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DR Medhat MRCP

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Nephritic syndrome<br />

Def :<br />

Clinical syndrome associated with underlying glomerulonephritis<br />

Features :<br />

Causes :<br />

Hematuria (usually microscopic).<br />

Proteinuria.<br />

Hypertension.<br />

Oliguria ( low GFR) / generalized oedema (salt & water retention).<br />

Acute or rapidly progressive renal impairment.<br />

Nephritic urinary sediment (hematuria ,dysmorphic RBCs,RBCs & granular casts,<br />

sub-nephrotic range proteinuria).<br />

Diffuse proliferative<br />

focal proliferative<br />

1. Post streptococcal GN 1. IgA nephropathy<br />

2. SLE 2. HSP<br />

3. MPGN (malaria,hepatitis,HUS/TTP,chr infection) 3. Alport syndrome<br />

4. RPGN (ANCA-associated GN, anti-GBM disease) 4. SLE<br />

5. Cryoglobulinemia 5. Coeliac disease<br />

6. Dermatitis herpitiformis<br />

Mechanisms of glomerular injury :<br />

1) Autoantibody/Antigen binding formation of<br />

2) Complement fixation & activation immune complexes<br />

3) Recruitment of inflammatory cells (neutrophils & macrophages)<br />

4) Relase of cytokines ,proteases ,growth factors ,vasoactive factors ,oxidant species &<br />

procoagulants) Damage to, and activation of, surrounding cells and matrix<br />

haematuria, proteinuria, and impairment of glomerular filtration.<br />

5) Cellular immunity may also contribute to structural glomerular damage — this is<br />

especially true of pauci-immune GN (e.g. the GN associated with ANCA-positive<br />

vasculitis) where ICs play no pathological role.<br />

6) Resolution of inflammation might return an infl amed glomerulus to normal or, if the<br />

healing phase is poorly regulated, may result in cellular dropout, scarring,<br />

glomerulosclerosis, and CKD.<br />

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