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• W1975914209 abstract "Dear Sir,A previously healthy 46-year-old man was found to have proteinuria at a medical checkup in 1991. In June 1993, he was admitted to the local hospital for renal biopsy, and IgA (Berger) nephropathy (diffuse proliferative glomerulonephritis of moderate severity) was diagnosed by light and electron microscopy and immunofluorescence. Despite treatment, azotemia rapidly worsened from April 1996, and he required hemodialysis for uremia from May 9, 1996.Also from about April 1996, he noted watery diarrhea, numbness of the lower extremities, and hypersensitivity of chest, abdomen, and lower extremities. These symptoms gradually worsened. On June 7, he was admitted for hemodialysis and to assess his sensory disturbances. On admission, neurological examination revealed reduced tendon reflexes (triceps, biceps, patellar, and Achilles tendons) and impairment of both touch and temperature sensation in the lower body. The grip power was 24 kg on the left and 30 kg on the right.Laboratory investigations showed proteinuria and hematuria. The white blood cell count was 5.8 × 109/l with 5.7% eosinophils, and anemia was present (hemoglobin 74 g/l). Hypoimmunoglobulinemia was also present (IgG 4.96 g/l, IgA 0.62, IgM 0.4 g/l). The blood urea nitrogen level was elevated (0.39 g/l) and so was the serum creatinine level (0.069 g/l). Blood glucose was normal (0.83 g/l). Antiganglioside antibodies (GM1, GD1a, GD1b, and GT1b) were not elevated. On examination of the cerebrospinal fluid, the albumin concentration was elevated (1.2 g/l), the cell count was 3/3, and the immunoglobulin levels were normal. Bone marrow was also normal. Nerve conduction studies showed that both motor and sensory nerve conduction velocities were reduced. A sural nerve biopsy specimen showed edema between the nerve fascicles and a decrease in the density of myelinated fibers, predominantly small fibers (fig. 1). Demyelinated fibers and slight macrophage infiltration were also seen, and the borders between nerve fascicles were unclear. From these findings, the diagnosis chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) was made. After admission, he received hemodialysis three times weekly and plasma exchange four times in total. However, his hypoimmunoglobulinemia, sensory disturbance, and diarrhea worsened. Edema of the lower extremities appeared, and his skin became dry with desquamation. Muscle weakness gradually increased until he had difficulty in climbing stairs. He is currently on hemodialysis, but shows no symptomatic improvement.A case of membranous glomerulonephritis associated with CIDP has been reported [1], but this appears to be the 1st case of IgA nephropathy associated with CIDP. Although no specific autoimmune antibodies were detected, other unknown autoantibodies may have been involved because of the myelin destruction seen on nerve biopsy and the eosinophilia. Neuropathy related to uremia usually features degeneration and atrophy of axons, and it showed no response to hemodialysis. There was also no evidence of diabetes, so neuropathy due to these common causes was ruled out. CIDP is related to cellular and humoral immunity [2], and IgA nephropathy is also associated with lymphocyte abnormalities [3], suggesting a possible relationship between these diseases. Several reports [4, 5]have suggested that high-dose intravenous immunoglobulin or plasma exchange can improve CIDP. Plasma exchange was not effective in our patient, probably because there was already progressive nerve degeneration. Thus, high-dose intravenous immunoglobulin may also have been ineffective. This patient fulfilled the diagnostic criteria for CIDP, but seemed to have a variant type because sensory disturbance was predominant and the serum IgG level decreased [4]. His IgA nephropathy was also atypical because of its relatively late onset and because the serum IgA level was decreased [3]. Rapid deterioration of the renal function coincided with the appearance of symptoms related to CIDP. Accordingly, both conditions may be related, and this case may represent a new disease combining demyelinating polyneuropathy and nephropathy, in which a common autoimmune mechanism damages the glomeruli and the myelin sheath." @default.
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• W1975914209 date "1998-01-01" @default.
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• W1975914209 title "Renal Failure due to IgA (Berger) Nephropathy with Inflammatory Demyelinating Polyradiculoneuropathy" @default.
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• W1975914209 doi "https://doi.org/10.1159/000045155" @default.
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