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Glomerulonephritis (Nephritic Syndrome (syndrome (haematuria (microscopic…

- - - - microscopic or macroscopic
      - red cell casts
      - podocytes develop large pores
    - - small
      - not always
    - - <300ml day
      - due to reduced renal function
  - - - weeks post streptococcus pyogenes
        
        URTI/sore throat
        
        skin infection
        
        afinity of bacterial antigen for the glomerular basement mebrane
        
        complement fixation
        
        hypocomplementaemia
        
        glomerular inflammation
        
        proliferation of mesangial and endothelial cells
        
        infiltrates with polymorphonuclear leukocytes
        
        on electron microscopy
        
        subepithelial hump-shaped immune deposits
      - supportive management
    - - day or two post URTI
      - biopsy
        
        expansion of the mesangium, both cells and matrix
        
        mesangial deposition of IgA
        
        typically in paramesangial areas immediately adjacent to a capillary loop
      - unkown cause
      - pts notice heamaturia with an URTI
      - increased serum IgA in 50% of cases
      - management is purely blood pressure control
        
        ACE inhibitor
        
        angiotensin 2 receptor blocker
        
        lifesyle
    - - goodpastures
        
        aka anti-glomerular basement membrane disease
        
        rare
        
        very bad
        
        pathophysiology
        
        severe necrotising glomeruloneophritis with cresent formation
        
        associated with alveolar damage in pre-existing lung disease
        
        autoantibodies against non-collagenous domain of the alpha-3 chain of type 4 collagen in the GBM
        
        investigations
        
        measure circulating anti-GBM antibodies
        
        renal biopsy
        
        a necrotising cresenteric glomerulonephritis
        
        immunohistological detection of linearly deposited antibody
        
        treatement
        
        immunosupression
        
        plasma exchange
      - vasculitic disorder
        
        Henoch-Schönlein purpura
        
        ANCA associated
        
        rare
        
        older patients
        
        focal necrotising GN with cresents
        
        macroscopic polyarteritis nodosa
    - - AKA mesangiocapillary GN
      - biopsy
        
        peripheral extension of mesagial matrix and cells
        
        thickening of capillary loops
        
        double contouring of basement mebrane
      - C3 deposition
- - - - hypoalbuminaemia <30g/L
      - oedema
        
        periorbital in kids
        
        primarily in feet and ankles
      - proteinuria >3g/24hr
        
        frothy urine
    - - cardiac failure
        
        oedema
        
        proteinuria
      - liver disease
        
        hypoalbuminaemia
    - - infection risk
        
        loss of immunoglobulin in urine
      - thromboembolism
        
        increase in clotting factors
        
        platelet abdnormalities
      - hyperlipideamia
        
        liver counteracting reduced oncotic pressure
        
        up to 5/6 x the normal limit
      - may have reduced eGFR
      - leukonychia
    - - urinalysis
        
        done for all patients with sudden onset oedema
      - hx to look for secondary causes
      - GFR measurement
      - serum albumin conc
      - albumin ratios
        
        ACR
        
        PCR
      - biopsy
        
        needed in adults to decide cause
        
        not in children - minimal change assumed
    - - oedema
        
        restrict salt intake
        
        increase sodium excretion
        
        loop diuretics
        
        if intractable
        
        add a thiazide
      - hypertension and proteinuria
        
        ACE inhibitor or angiotensin 2 receptor blocker
      - TREAT CAUSE
      - anticoagulation
        
        if serum albumin <20g/L
        
        not in minimal change
      - hyperlipideamia
        
        statin
  - - - Focal segmental glomerulosclerosis
        
        facts
        
        unknown pathogenesis
        
        likely to progress to end stage renal failure
        
        20%
        
        trial immunosupression
        
        underlying conditions
        
        genetics
        
        hyperfiltration
        
        obeisity
        
        HIV
        
        biopsy
        
        focal lesions affect deep juxtamedullary glomeruli first
        
        only a portion of some glomeruli affected
        
        sclerosis, mesangial expansion, capillary loop collapse
      - minimal change disease
        
        facts
        
        main cause in kids
        
        20-30% in adults
        
        likely to reoccur
        
        normal GFR except in prerenal AKI from hypovoleamia
        
        unknown pathogenesis
        
        treatement
        
        corticosteroids
        
        in relapse ciclosporin or tacrolimus
        
        excellent prognosis
        
        biopsy
        
        normal on light microscopy and immunohistochemisty
        
        fusion of podocyte foot processes on electron microscopy
      - membranous nephropathy
        
        facts
        
        ? autoantibodies to phospholipase A2 receptor
        
        1/3rd progress to end stage renal failure
        
        white adults
        
        30%
        
        immunosupression
        
        if deteriorating renal function
        
        ponticelli regimen
        
        may be due to underlying malignancy
        
        50yrs old
        
        lung, colon
        
        light microscopy of biopsy see thickening of glomerular basement membrane
        
        deposition of IgG-containing immune complexes
        
        deposition seen on outser side of membrane and subepithelial lying below the podocyte foot process
    - - SLE
      - Hep B and C
      - HIV
      - diabetes
      - malignancy