Acute Glomerulonephritis

Deepak Kumar GuptaInstitute of Dental Education and Advance

Studies, Gwalior

Glomerulonephritis

• Inflammation of glomeruli• Mainly Immunologically mediated• Classification of GN is based on

histopathological appearance.• Early investigation other than histological

examination is very difficult

Etiology

• Infectious diseases– Poststreptococcal glomerulnephritis– Infective endocaridtis– Syphilis– Viral – Mumps, measeles, hepatitis-b, c, inffectious

mononucleosis, Epstein Barr Virus (EPV),– Malaria

Etiology• Collagen Vasculitis disorder– Systemic lupus

erythematosus (SLE)– Good pasture’s syndrome– Henoch-schonlein purpura– Polyangitis– Wegner’s granulomatosis– Sickle cell nephropathy

Etiology

• Primary glomerular disease– Focal segmental glomerulonephritis– Minimal change disorder– Rapidly progressive GN - Crescentric

glomerulonephritis– Membranous glomerulonepritis – IgG nephropathy– Membranoproliferative GN – Mesengial proiliferative - IgA nephropathy– Meseangio-capillary glomerulonephritis

Etiology

• Miscellaneous– Malignancy– Eclampsia (A toxic condition characterized by

convulsions and possibly coma during or immediately after pregnancy)

– Penicillamine

Pathogenesis• Two chief pathogenesis are recognised:– Deposition of anitgen-antibody complexes in glomeruli– Deposiotion of an antibody in glomerular basement

membrane which then reacts with antigen in the basement membrane

Pathogenesis• Immune complexes are removed through hosts

reticuloendothelial system– Impaired ability of the same results in deposition in

glomerular capillary walls• Immune complex and antibody against glomerular

antigen trigger injury by following mechanism• Complement activation• Fibrin deposition • Platelet aggregation• Release of cytokines and free oxygen radical

Clinical features• Haematuria• Hypertension• Red blood cell casts• Proteinuria• Oliguria• Oedema – areas of low tissue pressure (periorbital areas),

but progresses to involve dependent portion of the body– May lead to ascitis or pleural effusion

• Uraemia• pyuria

Management

• Investigation– Urine microscopy – Red cell cast– Culture – throat swab α-beta hemolytic

streptococci in case of of poststreptoccal infection– Antistreptolysin – O (ASO titre) – eleveated– C3 Level – reduced– Urinary protein – increased– Urea & creatinine – may be eleveated– Renal biopsy – features of glomerulnepritis

Treatment

• Mainly supportive– Rest– Salt restriction– Diuretics – Anti-hypertensives– Antibiotics – in case of streptococcal infection– Dialysis – severe oliguria, fluid overload,

hyperkalemia

Complications

• Pulmonary edema• Hypertensive encephalopathy• Renal failure

Prognosis

• Excellent in children• Small number of adult develops persistant

hypertension or renal impairment later in life.

Poststreptococcal gomerulonephritis

• Most common cause of GN• PSGN occurs fater pharyngeal or cutaneous

attack with group A beta hemolytic streptococcus

• Latent period of infection– Pharyngeal – 6-10 days– Cutaneous – 2 weeks – Commonly associated with poor hygiene,

overcrowding & skin disease like scabies

Poststreptococcal gomerulonephritis

• Onset abrupt with– Puffness of face– Oliguria– Smoky urine– Reddish urine– Hypertension– Oedema

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