Proliferative glomerulonepheritis

Proliferative glomerulonepheritis

 

1. diffuse GN
2. focal segmental GN
3. rapidly progressive GN
4. mesangiocappilary GN
5. Ig A nephropathy

 

 

1-Diffuse glomerulonepheritis

 

Mostly young patients

Clinical features:

Minor Proteinurea

Nephritic syndrome

Mostly post infective

 

Good prognosis

Light microscopy: proliferation of the endothelial and mesangial cells with neutrophills.all glomeruli similarly affected

Immune florescence: Ig G,C3

Electrone microscopy: subepithilial deposits

 Treatment:

Acute phase: antihypertensive, duretics, salt restriction and dialysis if needed.

Steroids

 Associations:

Post streptococcal GN (group A β haemolytic streptococci)

  Typically preceded by sorethroat or skin disease (impetigo) 10-14 days

Endocarditis

SLE

 

 

 

2-Focal segmental glomerulonepheritis

 

any age

Clinical features:

Proteinurea

Nephrotic syndrome

Haematourea

Renal failure

 

Good prognosis

Light microscopy: focal sclerosis with hyaline deposits

                             Only some glomeruli show the Proliferative changes

Immune florecence: Ig M ,C3

Electrone microscopy:

 

Treatment;

Associations:

Shunt nephritis

SLE

SBE

HIV-AIDS

HLP

Obesity

IV drug user

 

 

 

 3-Rapidly progressive glomerulonepheritis

 

Mostly older pateints

Clinical features:

Acute renal failure

Haematourea

Olgourea

Hypertension

 

bad prognosis

 Light microscopy: hypercellularity

                              Crescent formation: aggregation of macrophages and epithelial cell         

                              In bowman capsule in 80% of glomeruli

Immune florescence: Ig G C3

Electrone microscopy:

 Treatment:

Steroids

Cyclophosphamide

 Associations:

Vasculitis

Anti GBM antibodies

Wegener’s

Goodpasture

Microscopic polyangitis

HLP

 

 

 

 

4-Mesangiocappilary glomerulonepheritis

 

under age

Clinical features:

Proteinurea, haematourea

Nephrotic syndrome

Renal failure

 

Bad prognosis

 Light microscopy: celluar expansion of the mesangium

                            BM appears split;tram track

Immune florecence:C3 nepheritic factor(Ig G to C3)

Electrone microscopy: type I subendothial deposits

                                    Type II basement membrane deposit

 Treatment:

 Associations:

Shunt nephritis

SBE

Cryoglobulinaaemia

Sickle cell disease

Alfa antitrypsin def

Lipodystrophy

C3 nepheritic factor

Measles

Kartager’s syndrome

Hep C

 

 

 

5-Ig A nephropathy (Berger’s disease)

 

Mostly young adults

The most common cause of microscopic haematourea

 

Clinical features:

Macro or microscopic haematourea

Minor proteinurea

Usually 0-3 days post URT infection

Increase serum Ig A in 50%

 

10% progress to renal failure

 Light microscopy: mesangial cell proliferation

Immune florecence:Ig A ,C3

Electron microscopy:

 Histology is similar to HLP

 

Treatment:

Proteinurea and mild disease: steroids

Progressive disease: prednisolone with Cyclophosphamide for 3 month

Consider tonsillectomy

 Associations:

Cirrohsis

Dermatitis herpictiformis

Celiac disease

Mycosis fungoides

Wiskott - Aldrich syndrome