scholarly journals Arginine Vasopressin-Independent Mechanism of Impaired Water Excretion in a Patient with Sarcoidosis Complicated by Central Diabetes Insipidus and Glucocorticoid Deficiency

2011 ◽  
Vol 2011 ◽  
pp. 1-5 ◽  
Author(s):  
Katsunobu Yoshioka ◽  
Nagaaki Tanaka ◽  
Keiko Yamagami ◽  
Takeshi Inoue ◽  
Masayuki Hosoi
Keyword(s):  
Diabetes Insipidus ◽  
Hypertonic Saline ◽  
Arginine Vasopressin ◽  
Plasma Levels ◽  
Human Study ◽  
Urine Osmolality ◽  
Water Excretion ◽  
Plasma Arginine ◽  
Glucocorticoid Deficiency ◽  
Saline Test

A 28-year-old man was admitted to our hospital because of reduced livido and increased fatigability. Four months before admission, he noticed polyuria, which was gradually relieved by admission. Magnetic resonance imaging revealed enhancing lesion centrally in the pituitary stalk. Biopsy from the skin revealed noncaseating granuloma composed of epithelioid cells, and a diagnosis of sarcoidosis was made. Although plasma arginine vasopressin (AVP) was undetectable after administration of hypertonic saline, urinary output was within normal range (1.5 to 2.2 L/day). The urine osmolality became above plasma levels during the hypertonic saline test. Hormonal provocative tests revealed partial glucocorticoid deficiency. Soon after the glucocorticoid therapy was begun, moderate polyuria (from 3.5–4.0 liters daily) occurred. At this time, plasma AVP was undetectable, and urine osmolality was consistently below plasma levels during the hypertonic saline test. In conclusion, we showed in human study that masked diabetes insipidus could be mediated by AVP-independent mechanisms.

scholarly journals Increases in Plasma ACTH and Cortisol after Hypertonic Saline Infusion in Patients with Central Diabetes Insipidus

2001 ◽  
Vol 86 (12) ◽  
pp. 5749-5754 ◽  
Author(s):  
Eiji Itagaki ◽  
Sachihiko Ozawa ◽  
Shinya Yamaguchi ◽  
Kenji Ushikawa ◽  
Teruaki Tashiro ◽  
...  
Keyword(s):  
Diabetes Insipidus ◽  
Hypertonic Saline ◽  
Plasma Osmolality ◽  
Central Diabetes Insipidus ◽  
Portal System ◽  
Plasma Acth ◽  
Acth Secretion ◽  
Acth Concentration ◽  
Plasma Arginine ◽  
Hypertonic Saline Infusion

To clarify the mechanism for the potentiation of CRH-induced ACTH response by the infusion of hypertonic saline, we investigated changes in plasma ACTH concentration after infusion of 5% hypertonic saline in five patients with untreated central diabetes insipidus (DI). Basal levels of plasma ACTH and cortisol in the DI group were not significantly different from those in normal control subjects. The infusion of hypertonic saline produced an increase in plasma arginine vasopressin (AVP) in controls, but did not elevate ACTH. However, in patients with DI, the plasma AVP concentration did not change, but circulating ACTH increased 3.6-fold (7.7 ± 1.5 to 23.0 ± 2.7 pmol/liter; P < 0.01), and plasma cortisol also increased significantly (298 ± 99 to 538 ± 124 nmol/liter; P < 0.05). Moreover, a positive correlation was observed between plasma ACTH and osmolality (r = 0.72; P < 0.005). These results indicate that ACTH secretion in DI patients is regulated by a mechanism distinct from that in healthy subjects. It seems possible that the increase in plasma osmolality promotes ACTH secretion in DI patients through AVP and/or urocortin via the hypophyseal portal system, independent of the AVP secretion from magnocellular neurons.

Familial hypothalamic diabetes insipidus in rats (Brattleboro strain)

1964 ◽  
Vol 206 (2) ◽  
pp. 425-430 ◽  
Author(s):  
H. Valtin ◽  
H. A. Schroeder
Keyword(s):  
Diabetes Insipidus ◽  
Hypertonic Saline ◽  
Supraoptic Nucleus ◽  
Spontaneous Mutation ◽  
Urine Osmolality ◽  
Urine Flow ◽  
Neurosecretory Material ◽  
Carrier Protein ◽  
Marked Diminution ◽  
Long Evans

Familial hypothalamic diabetes insipidus ( DI) has arisen as an apparently spontaneous mutation from a strain of Long-Evans hooded rats being bred for unrelated researches not involving radioactivity. The DI rats decrease water intake and urine flow, and increase urine osmolality in response to injected vasopressin. They concentrate their urines only minimally or not at all in response to dehydration, hypertonic saline, nicotine, or stress, and their serum osmolalities and sodium concentrations are significantly higher than those of normal animals. They show marked diminution of neurosecretory material in the neurohypophysis and supraoptic nucleus. The data suggest that the deficiency causing DI in these rats is a lack or dearth of synthesis of vasopressin or its carrier protein, or both.

