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Nephrotic syndrome
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Nephrotic syndrome

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    Nephrotic syndrome Nephrotic syndrome Presentation Transcript

    • By: Hamza AlGhamdi
    • NORMAL KIDNEY’S PHYSIOLOGY AND HISTOLOGY
    • Capillary Space Endothelium Urinary Space GBM Podocyte
    • NORMAL KIDNEY HISTOLOGY
    • Parietal Epithelium Visceral Epithelium Capillary Lumen Mesangial Cell Basement Membrane (GBM) Urinary Space RBC Endothelial Cell
    • NEPHROTIC SYNDROME IS NOT A DISEASE
      • Fluid retention -> abdominal distention , ascites , edema , puffy eyelids ,scrotal swelling , weight gain , shortness of breath
      • Anorexia
      • Hypertension
      • Oliguria
      • Orthostatic hypertension
      • Skin striae
      • Foamy urine
    • Periorbital edema Pitting edema of lower limbs
    • INVESTIGATIONS
      • Urine sample shows proteinuria (>3.5/day )
      • It is also examined for urinary casts
      • Comprehensive metabolic panel (CMP) shows Hypoalbuminemia
      • High levels of cholesterol (hypercholesterolemia), specifically elevated LDL
      • Electrolytes, urea and creatinine (EUCs): to evaluate renal function
      • Biopsy of kidney
      • Auto-immune markers
      • Excessive permeability of plasma proteins - >> heavy proteinuria
      • Depletion of plasma proteins , mainly albumin - hypoalbuminaemia
      • Liver compensates but not successful - >> reversed A:G ratio
      • Reduced albumin -> decreased colloid oncotic pressure of the blood -> oedema
      • ADH is stimulated - >> oedema
      • Increased Lipoprotein synthesis and decreased catabolism by liver ->> Hyperlipidaemia (mainly VLDL and /or LDL)
      • HDL is also lost in urine when heavy proteinuria occurs
      • Loss of body proteins (immunoglobulins /complement) -> frequent infection
      • Loss of anticoagulants antithrombin III , antiplasmin - > thrombotic and embolic phenomenon
    •  
    •  
      • Major cause of NS in adults
      • Characterised by presence of electron-dense immune deposits along the epithelial side of GBM (subepithelial )
      • Idiopathic in 85% of patients
      • The 15% remaining GN is associated with malignant tumors , SLE , drugs , infections or metabolic disorders
    •  
    • Membranous GN Sub-epithelial immune Complex deposits Thickened GBM
    • Membranous GN H&E
    • Membranous GN IF
    • Capillary Lumen GBM GBM Membranous GN EM
    • MINIMAL CHANGE DISEASE
      • the major cause of nephritic syndrome in Children
      • normal glomeruli on light Microscopy
      • uniform and diffuse effacement of the foot Processes of visceral epithelial cells on electron microscopy
      • Immunofluorescence shows no immune deposits
      • The cause and pathogenesis are unknown
      • dramatic response to corticosteroid therapy.
      • long-term prognosis is excellent.
    •  
    • MINIMAL CHANGE DISEASE Foot Process Fusion
    •  
    •  
      • sclerosis of some, but not all, glomeruli (thus, it is focal)
      • FSG can be.
      • * Idiopathic.
      • * A secondary evernt, refecting glomerular scarring, consequent to another primary glomerular disease (e.g., IgA nephropathy).
      • * associated to other known disorders (e.g. heroin abuse, HIV infection, obesity).
      • * The result of inherited mutations of proteins present in podocytes (podocin, a –actinin) or in the slit diaphragm between podocytes (nephrin).
      • 1- Light Microscopy:
      • Normal and diseased glomeruli (Focal)
      • Segmental tuft sclerosis in diseased glomeruli
      • 2- Immunofluorescence
      • No deposits
      • Deposits of IgM and C3
      • 3- EM:
      • Focal fusion of foot processes
      • Glomerular fibrosis
    • FSGS H&E
    • MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS
      • Thickness of capillary loops and glomerular cell proliferation
      • Glomeruli have a lobular appearance because of mesangial proliferation
      • Capillary walls often have a double-counter or tram-track appearance
    • MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS
      • Type 1 has subendothelial electron-dense deposits of immunoglobulins and complements
      • It occurs in patients with SLE , hepatitis B and other diseases
      • Type 2 has electron-dense GBM deposition in a confluent ribbon-like fashion
      • Type 2 is due to activation of alternative pathway of complement activation
    • Figure 8. Pathology of membranoproliferative glomerulonephritis type I. (a) Light microscopy shows a hypercellular glomerulus with accentuated lobular architecture and a small cellular crescent (methenamine silver).
    • IGA NEPHROPATHY (BERGER DISEASE)
      • the most common type of glomerulonephritis worldwide
      • major cause of recurrent glomerular hematuria
      • By light microscope, the glomeruli can appear nearly normal, showing only subtle mesangial hyprcellularity, or can reveal focal proliferative or sclerotic lesions
      • The pathogenesis is nuclear
      • although a genetic or acquired defect in immune regulation leading to increased mucosal IgA secretion. There isalso decreased clearance of IgA complexes by the liver.
      • Similar IgA deposits are seen in Henoch-Schönlein purpura in children
      • hematuria typically lasts for several days
      • chronic renal failure develops in 50% over a period of 20 years
    • THANK YOU Powerpoint presentation