Hyponatraemia caused by LGI1-associated limbic encephalitis

• Published in: Clinical kidney journal 2011-12, Vol.4 (6), p.424-426
• Main Authors: McQuillan, Rory F., Bargman, Joanne M.
• Format: Article
• Language: English
• Subjects: II. Clinical Reports
• ISSN: 2048-8505; 1753-0784; 2048-8513; 1753-0792
• DOI: 10.1093/ndtplus/sfr105

Limbic encephalitis (LE), once thought to be a rare paraneoplastic phenomenon, is increasingly diagnosed in patients without malignancy. Autoimmune LE has emerged as a distinct clinical entity. Autoantibodies to neuronal cell surface proteins have been described and may now be tested for. This has led to an exponential increase in the number of cases being reported. The most recently implicated autoantibody is to the leucine-rich anti-glioma 1 protein (LGI1). This protein is involved in synaptic transmission and inherited loss-of-function mutations cause autosomal dominant lateral temporal epilepsy. LGI1 is also expressed in specific tubules in the kidney. Anti-leucine-rich anti-glioma 1 protein (anti-LGI1) LE presents with sub acute onset of progressive neurological, cognitive and psychiatric disturbance. The condition is complicated in up to 60% of cases with severe and life threatening hyponatraemia. As well as causing significant morbidity, the co-existence of hyponatraemia may confuse the initial diagnosis. We present a case of anti-LGI1 which was complicated by hyponatraemia with a comprehensive review of the literature.