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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyponatraemia (HN) can result from a wide range of mechanisms, and therapy must be individualized. Two theories of the origin of HN in acute brain disease have prevailed. The first is the cerebral salt wasting syndrome (CSWS), where excessive natriuresis caused by some unknown cerebral natriuretic factor lowers the total sodium pool of the body and hence the plasma concentration. The second theory is the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), where an increase in total body water is caused by unphysiological secretion of ADH, lowering the concentration of sodium in the plasma. A third possibility is 'sodium shift', i.e. a displacement of sodium from the extracellular to the intracellular space with a simultaneous movement of potassium in the opposite direction. The morbidity and mortality associated with HN only arise in cases where the rate of development of HN was 0.5 mmol h-1 or more. Symptoms respond promptly when the HN is quickly corrected with furosemide and 3% sodium chloride.
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PMID:Hyponatraemia in acute brain disease. 132 60

A thirty-year-old male patient suffered subarachnoidal haemorrhage from an angioma positioned in the cranio-cervical transition. After rebleeding twice the patient developed a hydrocephalus internus malresorptivus and excessive natriuresis and polyuria, accompanied by depressed renin activity and extremely low aldosterone plasma levels. Neither fluid restriction and sodium substitution, nor administration of hydro-chlorothiazide/indomethacin affected natriuresis and polyuria. It was only after treatment with fludrocortisone-acetate/hydrocortisone that hyponatraemia and polyuria were resolved. At the same time a ventriculo-peritoneal shunt was applied. Differential diagnosis excluded the syndromes of inadequate antidiuretic hormone secretion, renal and cerebral diabetes insipidus, osmotic receptor hypofunction, chronic renal dysfunction and tubular necrosis. Natriuresis and polyuria developed under dexamethasone therapy. Since patient history, physical examination and laboratory criteria could not explain the electrolyte and fluid imbalance, this might be attributed to the hydrocephalus. Similar disturbances have been reported from other patients with intracranial disorders. Mechanical pressure exercised on the hypothalamus might cause the disturbance of fluid and sodium balance. Assuming a cerebral salt wasting syndrome, a putative natriuretic factor coming from the brain or an imbalance in the cerebral renin-angiotensin-system, as described in rats and dogs, must be discussed.
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PMID:[Massive natriuresis and polyuria after triple craniocervical subarachnoid hemorrhage: cerebral salt wasting syndrome?]. 148 43

The main objective of our study was to evolve a practical management protocol for neurosurgical patients with hyponatremia and natriuresis, based on their blood volume status and hematocrit. Twenty-one patients with hyponatremia and natriuresis and 3 control patients were studied. Patients with hyponatremia were categorized on the basis of their hematocrit, central venous pressure, and total blood volume. Group A consisted of patients with hypovolemia and anemia (16 patients); Group B patients had hypovolemia but no anemia (5 patients); Group C included those with hypervolemia (0 patients). Patients in Groups A and B received isotonic saline (> 50 ml/kg/d) and oral salt (12 g/d). Additionally, those in Group A were transfused with 500 ml of whole blood. The end points in the study were 72 hours after entry or two consecutive serum sodium values of > 130 mEq/L, whichever was earlier. Hyponatremia was corrected in all the patients within 72 hours (1 patient, < 24 h; 13 patients, < 48 h; and 7 patients, < 72 h). We conclude that most neurosurgical patients with hyponatremia and natriuresis have hypovolemia, with or without anemia. Fluid and salt replacement and a blood transfusion rather than fluid restriction often results in the correction of the hyponatremia. Our findings offer indirect evidence to support the hypothesis that in most of these patients, hyponatremia is caused by cerebral salt wasting syndrome, rather than the syndrome of inappropriate secretion of antidiuretic hormone.
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PMID:Management of neurosurgical patients with hyponatremia and natriuresis. 817 88

