Focal Proliferative Glomerulonephritis (AKA: Mesangial

Proliferative GN)

Focal proliferative GN is characterised by pathologic changes in

fewer than 50% glomeruli (focal), often confined to one or two

lobules of the affected glomeruli while other glomeruli are

normal. Focal GN is, thus, a pathologic diagnosis.

ETIOPATHOGENESIS: It may occur under following diverse

clinical settings:

a. As an early manifestation of a number of systemic diseases

such as SLE (class III), Henoch-Schonlein purpura,

subacute bacterial endocarditis, Wegener’s granulomatosis,

and polyarteritis nodosa, Goodpasture’s syndrome.

b. As a component of a known renal disease such as in IgA

nephropathy.

c. As a primary idiopathic glomerular disease unrelated to

systemic or other renal disease.

The diverse settings under which focal GN is encountered make

it unlikely that there are common etiologic agents or

pathogenetic mechanisms. However, the observation of

mesangial deposits of immunoglobulins and complement suggest

immune complex disease and participation of the mesangium.

MORPHOLOGIC FEATURES

By light microscopy, the single most important feature in focal

GN is the abnormality seen in certain number of glomeruli and

generally confined to one or two lobules of the affected

glomeruli i.e. focal and segmental glomerular involvement. The

pathologic change most frequently consists of focal and

segmental cellular proliferation of mesangial cells and

endothelial cells but sometimes necrotising changes can be seen.

The condition must be distinguished from focal segmental

glomerulo sclerosis.
By immunofluorescence microscopy, widespread mesangial

deposits of immunoglobulins (mainly IgA with or without IgG),

complement (C3) and fi brin are demonstrated in most cases of

focal GN.

CLINICAL FEATURES
The clinical features vary according to the condition causing it.

Haematuria is one of the most common clinical manifestation.

Proteinuria is frequently mild to moderate but hypertension is

uncommon.