Abnormalities in the response of plasma arginine vasopressin during hypertonic saline infusion in patients with eating disorders

1989 ◽  
Vol 26 (1) ◽  
pp. 73-86 ◽  
Author(s):  
J.Ken Nishita ◽  
Everett H. Ellinwood ◽  
W.J.Kenneth Rockwell ◽  
Cynthia M. Kuhn ◽  
Graham W. Hoffman ◽  
...  
Keyword(s):  
Eating Disorders ◽  
Hypertonic Saline ◽  
Arginine Vasopressin ◽  
Saline Infusion ◽  
Plasma Arginine ◽  
Hypertonic Saline Infusion

Plasma vasopressin and atrial natriuretic hormone levels in hypopituitarism with and without hydrocortisone treatments: responses to an acute water load

1992 ◽  
Vol 126 (3) ◽  
pp. 217-223 ◽  
Author(s):  
Tokihisa Kimura ◽  
Kozo Ota ◽  
Masaru Shoji ◽  
Minoru Inoue ◽  
Kazutoshi Sato ◽  
...  
Keyword(s):  
Arginine Vasopressin ◽  
Plasma Osmolality ◽  
Normal Subjects ◽  
Natriuretic Hormone ◽  
Water Load ◽  
Blood Volume Expansion ◽  
Atrial Natriuretic Hormone ◽  
Plasma Arginine ◽  
Glucocorticoid Deficiency ◽  
Atrial Natriuretic

To assess whether arginine vasopressin and atrial natriuretic hormone participate in impaired urinary dilution and excretion in glucocorticoid deficiency secondary to hypopituitarism. an acute oral water load of 20 ml·kg−1 BW was undertaken in the absence and presence of an oral hydrocortisone (60 mg) treatment in patients with ACTH deficiency (N= 7) and panhypopituitarism (N = 2). Plasma arginine vasopressin and atrial natriuretic hormone and renal water handling were simultaneously determined and compared with those in similarly water-loaded normal subjects. Plasma arginine vasopressin did not fall in response to decreased blood osmolality after an acute water load in the absence of hydrocortisone; plasma atrial natriuretic hormone did not change despite blood volume expansion; and impairment in urinary dilution and excretion remained. On the other hand, in the presence of hydrocortisone, plasma arginine vasopressin fell in response to a decrease in plasma osmolality and plasma atrial natriuretic hormone increased, thereby restoring urinary dilution and excretion. These results demonstrate that the impaired arginine vasopressin response to acute water loading play an essential role in deranged renal water and electrolyte handling in the state of glucocorticoid deficiency; the impaired release of atrial natriuretic hormone also may affect these disorders.

Regulation of vasopressin secretion in a patient with chronic hypernatraemia

1985 ◽  
Vol 110 (3) ◽  
pp. 346-351 ◽  
Author(s):  
Simon Smitz ◽  
Jean-Jacques Legros
Keyword(s):  
Hypertonic Saline ◽  
Arginine Vasopressin ◽  
Plasma Osmolality ◽  
Concomitant Increase ◽  
Specific Radioimmunoassay ◽  
Vasopressin Secretion ◽  
Plasma Arginine ◽  
The Brain ◽  
Unrestricted Diet ◽  
Hypertonic Saline Infusion

Abstract. A patient with the chronic hypernatraemia syndrome is described. Using a sensitive and specific radioimmunoassay, the plasma arginine-vasopressin (AVP) level was measured under various conditions. With an unrestricted diet, the plasma AVP level was inappropriately low for the degree of plasma hyperosmolality (0.9 pmol/l and 302 mOsm/kg, respectively). After chronic water loading, plasma osmolality was 271 mOsm/kg, plasma AVP level 1.5 pmol/l, and the urine remained hypertonic with respect to the plasma. During hypertonic saline infusion, plasma osmolality increased from 271 to 294 mOsm/kg without a concomitant increase in the plasma AVP concentration. After sc injection of apomorphine and after haemodynamic stimulation, the plasma AVP concentration increased from 0.8 to 36 pmol/l and from 1.2 to 6.3 pmol/I, respectively. These data demonstrate a selective deficiency in the osmoregulation of the AVP secretion. The observed neuroendocrine abnormalities may be linked to a congenital malformation of the brain.