The present study was undertaken to determine the pathophysiological role of arginine vasopressin (AVP) in elderly patients with hyponatremia, and the efficacy of fludrocortisone acetate in treating their hyponatremia. Eleven hospitalized patients aged 65 years or older whose serum sodium levels were less than 130 mEq/l were examined. The hyponatremic patients included two groups of patients: syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and central salt-wasting syndrome. And 24 healthy, young subjects aged 20 to 34 years, and 24 healthy, elderly subjects age 65 to 80 years were recruited by community announcement. The elderly subjects had decreased urinary concentrating ability and exaggerated response of AVP secretion to osmotic and nonosmotic stimuli, as compared to the young subjects. All the patients had hyponatremia, with the exaggerated urinary loss of Na. Plasma AVP levels were elevated despite hypoosmolality in all the 2 groups of hyponatremic, elderly patients. Plasma renin activity and plasma aldosterone concentrations were low in the patients with SIADH and central salt-wasting syndrome. Fludrocortisone acetate therapy was effective in the patients with central salt-wasting syndrome and 3 patients with SIADH whose hyponatremia remained unchanged after water restriction. Water restriction therapy normalized serum Na levels in only 3 patients with SIADH. These results indicate that AVP is involved in the mechanism for hyponatremia in the elderly patients with SIADH and central salt-wasting syndrome. Severe hyponatremia associated with SIADH and central salt-wasting syndrome responds well to mineralocorticoid therapy. Both the secretion of AVP and renal sodium handling may be involved in the mechanism of action of the disorders. The diagnostic criteria for SIADH in the elderly patients may have to be reevaluated and should be considered to indicate fludrocortisone acetate therapy.
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PMID:Involvement of arginine vasopressin and renal sodium handling in pathogenesis of hyponatremia in elderly patients. 873 59

A female aged 53 years was found to have a suprasellar lesion, which was shown to be a Rathke's cyst after removal by transsphenoidal surgery. She presented 16 days postoperatively, and following two grand mal seizures was found to be profoundly hyponatraemic (sodium 101 nmol/l). She was initially thought to have the syndrome of inappropriate antidiuretic hormone and was treated accordingly, but central venous pressure measurement revealed the hypovolaemia of cerebral salt wasting syndrome. The patient subsequently developed severe neurological sequelae after the correction of her hyponatraemia, following the development of extrapontine myelinolysis. Cerebral salt wasting syndrome is a rare cause of hyponatraemia following pituitary transsphenoidal surgery, which may mimic the syndrome of inappropriate antidiuretic hormone secretion. This case emphasizes the poor prognosis that may result from the rapid correction of profound hyponatraemia.
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PMID:Hyponatraemia secondary to cerebral salt wasting syndrome following routine pituitary surgery. 881 Jul 41

Hyponatremia is a common complication after subarachnoid hemorrhage (SAH). Although the mechanism of hyponatremia is still controversial, cerebral salt-wasting syndrome (CSNS) is currently regarded as being more responsible than the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). The aim of our study was to assess the plasma volume status of a patient with hyponatremia following subarachnoid hemorrhage. In doing this it may be possible to indirectly differentiate its pathogenesis. Fifty patients with SAH were studied. Twenty patients demonstrated hyponatremia (serum sodium < 135 mEq/L) during day 7 to 13 after subarachnoid hemorrhage. Patients with hyponatremia were categorized on the basis of their daily body weight, and central venous pressure. Group A consisted of patients with hypovolemia (16 patients), with the onset time of hyponatremia being day 7 to 9. Group B included those with hypervolemia (4 patients); hyponatremia was observed during day 10 to 11 and was corrected in all patients within 72 hours after induction of fluid restriction. Our findings suggest that hyponatremia following subarachnoid hemorrhage usually occurs due to CSWS, although SIADH remains as a minor pathogenesis. We conclude that the combination of daily body weight and CVP measurements is a simple and practical method to distinguish promptly SIADH from CSWS.
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PMID:[Differential diagnosis of hyponatremia following subarachnoid hemorrhage]. 963 2

