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Pathology of Kidney

Pathology of Kidney. Dr. Sachin Kale, MD. Associate Professor, Dept of Pathology. Anatomy of Kidney. Note the positions of Glomerulus PCT, DCT, CT Cortex, Medulla, Pelvis. Glomerular diseases:. Primary Acute diffuse post streptococcal RPGN Membranous GN FSGS MPGN

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Pathology of Kidney

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  1. Pathology of Kidney Dr. Sachin Kale, MD. Associate Professor, Dept of Pathology.

  2. Anatomy of Kidney Note the positions of Glomerulus PCT, DCT, CT Cortex, Medulla, Pelvis.

  3. Glomerular diseases: • Primary • Acute diffuse post streptococcal • RPGN • Membranous GN • FSGS • MPGN • Lipoid nephrosis or minimal change • IgA nephropathy • Secondary • SLE, Diabetes, Amyloidosis, Goodpasture’s syndrome, PAN, WG, HSP, Hypertension etc.

  4. Clinical Syndromes: • Nephritic syndrome. • Oliguria, Haematuria, Proteinuria, Oedema, Azotemmia, Hypertension. • Nephrotic syndrome. • >3.5 gm proteinuria, Hypoalbuminemia hyperlipidemia, Lipiduria • RPGN. • Nephritis, loss of Kidney function - within weeks • Chronic renal failure. • Azotemia/uremia progressing over months and years • Asymptomatic Hematuria or proteinuria

  5. CHRONIC RENAL FAILURE Fluid and Electrolytes:Dehydration, Edema, Hyperkalemia, Metabolicacidosis Calcium Phosphate and Bone:Hyperphosphatemia, Hypocalcemia, Secondary hyperparathyroidism, Renal osteodystrophy Hematologic:Anemia, Bleeding diathesis Cardiopulmonary:Hypertension, Congestive heart failure, Pulmonary edema, Uremic pericarditis Gastrointestinal:Nausea and vomiting, Bleeding, Esophagitis, gastritis, colitis Neuromuscular:Myopathy, Peripheral neuropathy, Encephalopathy Dermatologic:Sallow (greenish-yellow) color, Pruritus, Dermatitis

  6. ACUTE TUBULAR NECROSIS • Destruction of renal TUBULAR epithelium • Loss of renal function • 50% of ACUTE renal failure • Two types: ISCHEMIC NEPHROTOXIC -AMINOGLYCOSIDES -AMPHOTERICIN B -CONTRAST AGENTS

  7. NORMAL

  8. ATN

  9. ATN PATHOGENESIS • BLOOD FLOW DISTURBANCES (ISCHEMIC) • TUBULAR INJURY (NEPHROTOXIC)

  10. CLINICAL COURSE • INITIATION (36 hours) • Mild OLIGURIA • Mild AZOTEMIA • MAINTENANCE • More OLIGURIA • More AZOTEMIA • DIALYSIS NEEDED • RECOVERY • HYPOKALEMIA main problem • BUN, CREATININE return to normal

  11. Immune Mechanisms of Glomerular injury: • Antibody mediated: • In-Situ immune complex deposition • Tissue antigens - Goodpasture anti GBM Ag • Planted antigens - infections, toxins, drugs. • Circulating immune complex deposition. • Endogenous - DNA as in SLE • Exogenous – infections – HBsAg, Syphilis, Streptococcal, Falciparum, • Cell mediated Immune injury • Activation of alternate complement pathway

  12. Immune Glomerulonephritis: • Antigen or Antibody - Immune reaction • Activation of complements, Neutrophils… • destruction of glomerular structure • Inflammation, exudation  swelling. • ↓ blood flow, GFR, - • Oliguria, Proteinuria, Hematuria, Hypertension.

  13. Neutrophil Activity • Proteases – GBM degradation • Reactive oxygen metabolites – cell damage • Arachidonic acid metabolites –Reduction in GFR

  14. Other Mediators • Cytotoxic antibodies • Macrophages • Platelets • Resident glomerular cells • Fibrin related products

  15. Nephritic Syndromes : • Diffuse Proliferative GN • Post Streptococcal. • Rapidly Progressive GN (or Crescentic) • Post Streptococcal, Goodpasture’s, • Focal Glomerulonephritis • Primary: Bergers disease (IgA Nephritis) • Secondary IgA nephritis, Henoch Schonlein purpura, SBE, Coeliac Disease etc.

