Osmoregulation of Vasopressin Secretion in Patients with the Syndrome of Inappropriate Antidiuresis Associated with Central Nervous System Disorders.

Kamoi, Kyuzi; Toyama, Makoto; Takagi, Masaaki; Koizumi, Takayuki; Niishiyama, Ken-Ichi; Takahashi, Kinoe; Sasaki, Hideo; Muto, Terukazu

doi:10.1507/endocrj.46.269

Cited by 17 publications

(22 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Kamoi et al 8 observed this syndrome in patients with CNS disorders: subdural hematomas, closed head injury, epilepsy and ischemic cerebrovascular accident. Patients with SIADH and CNS disorders may present persistent AVP secretion with loss of hypotonic suppression, indicating that a careful assessment is required to determine the relationship between persistent AVP secretion and the pathogenesis of hyponatremic disorders 8 .…”

Section: Discussionmentioning

confidence: 98%

See 1 more Smart Citation

Vasopressin serum levels in patients with severe brain lesions and in brain-dead patients

Cintra

Maciel

Araújo

et al. 2004

Arq. Neuro-Psiquiatr.

View full text Add to dashboard Cite

-Introduction: Patients with severe brain lesions (SBL) and brain-dead patients (BD) frequently present with vasopressin (AVP) secretion disorders. Objective: To evaluate AVP serum levels in SBL and BD patients. Design: Prospective, open label, observational trial. Setting: A general teaching hospital. Method:Three groups of adult subjects (age ≥ 18y) of both sexes were included in this study: control group: 29 healthy volunteers; SBL group: 17 patients with Glasgow Coma Scale (GCS) ≤8; and BD group: 11 brain-dead patients. Samples of venous blood were collected in the morning at rest from healthy volunteers and at 8 hourly intervals over a period of 24h from SBL and BD patients for AVP determinations. Concomitantly, some clinical and laboratorial variables were also recorded. Results: AVP serum levels (pg/ml) were [mean (SD); median]: control [2.2(1.1); 2.0]; SBL [5.7(6.3); 2.9]; and BD [2.6(1.0); 2.8]. AVP serum levels varied greatly in SBL patients, but without statistically significant difference in relation to the other groups (p=0.06). Hypotension (p=0.02), hypernatremia (p=0.0001), serum hyperosmolarity (p=0.0001) and urinary hypoosmolarity (p=0.003) were outstanding in BD patients when compared with SBL. Conclusions: The AVP serum levels did not demonstrate significant statistical difference between the groups, only showing a greater variability in SBL patients (manifested as serum spike levels). Hypernatremia and hyperosmolarity were present in BD patients, indicating a failure of the hypothalamic-pituitary system in AVP production and release.KEY WORDS: brain lesion, brain death, vasopressin. Níveis séricos de arginina vasopressina em pacientes com lesão cerebral grave e em pacientes com morte encefálicaRESUMO -Introdução: Pacientes com lesão cerebral grave (LCG) ou com morte encefálica (ME) freqüentemente apresentam alterações na secreção de vasopressina (AVP). Objetivo: Avaliar os níveis séricos de AVP em pacientes com LCG e ME. Desenho: Estudo prospectivo, aberto, observacional. Local: Um hospital geral universitário. Método: Sujeitos adultos (idade ≥18 anos), de ambos os sexos, foram divididos em três grupos: grupo controle: 29 voluntários sadios; grupo LCG: 17 pacientes com pontuação na Escala de Coma de Glasgow (ECG) ≤8; grupo ME: 11 pacientes com diagnóstico de ME.Amostras de sangue venoso foram colhidas pela manhã, em repouso, nos pacientes do grupo controle, e de 8/8h, por 24h, nos pacientes dos grupos LCG e ME, para dosagens de AVP. Variáveis clínicas e laboratoriais de interesse foram anotadas concomitantemente. Resultados: Os valores da AVP (pg/ml) foram [média (DP); mediana]: grupo controle [2,2(1,1); 2,0]; grupo LCG [5,7(6,3); 2,9] e grupo ME [2,6(1,0); 2,8]. Observouse maior variação dos níveis séricos de AVP no grupo LCG, mas sem diferença estatisticamente significativa em relação aos demais (p=0,06). Hipotensão (p=0,02), hipernatremia (p=0,0001), hiperosmolaridade sérica (p=0,0001) e hiposmolaridade urinária (p=0,003) foram proeminentes no grupo ME em relação ao grupo LCG. Con...

