Chronic inflammatory demyelinating polyradiculoneuropathy and severe peripheral oedema: a renal explanation

• Published in: Journal of clinical neuroscience Vol. 7; no. 2; pp. 148 - 149
• Main Authors: Henderson, R.D, Healy, H.G, McCombe, P.A, Lander, C.M
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier Ltd 01.03.2000; Elsevier
• Subjects: Anti-Inflammatory Agents - therapeutic use; Biological and medical sciences; chronic inflammatory demyelinating polyradiculoneuropathy, focal sclerosing glomerulonephritis, oedema; Edema - drug therapy; Edema - etiology; Glomerulonephritis; Glomerulosclerosis, Focal Segmental - complications; Glomerulosclerosis, Focal Segmental - drug therapy; Humans; Kidney Glomerulus - drug effects; Kidney Glomerulus - physiopathology; Male; Medical sciences; Middle Aged; Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis; Nephrology. Urinary tract diseases; Nephropathies. Renovascular diseases. Renal failure; Neurology; Polyradiculoneuropathy, Chronic Inflammatory Demyelinating - complications; Polyradiculoneuropathy, Chronic Inflammatory Demyelinating - drug therapy; Prednisone - therapeutic use; Sacrococcygeal Region; Tropical medicine; chronic inflammatory demyelinating polyradiculoneuropathy, focal sclerosing glomerulonephritis, oedema; Kidney disease; Human; Glomerulonephritis; Nervous system diseases; Urinary system disease; Pathophysiology; Polyradiculoneuritis; Peripheral neuropathy; Case study; Concomitant disease; Chronic; Peripheral nerve disease; Sclerosing agent
• ISSN: 0967-5868; 1532-2653
• DOI: 10.1054/jocn.1999.0170

Inflammatory demyelinating neuropathies have been associated with membranous and focal sclerosing glomerulonephritis. Here we describe a 58 year old man with a clinical history, physical examination and laboratory investigations consistent with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), who also had severe lower limb and sacral oedema resistant to medical therapy. Mild proteinuria was present and a renal biopsy showed features consistent with focal sclerosing glomerulonephritis (FSGN). The patient’s weakness and oedema did not respond to i.v. immunoglobulin or plasmapheresis but responded to high dose oral prednisone. The oedema was not explained by immobility, hypoproteinaemia or local factors. The occurrence of the oedema in a person with CIDP and FSGN and its improvement with prednisone, together with improvement in CIDP and FSGN, suggests that it was immune mediated, possibly due to increased capillary permeability. The presence of renal disease in patients with inflammatory demyelinating neuropathies may be more common than currently realised.