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CHRONIC INFLAMMATORY DEMYELINATING POLYNEUROPATHY (CIDP) ASSOCIATED WITH MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS
Author(s) -
Capasso M.,
Di Muzio A.,
Amoroso L.,
Cappelli P.,
Di Liberato L.,
Di Stante S.,
Lupo S.,
Lugaresi A.
Publication year - 2002
Publication title -
journal of the peripheral nervous system
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 67
eISSN - 1529-8027
pISSN - 1085-9489
DOI - 10.1046/j.1529-8027.2002.7011_7.x
Subject(s) - membranoproliferative glomerulonephritis , medicine , chronic inflammatory demyelinating polyneuropathy , glomerulonephritis , pathology , rapidly progressive glomerulonephritis , focal segmental glomerulosclerosis , membranous nephropathy , immunology , kidney , antibody
The association between CIDP and glomerulonephritis has been rarely reported: membranous glomerulonephritis in five cases, focal‐segmental glomerulosclerosis in two, IgA nephropathy in one. A pathogenetic autoantibody towards a common antigen in myelin and glomerular basement membrane has been hypothesized. A 60‐year‐old man developed proteinuria (3.4 g/24 h) without clinical signs of nephrotic syndrome and, six months later, paresthesias and progressive limb weakness. Examination showed ataxic gait, predominantly distal weakness with bilateral foot drop, glove‐stocking sensory loss, reduced or absent reflexes, and postural tremor. Electrophysiological studies revealed a sensory‐motor demyelinating polyneuropathy with marked axonal loss in lower limbs. CSF examination showed increased proteins. HBV, HCV and HIV markers, rheumatoid factor, ANA, ANCA, ENA were negative. Monoclonal gammopathy and cryoglobulins were absent. C3 and C4 were normal. Circulating immune complexes were 37% (n.v. <35). Anti‐ganglioside (GM1, GM2, GA1, GD1a, GD1b), anti‐ sulfatide, and anti‐MAG antibodies were negative. Sural nerve biopsy showed small epineurial and perineurial infiltrates, marked loss of fibers, and no deposits of IgG and IgM or amyloid. Kidney biopsy revealed a membranoproliferative glomerulonephritis with associated interstitial nephritis. Neurological and renal abnormalities improved with plasmaphereses and prednisone. This patient represents the first with the association between membranoproliferative glomerulonephritis and CIDP, and the sixth, to our knowledge presenting with CIDP and glomerulonephritis. Our results seem to exclude a common pathogenetic role of antiganglioside, anti‐MAG and antisulfatide antibodies in this case.