Postinfectious glomerulonephritis(PIGN) is the most common cause of glomerular disorder in children between 5 and 15 years old. Most cases are caused by Group A nephritogenic strain of streptococcus although many other organisms also can cause disease. The proposed pathogenic mechanisms are immune complex formation between circulating antibody and glomerular “planted antigen”, reactivity of circulating autoantibody with normal glomerular tissue acting as autoantigen “molecular mimicry”, and trapping of circulating immune complex in the glomerulus. Activation of the complement system is also at the core of immune mediated renal damage. The typical clinical presentations of PIGN are hematuria, some degree of oliguria and azotemia , and hypertention. There may also be some degree of proteinuria and edema. In case of abnormal regulation of the complement pathway, the patient may present constant hypertension or edema in the absence of abnormal urine findings, which is called „atypical‟ postinfectious glomerulonephritis. Examination of urine typically reveals abnormal findings in patient with PIGN. The measurements of antecedent streptococcal infection and serum C3 level also help in diagnosis of PIGN. Renal biopsy is generally not indicated unless the existence of an atypical presentation and an atypical course or persistence of clinical features. Treatment of PSGN is mainly supportive and usually focuses on managing hypertension and treating volume overload. However, specific infections, such as hepatitis B, parvovirus B 19, or HIV, require treatment with specific antibiotic or antiviral agents.