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Glomerular injury results in what 3 basic functional changes (occuring singly or in combination)
  • Proteinuria
  • Hematuria
  • ↓GFR (Glomerular filtration rate)
Name 5 major groups of mechanisms of glomerular injury
  • Immune mechanisms
  • Hemodynamic changes
  • Podocyte injury
  • Polyanion loss
  • Metabolic
Define terminology:
  • Diffuse
  • Focal
  • Global
  • Segmental
  • Primary
  • Secondary 
  • Diffuse: All glomeruli
  • Focal: Only some glomeruli
  • Global: Entire tuft involved
  • Segmental: Only part of tuft involved
  • Primary: Kidney only or predominantly
  • Secondary: Kidney disease part of a systemic illness, or is a consequence of disease elsewhere in the body or non-glomerular renal disease
Differentiating between Nephrotic and Nephritic syndrome, name the 4 features of Nephrotic Syndrome
Nephrotic Syndrome
  • Proteinuria >3.5 g/day
  • Hypoalbuminemia
  • Edema
  • High serum cholesterol 
Differentiating between Nephrotic and Nephritic syndrome, name the 8 features of Nephritic Syndrome
Nephritic Syndrome
  • Sudden onset
  • Hypertension
  • Edema
  • ↓ urine output
  • ↑ serum creatinine
  • Proteinuria
  • Hematuria (w/ RBC casts)
  • Low serum C3
For Acute Postinfectious Glomerulonephritis, what group does it occur in most?
All ages, but mostly children
For Acute Postinfectious Glomerulonephritis, what infectious agent is the most common organism?
Group A Streptococcus (GAS)
For Acute Postinfectious Glomerulonephritis, what is the Pathogenesis?
Infection causes formation of immune complexes which deposit in glomeruli → activate complement → release chemotactic factor C5a → PMN and Monocyte infiltration → glomerular damage
For Acute Postinfectious Glomerulonephritis, what are 2 pathological findings?
  • Hypercellular glomeruli with many PMNs and monocytes

  • Immune complex deposits in glomeruli detected by direct immunofluorescence (IF) and electron microscopy (EM). Immune deposits have hump-like appearance.
For Acute Postinfectious Glomerulonephritis, what is the clinical course?
  • Acute nephritic syndrome develops 1-3 weeks after GAS infection

  • Signs/symptoms disappear after 1-2 weeks

  • Most patients recover, but chronic renal disease may result
For Acute Postinfectious Glomerulonephritis, describe the lab findings (5)
  • ↓ serum C3
  • ↑ creatinine
  • RBCs/Casts in urine
  • Variable proteinuria
  • Edema/HTN
     
  • anti-streptolysin O titre raised
For Acute Postinfectious Glomerulonephritis, explain the lab findings
  • Hematuria → due to breaks in GBM
     
  • GFR  →  reduced due to mechanical obstruction of capillaries by leukocytes
     
  • Edema/hypertension → due to salt/fluid retention, due to reduced GFR and RAAS activation
For Rapidly Progressive Glomerulonephritis, what is another name? Define this disease.
  • Crescentic glomerulonephritis
     
  • Inflammatory glomerular disease characterized by the presence of crescents in >50% of the glomeruli.
For Rapidly Progressive Glomerulonephritis, what is the incidence and etiology?
  • Uncommon
  • Adults affected more than kids
  • Unknown etiology 
For Rapidly Progressive Glomerulonephritis, what is the pathogenesis?
Variable
  • Anti-GBM antibodies
  • Immune complexes 
Crescents
  • Result due to severe injury to glomerular tuft resulting in breaks in the GBM, efflux of plasma, fibrin and monocytes in the urinary space
  • Parietal epithelial cells proliferate forming a crescent
Describe 5 Pathological findings of Rapidly Progressive Glomerulonephritis?
1. Crescents in >50% of glomeruli

2. Crescents can be cellular, fibrous or fibrocellular

3. Fibron often demonstrable

4. Endocapillary hypercellularity visible

5. Severe damage to glomerular tuft
What is the course of disease for Rapidly Progressive Glomerulonephritis?
  • Onset is insidious
     
  • Rapid progression from normal to oliguric renal failure
     
  • Prognosis is variable and depends on how many cells are crescented
What are the lab results (~4) for Rapidly Progressive Glomerulonephritis?
  • Non-specific
  • ↑ creatinine
  • Proteinuria
  • Hematuria
  • Serum C3 variable
Characterize Benign Nephrosclerosis in 1 sentence. What is the pathogenesis?
  • Very common condition frequently associated with hypertension and atherosclerosis.

  • Pathogenesis is ischemia resulting from arteriolar hyalinosis (ie. deposition of acellular protein materials in wall of artery)
Describe 3 pathology features of Benign Nephrosclerosis
  • Variable number of obsolete glomeruli
  • Non-obsolete glomeruli are normal
  • Focal tubular atrophy & interstitial fibrosis
What is the clinical course of benign nephrosclerosis?
Slowly progressive renal dysfunction with or without mild proteinuria
What are possible lab findings for benign nephrosclerosis (2)
  • ↑ serum creatinine
  • Mild proteinuria
For Focal Glomerulosclerosis, describe the incidence, etiology and pathogenesis.
  • Incidence: Relatively uncommon
     
  • Etiology: Unknown
     
  • Pathogenesis: Podocyte injury
For Focal Glomerulosclerosis, describe the pathogenesis in more detail (6)
  • Some, but not all glomeruli show segmental capillary loop sclerosis, increased mesangial matrix, hyaline deposition and adhesions to Bowman's capsule

  • Other glomeruli are normal
     
  • Glomeruli enlarged
     
  • No immune deposits
     
  • FOAM cells commonly seen
     
  • Focal tube atrophy
For Focal Glomerulosclerosis, describe the presentation
  • Some patients present with Nephrotic Syndrome

