Adolescent ; Female ; Glomerulonephritis, Membranous ; etiology ; Humans ; Tuberculosis, Pulmonary ; complications

IgA nephropathy is the most common form of primary glomerulonephritis which mainly accounts for the development of end-stage renal diseases. It is characterized by deposits of IgA1 in mesangium. The pathogenesis of IgA nephropathy is complicated. Moreover, there is a wide range of clinical features and variable histomorphologies in the diagnosed cases of IgA nephropathy. It was demonstrated that the galactose-deficient of IgA1 O-glycan chains led IgA1 to self-aggregation and eventual deposition in mesangium. Abnormality of glycosyltransferases, genetic mutation and immunologic disorder were involved in the aberrant glycosylation of IgA1 which was recognized as the key etiopathogenisis of IgA nephropathy. However, the exact source and the pathogenic mechanism of aberrantly glycosylated IgA1 remain obscure. The further studies on aberrant O-glycosylation of IgA1 would contribute to the understanding of IgA nephropathy and provide new therapeutical strategy.
Animals ; Glomerulonephritis, IGA ; etiology ; metabolism ; Glycosylation ; Humans ; Immunoglobulin A ; metabolism

Adult ; Glomerulonephritis, IGA ; etiology ; Hepatitis C ; complications ; Humans ; Male

Adult ; Cadmium ; Female ; Glomerulonephritis, IGA ; etiology ; Humans ; Occupational Exposure

Acute Disease ; Adult ; Glomerulonephritis ; etiology ; Hepatitis ; etiology ; Humans ; Male ; Meningitis, Aseptic ; etiology ; Pancreatitis ; etiology ; Typhoid Fever ; complications

We report treatment of a 24-year-old man with membranous glomerulonephritis (MGN) who developed a solitary choroidal tuberculoma in association with miliary tuberculosis during steroid therapy. In June 1995, the patient had developed nephrotic syndrome. He had refused renal biopsy at that time. So we treated him with corticosteroids having assumed a diagnosis of minimal change nephrotic syndrome. After initial corticosteroids and diuretics therapy for 5 months, his generalized edema resolved but proteinuria (3 positive) continued, suggesting the presence of other forms of glomerulonephritis. Renal biopsy performed in January 1996. The patient was diagnosed as having MGN. The patient was closely observed over a period of 34 months and remained stable without steroid therapy. However at 34 months, generalized edema was again noted and steroid therapy at high dosage was initiated. After 5 months of steroid therapy, he developed miliary tuberculosis and a solitary choroidal mass. An antituberculosis chemotherapeutic regimen was started and after a further 5 months, all clinical symptoms and signs of the pulmonary lesion were resolved and a measurable shrinking of the choroidal mass was recorded.
Adult ; Case Report ; Choroid Diseases/*etiology ; Glomerulonephritis, Membranous/*complications ; Human ; Male ; Tuberculoma/*etiology

Adult ; Atypical Hemolytic Uremic Syndrome ; etiology ; Female ; Glomerulonephritis, IGA ; complications ; Humans ; Puerperal Disorders ; etiology

Acute post-streptococcal glomerulonephritis (PSGN) is characterized by an abrupt onset of edema, hypertension, and hematuria. Life-threatening diffuse alveolar hemorrhage (DAH) is rarely associated with acute PSGN. There have been only two reported cases worldwide, and no case has been reported previously in Korea. Here, we present a patient who clinically presented with pulmonary-renal syndrome; the renal histology revealed post-infectious glomerulonephritis of immune complex origin. A 59-yr-old woman was admitted with oliguria and hemoptysis two weeks after pharyngitis. Renal insufficiency rapidly progressed, and respiratory distress developed. Chest radiography showed acute progressive bilateral pulmonary infiltrates. The clinical presentation suggested DAH with PSGN. Three days after treatment with high-dose steroids, the respiratory distress and pulmonary infiltrates resolved. Electron microscopy of a renal biopsy specimen sample revealed diffuse proliferative glomerulonephritis with characteristic subendothelial deposits of immune complex ("hump''). The renal function of the patient was restored, and the serum creatinine level was normalized after treatment.
Biopsy ; Female ; Glomerulonephritis/*etiology ; Hemorrhage/*etiology ; Humans ; Kidney/pathology ; Lung Diseases/etiology ; Middle Aged ; *Pulmonary Alveoli ; Streptococcal Infections/*complications

We treated a 54-year-old woman who was suffering from membranoproliferative glomerulonephritis associated with a complete type of hydatidiform mole. The renal manifestations were proteinuria and hematuria. A renal biopsy, performed before gynecologic management, disclosed focal and segmental subendothelial deposits with a proliferation of the mesangial cell and showed irregularly thickened capillary loops by light and electronmicroscoy. Genralized edema, proteinuria and hematuria were completely recovered by suction and curettage of the hydatidiform mole with prophylactic chemotherapy. The clinical manifestation of earlier presented 3 cases have been the nephrotic syndrome. The common feature of them was a complete remission of the nephropathy after the removal of the hydatidiform mole. The relationship between the hydatidiform mole and glomerulonephritis remains unresolved at present. But we concluded that the hydatidiform mole might be a cause of glomerulonephritis in this case.
Case Report ; Diagnosis, Differential ; Edema/etiology ; Female ; Glomerulonephritis, Membranoproliferative/pathology ; Glomerulonephritis, Membranoproliferative/etiology* ; Hematuria/etiology ; Human ; Hydatidiform Mole/therapy ; Hydatidiform Mole/diagnosis* ; Hydatidiform Mole/complications* ; Middle Age ; Pregnancy ; Proteinuria/etiology ; Uterine Neoplasms/therapy ; Uterine Neoplasms/diagnosis* ; Uterine Neoplasms/complications*

C1q nephropathy is a rare type of glomerulonephritis manifested as the deposition of C1q in the glomerular mesangium during immunofluorescent staining. Systemic lupus erythematosus and type I membranoproliferative glomerulonephropathy need to be excluded in the diagnosis of C1q nephropathy. C1q nephropathy has various manifestations under a light microscope, mainly including minimal change disease, focal segmental glomerulosclerosis, and proliferative glomerulonephritis. This disease is mainly manifested as persistent proteinuria or nephrotic syndrome and occurs more frequently in boys. Currently, glucocorticoids are mainly used for the treatment of this disease. Patients with C1q nephropathy show a good response to immunosuppressant treatment, but have a high rate of glucocorticoid resistance. Therefore, in this case, methylprednisolone pulse therapy or a combination with immunosuppressant treatment helps to achieve a good prognosis.
Complement C1q ; metabolism ; Diagnosis, Differential ; Glomerulonephritis ; diagnosis ; drug therapy ; etiology ; Glucocorticoids ; therapeutic use ; Humans ; Prognosis