Authors deal in detail with the pathophysiology of the osmolal regulation. Besides hyperosmolality the secretion of antidiuretic hormone (ADH) in increased by hypovolemia and hypotension. Secretion of ADH is lowered in hypoosmolal states. All other mechanisms are preferebly volume regulating and they influence mainly retention and excretion of sodium. Authors discuss homeostatic effects of the renin-angiotensin-aldosteron system, effects of renal failure with prevailing glomerular or tubular function disorder, impact of diuretics, natriuretic peptides, digitalis-like hormone, urodilantin and influence of the other solutes. Disorders of the effective osmolality regulation are frequent in the cerebral affections that originate from trauma, vascular disease, inflammation or tumors. Hypoosmolality and hyponatremia are presented in two different conditions: Inappropriate Vasopressin Secretion Syndrome (IADHS) and Cerebral Salt Wasting Syndrome (CSWS). Quick differential diagnose is important because the treatment of both syndromes is essentially different. Typical cause of hypernatremia is central diabetes insipidus (DI). The group of available calculated renal function parameters is applied in the differential diagnosis of these syndromes. They are creatinin clearance, excretion fraction of water and sodium, electrolyte clearance and electrolyte free water clearance. Investigation of ADH and natriuretic peptide could be even misleading. Pathophysiologic consequence of the state given by inappropriate elevation of one hormone can be the elevation of the second one.
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PMID:[Disturbances of effective osmolality regulation in disorders of the central nervous system and possible methods of monitoring]. 974 51

Uric acid metabolism is reviewed as it relates mainly to kidney and electrolyte disorders, with emphasis on the difficulties in understanding urate transport because of its bidirectional transport and the species differences in which animal data may not have relevance to the human condition. A critical review of the effects of pyrazinamide and extracellular volume expansion on urate transport raises questions about the current popular teachings that pyrazinamide exclusively blocks tubule urate secretion and extracellular volume expansion has a major role in controlling urate excretion. There appears to be a renal salt-wasting syndrome with overlapping clinical features that make it indistinguishable from the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), except possibly for extracellular volume depletion. Hypouricemia and the elevation in the fractional excretion of urate (%E/Furate) are extensively reviewed with a proposal to use the persistence of hypouricemia and elevated %E/Furate after the correction of hyponatremia to differentiate these patients from those with SIADH. An algorithm is proposed to differentiate one group from the other. A plasma natriuretic factor has been shown in some with probable renal salt wasting, which includes patients with AIDS, cancer, and pulmonary and intracranial diseases. The natriuretic factor may have etiologic implications and diagnostic and therapeutic applications.
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PMID:Regulation of renal urate excretion: a critical review. 1046 75

A four-year-old girl suffered difficult-to-diagnose hyponatremia resistant to treatment following surgery for a suprasellar tumor. The final diagnosis was diabetes insipidus evolving in three stages. Hyponatremia is a common problem following surgery to remove brain tumors. Early diagnosis and treatment of this electrolytic imbalance are essential for preventing serious neurological symptoms or death. The conditions most closely related to hyponatremia are inappropriate antidiuretic hormone secretion syndrome (IADHSS) and cerebral salt wasting syndrome (CSWS). The latter has become more common in recent years among patients undergoing brain surgery. Whereas IADHSS is treated by restricting fluids, CSWS requires administration of salt and volume fluid volume. We believe that for differential diagnosis of postoperative hyponatremia, a fluid restriction test takes priority over of fluid loading following neurosurgery. The course of hyponatremia must be carefully monitored and a complete endocrinological workup must be performed to detect the possible presence of hypophyseal deficiencies, particularly hypothyroidism and suprarenal insufficiency.
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PMID:[Hyponatremia in the postoperative period after a neurosurgical tumor condition]. 1007 82

Cerebral salt-wasting syndrome (CSWS) has been regarded as a misnomer of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). We take the position that CSWS does exist and might be more common than SIADH. Differentiation between groups has been difficult because of overlapping signs, symptoms, and associated diseases. Euvolemia in SIADH and hypovolemia in CSWS may be the only contrasting variables. However, clinical assessment of extracellular volume is accurate in about 50% of these patients. Determination of serum urate and fractional excretion rates of urate can differentiate one group from the other. In both groups, hyponatremia coexists with hypouricemia and increased fractional excretion of urate. When the hyponatremia is corrected by water restriction, hypouricemia and elevated FEurate correct in SIADH but persist in CSWS. Persistent hypouricemia and elevated FEurate were commonly noted with pulmonary and/or intracranial diseases. The absence of intracranial diseases in some patients suggests that renal salt wasting might be a more appropriate term than CSWS. A review of renal/CSWS reveals three studies involving hyponatremic neurosurgical patients who had decreased blood volume, decreased central venous pressure, and inappropriately high urinary sodium concentrations in the majority of them, suggesting that CSWS was more common than SIADH in neurosurgical patients. Evidence for the presence of a plasma natriuretic factor in CSWS is presented.
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PMID:Cerebral salt-wasting syndrome: does it exist? 1036


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