cryoglobulins GN Increased Cr over time with antibiotic use Acute interstitial nephritis Toxic ATN Acute unilateral flank pain / frank hematuria Renal emboli
- 23. • Post-streptococal GN • Endocarditis associated GN • Shunt nephritis
- 24. Shunt Nephritis Infected atrioventricular shunts; this may occur 2 months to many years after insertion - S. Epidermidis and S. aureus - Less frequently Propionibacterium acnes, diphtheroids, Pseudomonas, or Serratia. ventriculoperitoneal shunts are rarely complicated with GN.
- 25. Shunt Nephritis Complement Activation Low C3 / low C4
- 26. Shunt Nephritis Pathology IgM, IgG, and C3 deposits are present in the glomerular capillary and mesangium.
- 27. Shunt Nephritis Management prompt removal of the infected atrioventricular shunt, which is usually replaced by a ventriculoperitoneal shunt.
- 29. Viral Infection Related Glomerulopathy General Pathogenesis Pathogenetic mechanisms deposition of exogenous immune complexes in situ formation of immune complexes autoantibody formation directed to endogenous antigen modified by viral injury virus-induced release of proinflammatory cytokines, chemokines, adhesion molecules, and growth factors; and direct cytopathic effects of viral proteins
- 30. Hepatitis B Virus–Associated Renal Disease HBV & The Kidney Membranous Nephropathy MPGN Mesangial Proliferative GN Polyarteritis Nodosa
- 31. Hepatitis B Virus–Associated Renal Disease HBV & The Kidney Membranous Nephropathy • MN may occur in chronic HBV carriers Mesangial • Nephrotic Proliferative Polyarteritis MPGN • Often have impaired Glomerulonep renal function Nodosa • Clinically apparent liver hritis disease • C3 and C4 levels are decreased in 20% to 50% • Mesangial immune deposits may also be present
- 32. Hepatitis B Virus–Associated Renal Disease HBV & The Kidney Membranous Nephropathy MPGN • Type 1 MPGN • the most common glomerular Mesangial Proliferative Glomerulonep hritis Polyarteritis Nodosa lesion in adult HBV carriers • Cryoglobulinemia • Chronic liver disease (may be clinically asymptomatic) • Nephrotic or non nephrotic proteinuria, often associated with microhematuria
- 33. Hepatitis B Virus–Associated Renal Disease HBV & The Kidney Membranous Nephropathy MPGN Mesangial Proliferative GN Polyarteritis Nodosa • IgA Deposits • It is a consequence of chronic liver disease with impaired clearance of IgA circulating immune complexes
- 34. Hepatitis C Virus–Associated Renal Disease HCV & The Kidney MPGN with or without cryoglobu linemia MN fibrillary GN FSGS (especially in African Americans) TMA with anticardiolipin antibodies
- 35. Hepatitis C Virus–Associated Renal Disease HCV & The Kidney MPGN with or without cryoglobu linemia MN fibrillary GN FSGS (especially in African Americans) TMA with anticardiolipin antibodies
- 36. Hepatitis C Virus–Associated Renal Disease
- 37. Hepatitis C Virus–Associated Renal Disease Complement Activation Low C3 / low C4
- 38. MPGN Classification According to TYPE of deposits Algorithm source: Sanjeev Sethi et al. N Engl J Med 2012;366:1119-31.
- 39. MPGN Classification According to TYPE of deposits Algorithm source: Sanjeev Sethi et al. N Engl J Med 2012;366:1119-31. No C3 no Ig chronic phase of TMA
- 40. MPGN Classification According to TYPE of deposits Algorithm source: Sanjeev Sethi et al. N Engl J Med 2012;366:1119-31. No C3 no Ig chronic phase of TMA Always check the possibility of Infection
- 42. Always suspect infection whatever the type of the deposits
- 44. Suspect any organism as a cause of post infectious MPGN whenever there is an evidence of infection
- 46. Thank You Mohammed Abdel Gawad