Pathology of Kidney

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Pathology of Kidney

• Dr. Sachin Kale, MD.
• Associate Professor, Dept of Pathology.

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Anatomy of Kidney

• Note the positions of
• Glomerulus
• PCT, DCT, CT
• Cortex, Medulla, Pelvis.

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Glomerular diseases

• Primary
• Acute diffuse post streptococcal
• RPGN
• Membranous GN
• FSGS
• MPGN
• Lipoid nephrosis or minimal change
• IgA nephropathy
• Secondary
• SLE, Diabetes, Amyloidosis, Goodpastures
  syndrome, PAN, WG, HSP, Hypertension etc.

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Clinical Syndromes

• Nephritic syndrome.
• Oliguria, Haematuria, Proteinuria, Oedema,
  Azotemmia, Hypertension.
• Nephrotic syndrome.
• gt3.5 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

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CHRONIC RENAL FAILURE
Fluid and Electrolytes Dehydration, Edema,
Hyperkalemia, Metabolic acidosis 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
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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

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NORMAL
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ATN
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ATN PATHOGENESIS

• BLOOD FLOW DISTURBANCES (ISCHEMIC)
• TUBULAR INJURY (NEPHROTOXIC)

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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

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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

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Immune Glomerulonephritis

1. Antigen or Antibody - Immune reaction
2. Activation of complements, Neutrophils
3. destruction of glomerular structure
4. Inflammation, exudation ? swelling.
5. ? blood flow, GFR, -
6. Oliguria, Proteinuria, Hematuria, Hypertension.

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Neutrophil Activity

• Proteases GBM degradation
• Reactive oxygen metabolites cell damage
• Arachidonic acid metabolites Reduction in GFR

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Other Mediators

• Cytotoxic antibodies
• Macrophages
• Platelets
• Resident glomerular cells
• Fibrin related products

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Nephritic Syndromes

• Diffuse Proliferative GN
• Post Streptococcal.
• Rapidly Progressive GN (or Crescentic)
• Post Streptococcal, Goodpastures,
• Focal Glomerulonephritis
• Primary Bergers disease (IgA Nephritis)
• Secondary IgA nephritis, Henoch Schonlein
  purpura, SBE, Coeliac Disease etc.

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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.

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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

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• Normal

• Inflammation
• Proliferation
• Swelling.
• Narrow capillary
• ?GFR-Renin-BP

• Post Strepto GN

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Diffuse Proliferative GN

• Enlarged hypercellular glomeruli.
• Hyperplasia of epithelium endothelium. Cell
  Swelling.
• Inflammatory cells.
• Collapsed capillaries. Obstruction to blood flow.

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IF- Diffuse Proliferative GN
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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)

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Progression of DPGN
Rapidly Progressive GN

• Poststreptococcal DPGN

Complete Healing
Cardiac Failure or Uremia death in acute phase
CGN
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RPGN

• Clinicopathologic syndrome
• Glomerular damage
• Rapid progressive decline in renal function
• Histology accumulation of cells in Bowmans
  space in the form of Crescents

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RPGN Classification Pathogenesis

• Postinfectious
• GN associated with systemic diseases
• Idiopathic RPGN
• Glomerular injury is immunologically mediated.
• Goodpastures syndrome classic anti-GBM
  nephritis

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RPGN classification

• Post-infectious RPGN
• Systemic diseases
• SLE, Goodpastures, Vasculitis (PAN), Wegeners
  granulomatosus, HSP, Essential cryoglobulinemia
• Idiopathic RPGN

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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

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RPGN

• Formation of crescents
• Proliferation of parietal cells, migration of
  monocytes and macrophages into Bowmans space
• Crescents obliterate Bowmans space, compression
  capillary tuft
• Crescents undergo sclerosis

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RPGN Clinical features

• Goodpastures Syndrome recurrent hemoptasis
  renal manifestations
• Hematuria, Red cell casts, Moderate proteinuria,
• Variable HT and edema
• Oliguria

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Which of the following presents with hematuria,
proteinuria and hypertension

• Nephrotic syndrome
• Nephritic Syndrome
• UTI
• Renal Tubular Acidosis

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All of the following are seen in renal failure
except

• Hypercalcemia
• Hyperkalemia
• Bone lesions
• Metobolic Acidosis

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Anemia in renal failure is generally

• Microcytic hypochromic
• Normocytic normochromic
• Dimorphic
• megaloblastic

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Which of the following is not a primary GN

• Minimal Change disease
• Membranous GN
• Diabetes mellitus
• RPGN

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Which of the following is not part of nephrotic
syndrome

• Lipiduria
• Hypertension
• Proteinuria
• Edema

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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

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False about RPGN..

• Formation of crescents
• Small contracted kidneys
• Hematuria
• Oliguria

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Spot the diagnosis
RPGN
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Spot the diagnosis
ATN
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Spot the diagnosis
Post streptococcal GN
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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. 

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Thanks

• http//sachinkale1.tripod.com