acute poststreptococcal glomerulonephritis ( psagn ) is a common glomerular cause of gross hematuria in children . it commonly presents as nephritic syndrome with sudden onset of gross hematuria , edema , hypertension , and renal insufficiency . varied presentations have been reported such as asymptomatic , mild syndrome , or with complications , such as myocardial dysfunction , acute renal failure , or encephalopathy . we herein report a case of an 8-year - old boy with psagn , presenting as posterior reversible encephalopathy syndrome ( pres ) . an 8-year - old boy presented with complaints of headache and vomiting since 3 days . he had one episode of generalized tonic clonic convulsion on the day of admission lasting for about 5 min . there was no history of oliguria , drug intake , head injury , or koch 's contact . the child was unconscious with a pediatric glasgow coma scale score of 8/15 ( e2 v2 m4 ) . his heart rate was 110/min , respiratory rate was 24/min , and blood pressure was 160/120 mm hg in right upper arm ( > 95 percentile for age and sex ) . all his peripheral pulses were felt normally . there were no neurocutaneous markers on examination . his pupils were equal and reactive to light and fundoscopy was normal . there were no meningeal signs , focal neurological deficit , or cerebellar signs . laboratory studies revealed : hemoglobin 9.7 g / dl , white blood count 17,200/cumm ( neutrophils 70% , lymphocytes 30% ) , and platelet count 3.6 lac / cumm . blood urea nitrogen was 34 mg / dl and serum creatine was 1.2 mg / dl . urine microscopy showed 3 - 4 pus cells / hpf and 100 - 120 red blood cells / hpf . serum complement c 3 level was 26 mg / dl ( normal : 90 - 180 mg / dl ) . the child was started on nifedipine ( 0.3 mg / kg / dose , 6 hourly ) and intravenous furosemide ( 1 mg / kg / dose , 8 hourly ) . intravenous valproic acid ( 10 mg / kg / day ) and anticerebral edema measures ( i.e. intravenous mannitol and dexamethasone ) were also started . in view of the convulsion , severe hypertension , and persistent altered sensorium a magnetic resonance ( mr ) imaging with fluid - attenuated inversion recovery ( flair ) sequence was done . it showed hyperintense lesions in bilateral frontal and parietooccipital parenchyma on flair images suggestive of  pres  [ figure 1 ] . the blood pressure was controlled and he regained full consciousness within 48 h of admission . furosemide was omitted at the time of discharge and oral nifedipine was continued . on follow - up after 2 weeks , the child was asymptomatic with his blood pressure well - controlled . his nifedepine was also omitted and a repeat serum complement c3 done after 8 weeks was normal , that is , 110 mg / dl . magnetic resonance imaging brain with fluid - attenuated inversion recovery sequence shows bilateral symmetric hyperintense lesions in parieto - occipital parenchyma pres was first reported in 1996 by hinchey et al . it is a rare clinico - radiologic condition manifesting with headache , vomiting , seizures , confusion , visual disturbances , and occasionally focal neurological deficit . it is described mainly in conditions associated with an abrupt increase in blood pressure . in children , it has been reported in association with takayasu arteritis , ganglioneuroma , henoch - schnlein purpura , acute lymphoblastic leukaemia , steroids , hemolytic uremic syndrome , addison 's disease , hypertension , intraabdominal neurogenic tumours , porphyria , and bone marrow transplant . psagn typically follows infection of the throat or skin by nephritogenic strains of group - a beta hemolytic streptococci . the pathogenesis of psagn is immune - complex - mediated and results in depression in the serum complement ( c3 ) levels . hypertension is found in up to 60% of patients with psagn and may be associated with hypertensive encephalopathy in 10% of the cases . encephalopathy may also result from the toxic effects of the streptococcal bacteria on the central nervous system . the pathophysiology of pres in hypertensive encephalopathy has been explained by the  hyperperfusion injury " theory . a sudden rise of blood pressure overcomes the normal autoregulation of cerebral blood flow and causes dilatation of the cerebral arterioles , resulting in brain hyperperfusion . this increased perfusion pressure can overcome the blood - brain barrier , resulting in opening up of endothelial tight junctions , and leakage of plasma and red cells into the extracellular space , leading to cerebral edema ( vasogenic edema ) . the relative paucity of sympathetic innervation in the posterior brain results in increased susceptibility to hyperperfusion and vasogenic edema during acute blood pressure elevations . computed tomography ( ct ) scan reveals nonenhancing hypodensities of cerebral white matter in bilateral parietooccipital lobes . sparing of the calcarine fissure and paramedian occipital lobe structures helps differentiate pres from bilateral infarction of the posterior cerebral artery territory . involvement of brain stem , cerebellum , basal ganglion , and frontal lobes has also been reported . t2-weighted mr images , at the height of symptoms , characteristically show diffuse hyperintensity selectively involving the parietooccipital white matter . children develop pres at a lower absolute pressures than adults owing to the relative  left shift  of their range of cerebral blood flow autoregulation . early recognition of the condition , adequate control of hypertension , and appropriate anticonvulsant treatment are important in the management . anticonvulsant therapy is usually given for a short period due to the reversible nature of the condition . however , irreversible cytotoxic edema , ischemia , and infarction in brain can occur due to delay in the diagnosis and treatment . this can result in long - term sequelae including neurodevelopmental delay , neurological deficits , epilepsy , persistent vision abnormalities , or even death . in conclusion , we highlight this unusual presentation of psagn as posterior reversible encephalopathy syndrome . also , physicians should maintain a high index of suspicion and consider psagn in their differential diagnosis when treating patients with posterior reversible encephalopathy syndrome .