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[Renal glucosuria and membranous glomerulonephritis in chronic inflammatory demyelinating polyradiculoneuropathy: CIDP].

医学 肾活检 近端肌无力 泼尼松龙 肌肉活检 体格检查 蛋白尿 病理 肾小球肾炎 活检 神经系统检查 内科学 胃肠病学 外科
作者
Koji Kanemoto,C Nakahara,H Saitoh,T Fukushima,Ryoichi Kashiwagi,Masahide Takahashi,Naomi Iwasaki,Tomohiro Kamoda,Norio Ohkoshi,M. Nagata,Akio Kôyama,Tsuyoshi Watanabe,Akira Matsui
出处
期刊:PubMed 卷期号:41 (5): 511-6 被引量:10
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Glucosuria was detected in a 7-year-old boy by a routine school mass examination in April 1991. The diagnosis of renal glucosuria was made in the affiliated hospital of the University of Tsukuba. The patient developed muscle weakness and gait disturbance in February 1993. Spinal fluid examination revealed a protein level of 62 mg/dl and a cell count of 4/3. Under the diagnosis of Guillain-Barré syndrome, he was treated with i.v. immunoglobulin and oral prednisolone. Although the therapy somewhat improved the symptoms, his muscle strength had not fully recovered at the end of the treatment. In November 1995, the muscle weakness became worse; he could not go up stairs, nor stand upright on one leg. In April 1996, proteinuria was detected in a school mass examination. He was referred to the University Hospital of Tsukuba for a full renal study in March 1997. Renal biopsy revealed global sclerosis in 16 of 19 glomeruli with extensive interstitial fibrosis and mononuclear cell infiltration. A diagnosis of membranous glomerulonephritis was established based on the findings of spikes in PASM staining, weak IgG deposition in the glomerular capillary and subepithelial deposits by electron microscopic study. Additionally, pituitary growth hormone deficiency was found by endocrinological examination. The diagnosis of CIDP was established by fibulal neuron biopsy, which revealed neuronal degeneration and profound demyelinization. The clinical course of the present case was unlike that of the few reported cases of MGN associated with CIDP described in the literature. The initial renal symptom was glucosuria, which started 5 years prior to the onset of proteinuria. Second, glomerulosclerosis was more extensive than that seen in the literature. We surmise that chronic interstitial nephritis of insidious onset was followed by MGN which developed subsequently, probably at the time of the start of proteinuria.

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