  • Others just show proteinuria

  • Progression can be quick (a few years) or long (20 years)
     
  • Some people respond to steroids 
For Focal Glomerulosclerosis, describe the lab results
  • Normal: Serum C3, Cr
     
  • Or, hallmarks of Nephrotic Syndrome (hypoalbuminemia, hyperlipidemia, proteinuria, hematuria)
For Minimal Change Disease, describe the incidence, etiology and pathogenesis.
  • Most common cause of Nephrotic Syndrome in kids. Uncommon in adults
  • Unknown etiology
  • Unknown pathogenesis (possibly T-cell disorder?)
Describe pathological features in Minimal Change Disease
  • Glomeruli appear normal histologically
     
  • Widespread effacement of foot processes on EM
     
  • No immune complexes
What are labs results in Minimal Change Disease?
  • Normal renal function
  • Marked proteinuria
  • Hypoalbuminemia
  • Hyperlipidemia
  • Normal: Serum C3
For Diabetic Glomerulonephritis, describe the incidence and etiology
  • Incidence: Relatively common (as many as half of diabetics on autopsy).
  • 5% of diabetics die of renal failure.
  • Renal disease occurs with duration of disease (rare in kids)
  • Etiology: unknown
Describe the pathogenesis of Diabetic Glomerulosclerosis
Glomerular and vascular changes (related to hyperglycemia)
Describe the pathological features (4) of Diabetic Glomerulonephritis
  • Mesangial expansion and thickening of glomerular basement membranes (diffuse glomerulosclerosis)
     
  • Mesangial nodules (in long-standing disease)

  • Extensive hyalinization of arterioles 
What is the clinical course (2) of Diabetic Glomerulosclerosis?
  • Present with mild proteinuria
  • When protein >3gm/day, the deterioration accelerates and renal failure ensues within 5 years
What are the lab results for Diabetic Glomerulosclerosis?
Non-specific
Summarize Acute Postinfectious Glomerulonephritis
  • Relatively common

  • Occurs following infection. Most common agent is Group A Strep (GAS)

  • Immune complexes deposit on glomeruli activating complement and recruiting PMNs and Monocytes

  • Hypercellular glomeruli and immune complexes can be observed

  • Acute Nephritic syndrome develops 1-3 weeks after infection, resolving 1-2 weeks later

  • Lab results show:

    ↓C3
    ↑creatinine
    RBC casts in urine
    Variable proteinuria
     
  • Hematuria (due to breaks in GBM)

    GFR reduced (due to mechanical obstruction of capillaries by WBCs)

    Edema and hypertension (due to salt/fluid retention) due to RAAS activation 
Summarize Rapidly Progressive Glomerulonephritis
  • Also known as Crescentic Glomerulonephritis

  • >50% of glomeruli have crescents

  • Relatively uncommon, affects adults

  • Can be due to immune complexes or anti-GBM antibodies

  • Most cases immunological mechanisms not known

  • Crescents result from severe damage to glomerular tuft, resulting in breaks in GBM and efflux of plasma, fibrin, monocytes into urinary space. Results in proliferation of parietal epithelial cells

  • Crescents (fibrous, cellular, both) result in >50% of glomeruli; fibrin can be demonstrated; endocapillary hypercellularity visible; sever damage to tuft visible

  • Onset insidious

  • Progression from normal function to failure is rapid (weeks to months)

  • Prognosis variable, bad if large number (>80%) glomeruli have crescents

  • Lab results:

    ↑ creatinine
    Proteinuria
    Hematuria
    Serum C3 (variable) 
Summarize Benign Nephrosclerosis
  • Common condition frequently associated with hypertension and atherosclerosis

  • Ischemia results from arteriolar hyalinosis

  • Variable number of obsolete glomeruli showing ischemic change; non-obsolete glomeruli are normal; focal tubular atrophy and interstitial fibrosis

  • Progressive renal dysfunction (with/without proteinuria)

  • Lab results:

    ↑ creatinine (sometimes)
    proteinuria (sometimes) 
Summarize Focal Glomerulosclerosis
  • Relatively uncommon

  • Unknown etiology

  • Podocyte injury

  • Glomeruli show segmental capillary loop sclerosis; increased mesangial matrix; hyaline deposition; adhesions to Bowman's capsule

  • Other glomeruli appear normal; no immune deposits; FOAM cells seen in affected segments; focal tubular atrophy

  • Presentation is variable; some patients have Nephrotic Syndrome, others just have proteinuria

  • Progression from 1-20 years, patients can respond to steroids

  • Lab results:

    C3 normal
    creatinine normal
    If NS, then symptoms of NS: hyperlipidemia, hypoalbuminemia, proteinuria, hematuria 
Summarize Minimal Change Disease
  • Most common cause of Nephrotic Syndrome in children

  • Etiology/pathogenesis unknown

  • Glomeruli appear normal histologically, however: widespread effacement of foot processes; no immune complexes

  • Lab results:

    Normal renal function
    Marked proteinuria
    Serum C3 normal
    Hypoalbuminemia
    Hyperlipidemia 
Summarize Diabetic Glomerulosclerosis
  • Relatively common

  • Present in 5-50% of patients on autopsy (5% of diabetics die of renal failure)

  • Rare in children with diabetes (renal disease due to long-term)

  • Etiology unknown

  • Glomerular and vascular changes appear to be related to hyperglycemia

  • Pathology involves: mesangial expansion and thickening of glomerular basement membranes; mesangial nodules in long-term disease; extensive hyalinization or arterioles

  • Patients present with mild proteinuria, which may remain static or worsen

  • If proteinuria >3gm/day, rapid deterioration ensues 
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