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首页> 外文期刊>Neuron >Autoimmunity to the sodium-level sensor in the brain causes essential hypernatremia.
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Autoimmunity to the sodium-level sensor in the brain causes essential hypernatremia.

机译：对脑中钠水平传感器的自身免疫会导致原发性高钠血症。

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摘要

Na(x) is the sodium-level sensor of body fluids in the brain involved in sodium homeostasis. Na(x)-knockout mice do not stop ingesting salt even when dehydrated. Here we report a case with clinical features of essential hypernatremia without demonstrable hypothalamic structural lesions, who was diagnosed as a paraneoplastic neurologic disorder. The patient had autoantibodies directed against Na(x), along with a ganglioneuroma composed of Schwann-like cells robustly expressing Na(x). The removal of the tumor did not reduce the autoantibody levels or relieve the symptoms. Intravenous injection of the immunoglobulin fraction of the patient's serum into mice induced abnormalities in water/salt intake and diuresis, which led to hypernatremia. In the brains of these mice, cell death was observed along with focal deposits of complement C3 and inflammatory infiltrates in circumventricular organs where Na(x) is specifically expressed. Our findings thus provide new insights into the pathogenesis of hypernatremia relevant to the sodium-level-sensing mechanism in humans.
机译：Na（x）是参与钠稳态的大脑中体液的钠水平传感器。 Na（x）敲除小鼠即使脱水也不会停止摄取盐分。在这里，我们报告一例具有原发性高钠血症但无明显下丘脑结构性病变临床特征的病例，该病例被诊断为副肿瘤性神经系统疾病。该患者具有针对Na（x）的自身抗体，以及由强烈表达Na（x）的雪旺氏样细胞组成的神经节神经瘤。切除肿瘤并不能降低自身抗体水平或减轻症状。向小鼠静脉内注射患者血清的免疫球蛋白部分会引起水/盐摄入和利尿异常，从而导致高钠血症。在这些小鼠的大脑中，观察到细胞死亡以及补体C3的局灶性沉积和炎性浸润，尤其是在表达Na（x）的室间隔器官中。因此，我们的发现为与钠水平感应机制有关的高钠血症的发病机理提供了新的见解。

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