Clinical syndromes related to renal disease
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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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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


Tubular defects, Urinary infections, Nephrolithiasis, Obstruction, Tumors

Clinical syndromes related to renal disease

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.

Renal failure - Acute

  • Pathogenesis..

  • Failure of glomerular filtration due to hypo-perfusion

  • Renal causes

  • Post-renal causes

  • End result is a decrease of GFR

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.

Pathogenesis of glomerulonephritis
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.

Pathogenesis of glomerulonephritis1
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


Pathogenesis of glomerulonephritis2
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

Pathogenesis of glomerulonephritis3
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

  • Immunological studies in glomerulonephritis

  • .

  • Immunofuorescence on biopsy

  • Complement levels

  • Circulating antibodies (ANA, GBM, ANCA)

Pathogenesis of glomerulonephritis4
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