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Clinical syndromes related to renal disease

Clinical syndromes related to renal disease. Acute nephritis. Hematuria, proteinuria, hypertension. Nephrotic synd. Proteinuria > 3.5 g/day, hypoalbuminemia <2 g/dl, edema, hyperlipidemia, lipiduria. Asymptomatic hemat / proteinuria. Due to subtle glomerular abnormalities. Ac renal failure.

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Clinical syndromes related to renal disease

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  1. Clinical syndromes related to renal disease

  2. Acute nephritis Hematuria, proteinuria, hypertension Nephrotic synd Proteinuria > 3.5 g/day, hypoalbuminemia <2 g/dl, edema, hyperlipidemia, lipiduria Asymptomatic hemat / proteinuria Due to subtle glomerular abnormalities Ac renal failure Oliguria / anuria, azotemia, (Anuria <100 ml; oliguria 100-400 ml) Chr renal failure Uremia Tubular defects, Urinary infections, Nephrolithiasis, Obstruction, Tumors Clinical syndromes related to renal disease

  3. Renal failure - Acute Syndrome characterized by acute suppression of renal function with oliguria / anuria, azotemia. Major causes are - Vascular obstruction, Severe glomerular disease, Acute tubulo-interstitial nephritis, Severe pyelonephritis with papillary necrosis, Urinary obstruction, Acute tubular necrosis.

  4. Renal failure - Acute • Pathogenesis.. • Failure of glomerular filtration due to hypo-perfusion • Renal causes • Post-renal causes • End result is a decrease of GFR

  5. Renal failure - Chronic • End result of various renal diseases. Four stages: • Diminished renal reserve: GFR > 50%. Asymptomatic but susceptible • Renal insufficiency: GFR 20-50%. Azotemia, anemia, hypertension, polyuria. Sudden stress ----- Uremia • Renal failure: GFR < 20%. Edema, metabolic acidosis, hypocalcemia, uremia with systemic complications. • End-stage renal disease: GFR < 5%. Terminal stage of uremia.

  6. Pathogenesis of Glomerulonephritis

  7. Pathogenesis of glomerulonephritis Immune mechanisms underlie majority of the primary glomerulonephritis 1. In situ immune complex deposition a. Intrinsic (fixed) glomerular antigens Anti GBM, Heymann nephritis, membranous nephropathy b. Planted antigens (proteins, bacterial, viral) 2. Circulating immune complexes Others: cytotoxic antibodies, chemical mediators, cell mediated injury, non-immune mechanisms.

  8. Pathogenesis of glomerulonephritis Intrinsic (fixed) glomerular antigens - Anti GBM Antibodies directed against non-collagenous domain of type IV collagen. Linear pattern of fluorescence for IgG Underlying cause in Goodpasture’s syndrome

  9. Pathogenesis of glomerulonephritis Intrinsic (fixed) glomerular antigens Heymann nephritis, membranous nephropathy Animal model - rats immunized with preparations of PCT brush border developed antibodies. Manifested as membranous glomerulonephritis closely resembling human MGN. Sub-epithelial granular deposits of immunoglobulin. Heymann antigen is a 30 kd protein located in pits on the basal surface of podocyte. Nature of antigen in man is unknown

  10. Pathogenesis of glomerulonephritis Circulating immune complexes - Localize in glomeruli due to physicochemical and hemodynamic factors Evocative antigen may be endogenous (SLE) or exogenous (PSGN, malaria etc) Immune complexes lie in mesangium and sub-endothelial region of glomerulus or in sub-epithelial region. Deposits are granular. Localization of complexes is dependant on: - Molecular charge: Cationic particles pass through GBM - Molecular size

  11. Immunological studies in glomerulonephritis • . • Immunofuorescence on biopsy • Complement levels • Circulating antibodies (ANA, GBM, ANCA)

  12. Pathogenesis of glomerulonephritis Cell mediated glomerular injury: By activated T cells, monocytes and macrophages - Delayed hypersensitivity by ag specific T cells - Direct action by cytotoxic T cells - Cytokine mediation • Tubulointerstitial nephritis • ? Pauci-immune crescentic nephritis • Minimal change nephropathy • Focal segmental glomerulosclerosis

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