Prolonged antidiuresis by 1-desamino-8-D-arginine vasopressin (DDAVP): Correlation to its plasma levels and nephrogenous cyclic AMP production.

Katayama, Shigehiro; Itabashi, Akira; Yamaji, Taketo

doi:10.1507/endocrj1954.27.363

Cited by 5 publications

(2 citation statements)

References 14 publications

(23 reference statements)

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“…This may be explained by the decreased sensitivity of plasma AVP to renal tubules due to a long-term deficiency of AVP secretion. In this case, the increase in urine osmolality and the decrease in free water clearance 4 hours after nasal administration of DDAVP was half as compared with those using the same method as this case in patients with NDI reported by Katayama et al [21], indicating that the response of plasma AVP to renal tubules was diminished.…”

Section: Discussionsupporting

confidence: 59%

“…Indeed, the lack of Glu-47 enhances dimerization or tetramerization of the neurophysin molecule and accumulates large amounts of mutant prohormone in the endoplasmic reticulum with the resulting that stimulated secretion of stored AVP is impaired as in the state of osmoreceptor defect of type 2 [11]. In this case, administration of DDAVP suppressed plasma AVP concentration and its response to urinary concentration diminished in comparison with that in other patients with NDI [21], indicating functions of secretion and activity of AVP may be normally reserved.…”

Section: Discussionmentioning

confidence: 90%

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Novel Mutant Vasopressin-neurophysin II Gene Associated with Familial Neurohypophyseal Diabetes Insipidus

et al. 2004

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Abstract. We describe a novel missense mutant of arginine vasopressin (AVP)-dependent neurohypophyseal diabetes insipidus in an autosomal dominant family. A 54-year-old woman was admitted to our hospital because of thyroidectomy for thyroid cancer. After thyroidectomy she was found to have hypernatremia and polyuria and polydipsia both of which had been present from childhood. She had no obstructive hydronephrosis. Her father, father's younger sister and her third son also had polyuria and polydipsia. Basal plasma AVP concentration at normal plasma osmolality was normal but did not respond to increased plasma osmolality despite hyperosmolality during infusion of hypertonic saline infusion, indicating that plasma AVP secretion was impaired. Sodium concentration in urine and urine osmolality were low and increased after nasal administration of DDAVP. There was a diminished but bright signal of pituitary posterior gland on magnetic resonance T1 weighted image. Molecular genetic analysis demonstrated that the patient and her son had a single heterozygous missense mutation (G®A) at nucleotide 1829 in 1 AVP allele, yielding an abnormal AVP precursor with lacking Glu-47 in its neurophysin II moiety. The abnormal AVP precursor may be related to the impaired AVP secretion.

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Section: Discussionsupporting

confidence: 59%

Section: Discussionmentioning

confidence: 90%