IgA Nephropathy with Pathologic Features of Membranoproliferative Glomerulonephritis following Burn Injury
A 46-year-old male patient with scrotal and pedal edema was admitted to our department in August 2012. He had been burned in a gas leakage accident 2 weeks ago. 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 36.6°C, 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. ). Severe edema in the bilateral lower extremities and scrotums were also observed.\nNo lymphadenopathy, hepatosplenomegaly, or neurological abnormalities were shown. Electrocardiogram and chest X-ray were normal. Abdominal ultrasonography showed bilateral normal-sized kidneys. No antineutrophil cytoplasmic antibodies, antiglomerular basement membrane antibodies and antinuclear antibodies were detected. The laboratory test results of the urine and blood for this patient are listed in table . 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.\nA 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. Hyaline droplets containing proteins and lipids in tubules were observed. Meanwhile, red blood cells in some tubules were also observed. The interstitium showed diffuse edema and scattered infiltration of mononuclear cells. Arterioles presented as normal status. Neither tubular atrophy nor interstitial fibrosis was found, as shown in figure .\nIgA and C3 are predominant immunoreactants for the diagnosis of IgAN. Immunofluorescence revealed IgA (3+), trace IgM, C3 (3+), IgG (–), C4 (–) and C1q (–) in a coarse granular pattern with mesangial and capillary distribution (fig. ), 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.\nUltrastructural studies showed high-density deposits of mesangial and subendothelial cells. 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. ).\nBased 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. Then, the patient was discharged and treatment was continued at the outpatient section. The patient had been followed up to date and showed normal renal function and mild proteinuria.