scholarly journals Unmasking of Neurosarcoidosis

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A618-A618
Author(s):  
Sharini Venugopal ◽  
Binita Neupane ◽  
Mahesh Nepal ◽  
Luis F Chavez
Keyword(s):  
Diabetes Insipidus ◽  
Medical History ◽  
Case Reports ◽  
Rare Complication ◽  
Case Series ◽  
Primary Hypothyroidism ◽  
Past Medical History ◽  
Water Excretion ◽  
History Of ◽  
Glucocorticoid Deficiency

Abstract Introduction: Central diabetes insipidus is a rare complication of neurosarcoidosis. In patients with concomitant adrenal insufficiency (AI), the symptoms of Diabetes Insipidus (DI) can be masked. Case: A 55-year-old female with past medical history of sarcoidosis presented to the hospital with hematemesis, nausea and dizziness. She has a past medical history of cardiac sarcoidosis that was revealed on a PET scan done before 10 years for which she was being treated with methotrexate and prednisone. She was off prednisone for a year prior to hospitalization. She underwent an upper endoscopy that showed diffusely erythematous gastric mucosa in the antrum. She was also hypotensive on admission, and she received packed red blood transfusions after which her sodium increased from 145mmol/L to 165mmol/L (Normal: 135-145mmol/L) in 48 hours. Further workup revealed persistent hypernatremia and urine osmolality was 75mOsm/kg H2O. (Normal: 50-1200mOsm/kg H2O). She was also hypoglycemic and hypotensive requiring multiple fluid boluses throughout her hospitalization. This prompted us to perform a random cortisol that came back at 2.1ug/dl (Normal: 3-23ug/dl) and 1.8ug/dl on two occasions. Cortisol Stimulation test was subsequently ordered, but was done only at 30 minutes, and Cortisol increased from 1.8ug/dl to 6.3ug/dl. Free thyroxine was 0.5 ng/dl (Normal: 0.9-1.8 ng/dl) and her TSH was 7.58uIU/ml (Normal: 0.55-4.78uIU/ml). MRI of the brain revealed extensive areas of extra-axial supra-sellar/infundibular nodular homogeneous intense enhancement that is most consistent with neuro-sarcoid. She was started on prednisone 40 mg daily, Desmopressin 0.05 mg twice daily, and levothyroxine as well. Her sodium level normalized and was 137mmol/L at discharge. She followed up later with outpatient Endocrinology and reported around 90lbs weight gain and no more episodes of nausea or vomiting or epistaxis or lightheadedness. Conclusion: The involvement of the hypothalamic-pituitary axis in sarcoidosis is extremely rare and attributes to < 1% of patients with a sellar mass. Small case series have shown that hypogonadism is the most common endocrine abnormality followed by DI. Our patient had a long-standing history of sarcoidosis with her pituitary dysfunction unmasked only on admission for other causes. She did not manifest any symptoms of DI or AI. There have been case reports where the symptoms of DI are masked due to underlying glucocorticoid deficiency. There have been theories that glucocorticoid deficiency impairs renal water excretion by both ADH (Anti-diuretic hormone) dependent and ADH independent pathways. Another notable feature in our case is that our patient presented with primary hypothyroidism. In fact, sarcoidosis has been commonly implicated in auto-immune polyglandular syndromes type 3, which can present with auto-immune thyroiditis more so in females.

Plasma vasopressin responses in postpartum hypopituitarism: impaired response to osmotic stimuli

1992 ◽  
Vol 127 (6) ◽  
pp. 494-498 ◽  
Author(s):  
MA Arnaout ◽  
K Ajlouni
Keyword(s):  
Diabetes Insipidus ◽  
Hypertonic Saline ◽  
Arginine Vasopressin ◽  
Plasma Osmolality ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Plasma Vasopressin ◽  
Basal Plasma ◽  
The Mean ◽  
Thyroxine Replacement Therapy

