focal and diffuse mesangial proliferative glomerulonephritis reveal the most common histologic lesions observed on renal biopsies from patients with iga nephropathy ( igan ) . however , histologic variability is also observed in this disease , which is the same as with lupus nephritis . in some cases , endocapillary hypercellularity is accompanied by segmental duplication of the glomerular basement membrane , and there is rarely diffuse endocapillary proliferation with lobular accentuation and multiple double contours , resembling type i membranoproliferative glomerulonephritis ( mpgn ) . tanaka and waga   have reported a biopsied patient with acute igan following the formation of keloid scars due to a burn injury . however , further reports regarding the correlation between igan and burn injury are rare . a 46-year - old male patient with scrotal and pedal edema was admitted to our department in august 2012 . laboratory examination showed proteinuria ( 4 + ) and more than 775 red blood cells in the urine without casts . this patient had been treated for his 2nd- to 3rd - degree burn injuries in a local burn center . he had no inhalation injury or sepsis during the whole treatment process . at the admission time , he had a body temperature of 36.6c , a pulse rate of 75 beats / min , a respiratory rate of 16/min , and a blood pressure of 118/80 mm hg . physical examination revealed cutaneous convalescence after full - thickness burns of both hands , the coronal plane of the body and both legs . the skin showed fuscous , slight exudation , bleeding cracks , mild scaling and itch during the treatment process ( fig . the laboratory test results of the urine and blood for this patient are listed in table 1 . he was diagnosed as having nephrotic syndrome on the basis of a diminished serum albumin level of 23 g / l and an increased proteinuria excretion of 10.0 g/24 h. during the treatment course , microbiological examination of wound secretion was performed twice a week and no infection was observed . a percutaneous renal biopsy was performed on september 11 , 2012 ( day 57 after burn injury ) to explore the cause of proteinuria . the examination under light microscopy revealed a diffuse and moderate proliferation of mesangial cells and endothelial cells without observable crescents in 20 glomeruli . arterioles presented as normal status . neither tubular atrophy nor interstitial fibrosis was found , as shown in figure 2a  c . immunofluorescence revealed iga ( 3 + ) , trace igm , c3 ( 3 + ) , igg (  ) , c4 (  ) and c1q (  ) in a coarse granular pattern with mesangial and capillary distribution ( fig . 2d , e ) , and inconspicuous staining for igm along the glomerular capillary walls in a granular pattern . in addition , this patient showed negative staining of hbsag and hbcag . the mesangial hypercellularity and increased mesangial matrix were present between the glomerular basement membrane and glomerular endothelium . the thickened capillary wall was composed of basement membrane - like materials , interposed mesangial cells , and electron - dense immune - type deposits ( fig . based on the proliferative properties of glomerular lesions , the patient was started on therapy with oral prednisone at a dose of 1 mg / kg / day . after treatment , the excretion of urinary protein revealed a significant decrease from 10.0 to 5.20 g/24 h in 2 weeks . the patient had been followed up to date and showed normal renal function and mild proteinuria . the glomerular filtration rate is increased after burn injuries , which is accompanied by vascular dysfunction and increased cardiac output . renal disease and acute kidney injury remains prevalent and is associated with the increased mortality of patients with severe burn injuries . this case shows the pattern of diffuse proliferative type i mpgn - like symptoms with mesangial interposition and double contours of the glomerular basement membrane present on periodic acid - schiff and silver stains ( fig . the following reasons are considered as a close correlation between burn injury and the onset of igan . first , this patient did not have any urinary abnormalities or chronic kidney diseases before and at the early stage of burn injury . second , nephrotic syndrome was observed at the 2nd week after the injury , and the patient did not have a history of infection such as inflammation of the respiratory tract although concurrent nephrotic syndrome in convalescence was observed . in addition , the patient suffered from skin problems with slight exudation , bleeding cracks , mild scaling and itch during the treatment process ( fig . although a causal relationship between igan and burn injury has not been established , an association of cutaneous lesions after burn injury with igan has been reported in a few patients [ 2 , 4 ] . tanaka and waga   mentioned a biopsied patient with acute igan following the formation of keloid scars due to burn injury . the patient revealed a rapid recovery after complete removal of the scars without any medication . wang et al .   have reported that acute igan is closely related to high - voltage electrical burn injury . in this study , all those case reports revealed a close relationship between igan and burn injury . because of trauma , infection , tissue necrosis , allogeneic plasma transfusion , increased concentrations of circulating immune complexes were observed . this situation is similar to the immune dysfunction of igan . both have inherent genetic predisposition and external infections , which may induce igan . if the pathogenesis of igan is not correlated with the concurrent burn injury , what is the cause of the nephrotic sydrome ? we hypothesize that an autoimmune dysregulation due to a sequestered antigen induced by skin infection and pruritus after burn injury may have an important role in the pathogenesis of igan . the persistent skin lesions with dry , itch and crusting properties can trigger iga deposition and promote the depositions in the mesangium and subendothelium of the patient . after serious burns , the immune system is disordered , the immune complex is increased in the circulation , and macrophages are excessively activated . numerous studies have provided evidence that burns upregulate inflammatory cytokines such as tnf- and il-1 . those cytokines can interfere with the hemodynamics of intraglomerular microcirculation , the coagulation - fibrinolysis system and the infiltration of inflammatory cells after burns . nephritis is a rare complication of burn injury , and once this happens , it will affect the recovery and prognosis of the patient . regular urine analysis will contribute to the early detection and diagnosis of glomerular diseases while treating burn injury . it is difficult to measure the blood pressure of burned patients , but blood pressure should be monitored as early as possible . because of wound exudation , infection and other reasons , the patients with large burned areas often have some degree of hypoalbuminemia . once persistent hypoalbuminemia exist , the burned patients need further examination to diagnose whether they have chronic glomerulonephritis or nephrotic syndrome . if the burned patient has nephrotic syndrome , enough glucocorticoid should be administered in order to alleviate proteinuria effectively and for the recovery of burn wounds . the casual relationship between the onset of igan and burn injury remains speculative and needs to be explored further .