  16. Diffuse Proliferative GN: • Post streptococcal* common – • Primary infection - Pharynx, skin, ear etc.. • Kidney damage – 1-4 weeks after infection. • Malaise, fever, nausea, edema*, ↑ASO, ↓C3 • Resolution in 6-8 weeks.

  17. Post Streptococcal GN (Prol.GN): • 1-4 weeks following streptococcal infection by nephritogenic strains (time for Ab formation) • Immune mediated • Granular deposits of IgG,IgM & C3 in GBM, (subepithelial location common) • Humps in GBM on EM or IF Microscopy

  18. Normal • Inflammation • Proliferation • Swelling. • Narrow capillary • ↓GFR-Renin-BP • Post Strepto GN

  19. Diffuse Proliferative GN: • Enlarged hypercellular glomeruli. • Hyperplasia of epithelium & endothelium. Cell Swelling. • Inflammatory cells. • Collapsed capillaries. Obstruction to blood flow.

  20. IF- Diffuse Proliferative GN

  21. Pathogenesis of Diffuse PGN: • Streptococcal infection – Antibody attack GBM - inflammation & proliferation. • Glomerular capillary obstruction: • J.G.A stimulation – Renin – high blood pressure • Reduced filtration – raised blood urea • Fluid retention – Oedema • Damage to GBM: • Unselective proteinuria (form Pr. casts in tubule) • Haematuria (form RBC casts in tubule)

  22. Progression of DPGN: Rapidly Progressive GN Poststreptococcal DPGN Complete Healing Cardiac Failure or Uremia; death in acute phase CGN

  23. RPGN • Clinicopathologic syndrome • Glomerular damage • Rapid progressive decline in renal function • Histology: accumulation of cells in Bowman’s space in the form of “Crescents”

  24. RPGN: Classification & Pathogenesis • Postinfectious • GN associated with systemic diseases • Idiopathic RPGN • Glomerular injury is immunologically mediated. • Goodpasture’s syndrome – classic anti-GBM nephritis

  25. RPGN classification • Post-infectious RPGN • Systemic diseases – • SLE, Goodpasture’s, Vasculitis (PAN), Wegener’s granulomatosus, HSP, Essential cryoglobulinemia • Idiopathic RPGN

  26. RPGN cont.. • Idiopathic : ½ the cases, • Linear, Granular or minimal to none immune deposits • Gross: Enlarged pale kidneys Large white kidney • Petechial hemorrhages in cortex • M/E: Glomeruli: focal necrosis, endothelial proliferation

  27. RPGN… • Formation of crescents: • Proliferation of parietal cells, migration of monocytes and macrophages into Bowman’s space • Crescents obliterate Bowman’s space, compression capillary tuft • Crescents undergo sclerosis

  28. RPGN: Clinical features • Goodpasture’s Syndrome: recurrent hemoptasis & renal manifestations • Hematuria, Red cell casts, Moderate proteinuria, • Variable HT and edema • Oliguria

  29. Which of the following presents with hematuria, proteinuria and hypertension • Nephrotic syndrome • Nephritic Syndrome • UTI • Renal Tubular Acidosis

  30. All of the following are seen in renal failure except • Hypercalcemia • Hyperkalemia • Bone lesions • Metobolic Acidosis

  31. Anemia in renal failure is generally • Microcytic hypochromic • Normocytic normochromic • Dimorphic • megaloblastic

  32. Which of the following is not a primary GN • Minimal Change disease • Membranous GN • Diabetes mellitus • RPGN

  33. Which of the following is not part of nephrotic syndrome • Lipiduria • Hypertension • Proteinuria • Edema

  34. True about Post-strepto GN - • Occurs 1 – 4 months after infection • Occurs 1 – 4 days after infection • Occurs 1 – 4 weeks after infection • Non of the above

  35. False about RPGN.. • Formation of crescents • Small contracted kidneys • Hematuria • Oliguria

  36. Spot the diagnosis RPGN

  37. Spot the diagnosis ATN

  38. Spot the diagnosis Post streptococcal GN

  39. Thought for the day… • Ours is a world where people don't know what they want and are willing to go through hell to get it. 

  40. Thanks… • http://sachinkale1.tripod.com

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