The neurohypophyseal function was assessed in a group of 15 patients with postpartum hypopituitarism by measuring plasma arginine-vasopressin concentrations during 5% hypertonic saline infusion. None of the patients had symptoms of diabetes insipidus and all patients were on adequate cortisone and thyroxine replacement therapy before testing. The mean basal plasma vasopressin value in the patients (0.6±0.1 pmol/1) was significantly lower than that in the normal subjects (2.9±0.3 pmol/l; p<0.01), whereas the mean serum sodium, plasma osmolality, plasma renin activity and serum aldosterone values were similar in the two groups. During the osmolar load (5% hypertonic saline), the patients revealed varying degrees of arginine-vasopressin responses to the increase in plasma osmolality. Three patients showed normal arginine-vasopressin responses, 10 had subnormal responses, and 2 had no response. During the dehydration test, the patients revealed significantly lower maximum urine osmolalities (p<0.0025) with significantly higher concurrent mean plasma osmolality (p<0.0025) than the controls. None of the patients showed overt polyuria at the time of the study. The results indicate the impaired osmoregulation of arginine-vasopressin secretion to an osmolar stimuli in patients with postpartum hypopituitarism, suggesting neurohypophyseal damage. In patients with Sheehan's syndrome, partial diabetes insipidus seems to be much more frequent than previously believed.

Oral hypertonic saline causes transient fall of vasopressin in humans

1986 ◽  
Vol 251 (2) ◽  
pp. R214-R217 ◽  
Author(s):  
J. R. Seckl ◽  
T. D. Williams ◽  
S. L. Lightman
Keyword(s):  
Drinking Water ◽  
Plasma Renin Activity ◽  
Hypertonic Saline ◽  
Arginine Vasopressin ◽  
Total Protein ◽  
Tap Water ◽  
Plasma Osmolality ◽  
Plasma Renin ◽  
Oral Rehydration ◽  
Plasma Arginine

After dehydration, oral rehydration causes a fall in plasma arginine vasopressin (AVP) that precedes changes in plasma osmolality. To investigate further the stimulus for this effect, its specificity, and association with thirst, six volunteers were deprived of water for 24 h and given a salt load on two separate occasions. On each study day they then drank rapidly 10 ml/kg of either tap water or hypertonic saline (360 mosmol/kg). There was a significant fall in plasma AVP from 2.0 +/- 0.3 to 1.2 +/- 0.4 pmol/l (P less than 0.05) 5 min after drinking water and from 1.8 +/- 0.3 to 0.9 +/- 0.2 pmol/l (P less than 0.05) after hypertonic saline. Plasma osmolality fell 30-60 min after water and was unchanged after saline. Plasma renin activity, oxytocin, and total protein all remained unchanged. All subjects reported diminished thirst after hypertonic saline. Gargling with water reduced thirst but did not affect plasma AVP. There appears to be a drinking-mediated neuroendocrine reflex that decreases plasma AVP irrespective of the osmolality of the liquid consumed. The sensation of thirst did not correlate with plasma osmolality and was not always related to plasma AVP concentration.

Hyponatraemia in quadriplegic patients

1988 ◽  
Vol 75 (4) ◽  
pp. 441-444 ◽  
Author(s):  
David J. Leehey ◽  
Alicia A. Picache ◽  
Gary L. Robertson
Keyword(s):  
Arginine Vasopressin ◽  
Fluid Intake ◽  
Plasma Osmolality ◽  
Free Water ◽  
Plasma Sodium ◽  
Free Water Clearance ◽  
Water Excretion ◽  
Water Load ◽  
Daily Urine ◽  
Plasma Arginine

1. Studies were performed in five hyponatraemic (plasma sodium 129 ±1.6 mmol/l; plasma osmolality 268 ±3.0 mosmol/kg) quadriplegic patients in order to elucidate its aetiology. Five age- and sex-matched healthy subjects served as controls. 2. Daily urine volumes were high (4454 ± 624 ml) in the quadriplegic patients secondary to habitually increased fluid intake. 3. All quadriplegic patients had suppressed plasma arginine vasopressin levels (< 0.8 pmol/l) and were able to form dilute urine after a water load (20 ml/kg). However, free water clearance and the ability to excrete the water load were frequently impaired, and these defects were associated with reductions in both osmolar clearance and delivery of filtrate to the distal diluting sites of the nephron. 4. During hypertonic saline (5%, w/v, NaCl) infusion, plasma arginine vasopressin rose progressively before plasma osmolality reached the normal range, consistent with a resetting of the osmostat. 5. We conclude that hyponatraemia in quadriplegic patients is related to an intrarenal defect in water excretion and resetting of the osmostat coupled with increased fluid intake.

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