The Japanese Journal of Nephrology
Online ISSN : 1884-0728
Print ISSN : 0385-2385
ISSN-L : 0385-2385
Renal glucosuria and membranous glomerulonephritis in chronic inflammatory demyelinating polyradiculoneuropathy:CIDP
Katsuyoshi KANEMOTOChieko NAKAHARAHisako SAITOHTakashi FUKUSHIMARyouichi KASHIWAGIMiho TAKAHASHINobuaki IWASAKITomohiro KAMODANorio OHKOSHIMichio NAGATAAkio KOYAMATeruo WATANABEAkira MATSUI
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1999 Volume 41 Issue 5 Pages 511-516

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Abstract

Glucosuria was detected in a 7-year-old boy by a routine school mass examination in . The diagnosis of renal glucosuria was made in the affiliated . The patient developed muscle weakness and gait disturbance in . Spinal fluid examination revealed a protein level of 62 mg/dl and a cell count of 4/3. Under the diagnosis of Guillain-Barre syndrome, he was treated with IV 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 the muscle weakness became worse;he could not go up stairs, nor stand upright on one leg. In proteinuria was detected in a school mass examination. He was referred to for a full renal study in 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 fbulal 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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