Cellular and Subcellular Aquaporin-4 Distribution in the Mouse Neurohypophysis and the Effects of Osmotic Stimulation

Mesbah-Benmessaoud, Ouahiba; Benabdesselam, Roza; Hardin‐Pouzet, Hélène; Dorbani-Mamine, Latifa; Grange-Messent, Valérie

doi:10.1369/jhc.2010.956805

Cited by 6 publications

(3 citation statements)

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“…1 Compelling evidence supports this IgG having a central role in the pathogenesis of NMO. 2 A single case of the syndrome of inappropriate antidiuresis (SIAD) has been described in NMO. 2 A single case of the syndrome of inappropriate antidiuresis (SIAD) has been described in NMO.…”

mentioning

confidence: 99%

Syndrome of inappropriate antidiuresis may herald or accompany neuromyelitis optica

Iorio¹,

Lucchinetti²,

Lennon³

et al. 2011

Neurology

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HERALD OR ACCOMPANY NEUROMYELITIS OPTICAAquaporin-4 (AQP4) is the target autoantigen of an immunoglobulin G (IgG) autoantibody that distinguishes a spectrum of inflammatory demyelinating CNS disorders (the neuromyelitis optica [NMO] spectrum) from multiple sclerosis (MS) and other CNS demyelinating disorders. 1 Compelling evidence supports this IgG having a central role in the pathogenesis of NMO. AQP4 is concentrated in astrocytic foot processes at interfaces between CNS parenchyma and fluid compartments, both CSF and blood, 1 and in areas involved in osmosensitivity and osmoregulation, including supraoptic and paraventricular nuclei of the hypothalamus and sensory circumventricular organs, the subfornical organ, the organum vasculosum of the lamina terminalis, and the area postrema. 2 A single case of the syndrome of inappropriate antidiuresis (SIAD) has been described in NMO. 3 Here we report the frequency of SIAD in NMO.Methods. Standard protocol approvals, registrations, and patient consents. The study was approved by the Institutional Review Board. The study involved retrospective chart review of 160 AQP4-IgG seropositive Mayo Clinic patients identified though the Neuroimmunology Laboratory's NMO database who provided consent to have their records reviewed.Our inclusion criterion, hyponatremic patients fulfilling modified Bartter and Schwartz criteria for SIAD, 4 required that data be available for both serum sodium concentration and blood/urine osmolality, at the onset of NMO or during a relapse of the disease. We excluded patients whose hyponatremia was attributable to carbamazepine or diuretic therapy (3), lymphoma (1), or thyroid dysfunction (1). No patient had signs of cerebral salt wasting syndrome.Results. Among 160 patients with NMO or NMO spectrum disorder, 43 had sufficient data for the study. Seven patients (16%) met diagnostic criteria for SIAD (table). The median age at disease onset was 55 years (range 15-72). The median follow-up interval was 67 months (range 24 -150). SIAD was the initial symptom of the attack in 5 of the 43 patients (12%). Hyponatremia was mild (130 mmol/L) in 1 patient, moderate (120 -130 mmol/L) in 4, and severe (Ͻ120 mmol/L) in 2. Only 1 patient experienced confusion and decreased consciousness attributable to hyponatremia. No information about sodium urinary concentration and plasma vasopressin levels was available. No patient was on any diuretic therapy or had adrenal insufficiency. Creatinine and BUN were unremarkable in all patients. Two patients experienced intractable vomiting, 2 had nausea, and 1 patient developed a syndrome of posterior reversible encephalopathy at the time of documented hyponatremia. Hyponatremia resolved in all patients after fluid intake was restricted to 1 L per day. No patient experienced a recurrence of hyponatremia.MRI revealed brain abnormalities in 4 patients; 1 had fluid-attenuated inversion recovery and T2weighted signal abnormalities extending from the brainstem into the area postrema region. Five patients had radiologic signs compa...

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mentioning

confidence: 99%

Syndrome of inappropriate antidiuresis may herald or accompany neuromyelitis optica

Iorio¹,

Lucchinetti²,

Lennon³

et al. 2011

Neurology

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“…These patients mainly present with an acute diencephalic or brainstem syndrome [1]. Hyponatremia in AQP4 positive patients is thought to be a result of demyelinating lesions in hypothalamic osmoregulatory centers, mainly the supraoptic and paraventricular nuclei, as a consequence of high AQP4 expression in these areas [5]. Treating hyponatremia can bear the formidable consequence of sodium correction-ODS.…”

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confidence: 99%

Neuromyelitis optica spectrum disorder associated with osmotic demyelination syndrome

et al. 2016

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“…AQP4 is highly expressed in astrocytic end‐feet at the blood–brain barrier, surrounding CNS synapses and nodes of Ranvier, and in areas involved in osmosensitivity and osmoregulation, including supraoptic and paraventricular nuclei of the hypothalamus and circumventricular organs (e.g. the subfornical organ, the organum vasculosum of the lamina terminalis, and the area postrema) . AQP4 is also expressed in epithelial cells of the collecting ducts of the kidney, in the parietal cells of the stomach and in the skeletal muscle.…”

Section: Introductionmentioning

confidence: 99%

Neuromyelitis optica and the evolving spectrum of autoimmune aquaporin‐4 channelopathies

Iorio

Pittock

2014

Clinical & Exp Neuroim

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Water channels are a recognized "novel" target for central nervous system, inflammatory, autoimmune, demyelinating diseases, and represent an evolving spectrum of disorders termed neuromyelitis optica (NMO) spectrum disorders (SD). These disorders should now be considered under the umbrella term "autoimmune aquaporin-4 channelopathy". NMOSD represent the first multiple sclerosis (MS)-like disease for which a specific antigen has been identifiedthe astrocytic water channel aquaporin-4 (AQP4). MS lacks a distinguishing biomarker. This discovery represents a seismic shift from historic emphasis on the oligodendrocyte and myelin to the astrocyte. The NMO of today represents a relapsing spectrum of disease, not necessarily restricted to the optic nerves and spinal cord, that is different from the monophasic disorder in which near simultaneous bilateral optic neuritis and transverse myelitis occur, as was originally described by Devic. Recent clinical, radiological and pathological findings have documented brain involvement in NMO spectrum disorders, particularly in children. Most patients with NMOSD have brain abnormalities on magnetic resonance imaging, and these are consistent with MS in up to 10% of patients. Others have lesions in areas that highly express AQP4 including the circumventricular organs accounting for intractable nausea and vomiting, and the syndrome of inappropriate antidiuresis as presenting symptoms or heralds of relapse. Diencephalic involvement might explain recently recognized sleep disorders and endocrinopathies. Continued progress in our understanding of the immunobiology of AQP4 autoimmunity necessitates continuing revision of the clinical diagnostic criteria for NMO spectrum disorders. As the clinical spectrum broadens, the importance of highly specific assays that detect pathogenic AQP4-immunoglobulin G targeting extracellular epitopes of AQP4 cannot be overemphasized. (Clin. Exp. Neuroimmunol.

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Cellular and Subcellular Aquaporin-4 Distribution in the Mouse Neurohypophysis and the Effects of Osmotic Stimulation

Cited by 6 publications

References 61 publications

Syndrome of inappropriate antidiuresis may herald or accompany neuromyelitis optica

Syndrome of inappropriate antidiuresis may herald or accompany neuromyelitis optica

Neuromyelitis optica spectrum disorder associated with osmotic demyelination syndrome

Neuromyelitis optica and the evolving spectrum of autoimmune aquaporin‐4 channelopathies

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