show abstract

Section: Discussionmentioning

confidence: 98%

“…However, these disorders still need to be clarified 8,9 . Currently, no consensus has been found in the literature regarding the behavior of AVP in patients with SBL and in those with brain death.…”

mentioning

confidence: 99%

Vasopressin serum levels in patients with severe brain lesions and in brain-dead patients

Cintra

Maciel

Araújo

et al. 2004

Arq. Neuro-Psiquiatr.

View full text Add to dashboard Cite

show abstract

“…Changes in blood volume were determined from the changes in hematocrit using the formula BV2/BV1=Hct1/ Hct2, assuming no changes in circulating erythrocyte volume. 30 …”

Section: Clinical and Biochemical Assessmentmentioning

confidence: 99%

A Copeptin-Based Classification of the Osmoregulatory Defects in the Syndrome of Inappropriate Antidiuresis

Fenske

Christ‐Crain

Hörning

et al. 2014

Journal of the American Society of Nephrology

View full text Add to dashboard Cite

Hyponatremia, the most frequent electrolyte disorder, is caused predominantly by the syndrome of inappropriate antidiuresis (SIAD). A comprehensive characterization of SIAD subtypes, defined by type of osmotic dysregulation, is lacking, but may aid in predicting therapeutic success. Here, we analyzed serial measurements of serum osmolality and serum sodium, plasma arginine vasopressin (AVP), and plasma copeptin concentrations from 50 patients with hyponatremia who underwent hypertonic saline infusion. A close correlation between copeptin concentrations and serum osmolality existed in 68 healthy controls, with a mean osmotic threshold6SD of 28264 mOsM/kg H 2 O. Furthermore, saline-induced changes in copeptin concentrations correlated with changes in AVP concentrations in controls and patients. With use of copeptin concentration as a surrogate measure of AVP concentration, patients with SIAD could be grouped according to osmoregulatory defect: Ten percent of patients had grossly elevated copeptin concentrations independent of serum osmolality (type A); 14% had copeptin concentrations that increased linearly with rising serum osmolality but had abnormally low osmotic thresholds (type B); 44% had normal copeptin concentrations independent of osmolality (type C), and 12% had suppressed copeptin concentrations independent of osmolality (type D). A novel SIAD subtype discovered in 20% of patients was characterized by a linear decrease in copeptin concentrations with increasing serum osmolality (type E or "barostat reset"). In conclusion, a partial or complete loss of AVP osmoregulation occurs in patients with SIAD. Although the mechanisms underlying osmoregulatory defects in individual patients are presumably diverse, we hypothesize that treatment responses and patient outcomes will vary according to SIAD subtype.

show abstract

“…She received hysterectomy for myoma uteri at the age of 40 years in Yukiguni-Yamato General Hospital. At the time, she was diagnosed as primary polydipsia with bilateral non-obstructive hydronephrosis as shown by drip infusion pyerography, since she had normal level of plasma AVP concentration (0.6 pg/ml) as measured by the RIA method previously reported [12][13] although she had polyuria (5000-7000 ml/day) and polydipsia (5000-7000 ml/ day). Before admission, she received Ca ++ antagonist for hypertension.…”

Section: Case Report and Methodsmentioning

confidence: 95%

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

et al. 2004

Self Cite

View full text Add to dashboard Cite

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.

show abstract

Osmoregulation of Vasopressin Secretion in Patients with the Syndrome of Inappropriate Antidiuresis Associated with Central Nervous System Disorders.

Cited by 17 publications

References 30 publications

Vasopressin serum levels in patients with severe brain lesions and in brain-dead patients

Vasopressin serum levels in patients with severe brain lesions and in brain-dead patients

A Copeptin-Based Classification of the Osmoregulatory Defects in the Syndrome of Inappropriate Antidiuresis

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

Contact Info

Product

Resources

About