We conclude that measurement of AVP by RIA during a hypertonic saline infusion test can differentiate patients with CDI from those without CDI with a high degree of accuracy.
The most frequent hyponatremic disorders related to AVP in these patients are the syndrome of inappropriate ADH secretion (SIADH) and the cerebral/renal salt wasting syndrome (C/RSW), while hypernatremic conditions include central diabetes insipidus (CDI) and adipsic CDI.
While DI symptoms develop prior to detectable cell death in transgenic DI mice, the eventual loss of vasopressinergic neurons is accompanied by autophagy, but the mechanism leading to cell degeneration in autosomal dominant neurohypophysealDI still remains unknown.
Our findings showed that AVP neurons underwent apoptosis induced by ER stress, and ER stress might play a vital role in CDI condition through the PI3K/Akt and ERK pathways.
A marked copeptin peak was identified at 1 hour after extubation, when a value below or equal to 12.8 pmol/L had a good accuracy in identifying CDI cases (AUC 0.866, 95% CI 0.751 - 0.941).
In the present study, the AVP-NPII gene of a Chinese adult patient with central diabetes insipidus, the patient's symptomatic mother and an asymptomatic sister of the patient was sequenced.
We present here an extraordinary case of developing permanent DI after mild TBI with the absence of neurohypophyseal bright spot on MRI with no other abnormal findings.
Hydranencephaly is a congenital condition characterized by the complete or near-complete absence of the cerebral cortex and basal ganglia, while central diabetes insipidus (CDI) is a condition characterized by the inability to concentrate urine due to a deficiency in antidiuretic hormone (ADH).
These data demonstrate that chronic AVP deficiency impacts behavioral arousal during adolescence and support the hypothesis that AVP influences adolescent social development, in part, through its regulation of arousal.
Copeptin identified CDI with an AUC of 0.99 (95% CI 0.97-1.00), and a cut-off value ≤ 4.4pmol/L showed a sensitivity of 100% and a specificity of 99% to predict CDI.
In addition, the number of AVP-positive cells in supraoptic nucleus (SON) and paraventricular nucleus (PVN) decreased after PEL, which confirmed the success of the CDI model.
Disturbances in these regulatory mechanisms can lead to polyuria-polydipsia syndrome, which comprises of three different conditions: central diabetes insipidus (DI) due to insufficient secretion of AVP, nephrogenic DI caused by renal insensitivity to AVP action and primary polydipsia due to excessive fluid intake and consequent physiological suppression of AVP.
Rabphilin-3A has been suggested as a novel autoantigen in infundibulo-neurohypophysitis (LINH), which leads to central diabetes insipidus through insufficient secretion of AVP.
Central diabetes insipidus (DI) is a rare disease characterized by the excretion of excessive volumes of dilute urine due to reduced levels of the antidiuretic hormonearginine vasopressin (AVP), caused by an acquired or genetic defect in the neurohypophysis.
Diabetes insipidus is a disease characterized by polyuria and polydipsia due to inadequate release of arginine vasopressin from the posterior pituitary gland (neurohypophyseal diabetes insipidus) or due to arginine vasopressin insensitivity by the renal distal tubule, leading to a deficiency in tubular water reabsorption (nephrogenic diabetes insipidus).
We investigated the clinical relationship between AVP, copeptin (the C-terminal fragment of the AVP precursor), and the development of relative AVP deficiency following hemorrhagic shock.
Central diabetes insipidus (CDI) is the result of a deficiency of arginine vasopressin, and its major causes are idiopathic, primary or secondary tumors, neurosurgery and trauma.