Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although the aldosterone-responsive segments of the nephron together reabsorb <10% of the filtered Na+, certain single-gene defects that affect the epithelial Na+ channel (ENaC) in the luminal membrane of the collecting duct (CD) or its regulation by aldosterone cause severe hypertension, whereas others cause salt wasting and hypotension. These rare defects illustrate the key role of the distal nephron in maintaining normal extracellular volume and blood pressure. Genetic defects that increase the Cl- conductance of the junctional complexes may also lead to salt retention and hypertension. Less dramatic alterations in regulatory actions of other hormones such as vasopressin (VP), either alone or with other genetic variations, diet, or environmental factors, may also produce Na+ retention or loss. Although VP acts primarily to regulate water balance, it is also an antinatriuretic hormone. Elevated basal plasma VP levels, and/or augmented VP release with increased Na+ intake, have been linked to essential hypertension in humans and in animal models of congestive heart failure and cirrhosis. Norepinephrine, dopamine, and prostaglandin E2 can inhibit the antinatriuretic effects of VP, and changes in the actions of these autocrine and paracrine regulators may also be involved in abnormal regulation of Na+ reabsorption.
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PMID:Abnormal regulation of ENaC: syndromes of salt retention and salt wasting by the collecting duct. 1211 May 5

The syndromes of inappropriate antidiuretic hormone secretion (SIADH) and cerebral salt wasting (CSW) are two potential causes of hyponatremia is patients with disorders of the central nervous system. Distinguishing between these two causes can be challenging because there is considerable overlap in the clinical presentation. The primary distinction lies in the assessment of the effective arterial blood volume (EABV). SIADH is a volume-expanded state because of antidiuretic hormone-mediated renal water retention. CSW is characterized by a contracted EABV resulting from renal salt wasting. Making an accurate diagnosis is important because the treatment of each condition is quite different. Vigorous salt replacement is required in patients with CSW, whereas fluid restriction is the treatment of choice in patients with SIADH. Although most physicians are familiar with SIADH, they are much less familiar with CSW. This review emphasizes the need for CSW to be included in the differential diagnosis of hyponatremia in a patient with central nervous system disease. Distinguishing between these two disorders is of crucial importance because therapy indicated for one disorder but used in the other can result in negative clinical consequences.
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PMID:Hyponatremia in patients with central nervous system disease: SIADH versus CSW. 1271 79

We describe a case of severe hyponatremia following chemotherapy administration in a patient with small-cell lung cancer. There was no evidence of the syndrome of inappropriate antidiuretic hormone (SIADH) secretion. The clinical and laboratory findings were consistent with a sodium-wasting nephropathy complicating cisplatin administration. There are few well-documented reports of cisplatin-associated hyponatremia in the medical literature. We have summarized the relevant literature and attempted to define the differential diagnosis of hyponatremia in this setting. Most cases are accounted for by sodium-losing nephropathy of SIADH, but many reported cases contain insufficient data for classification. Appropriate attention to the evaluation of hyponatremia following platinum-based chemotherapy is needed to properly treat these conditions.
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PMID:Sodium-wasting nephropathy caused by cisplatin in a patient with small-cell lung cancer. 1466 76

Hyponatremia is frequently encountered in patients who have undergone neurosurgery for intracranial processes. Making an accurate diagnosis between the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and cerebral salt wasting (CSW) in patients in whom hyponatremia develops is important because treatment differs greatly between the conditions. The SIADH is a volume-expanded condition, whereas CSW is a volume-contracted state that involves renal loss of sodium. Treatment for patients with SIADH is fluid restriction and treatment for patients with CSW is generally salt and water replacement. In this review, the authors discuss the differential diagnosis of hyponatremia, distinguish SIADH from CSW, and highlight the diagnosis and management of hyponatremia, which is commonly encountered in patients who have undergone neurosurgery, specifically those with traumatic brain injury, aneurysmal subarachnoid hemorrhage, recent transsphenoidal surgery for pituitary tumors, and postoperative cranial vault reconstruction for craniosynostosis.
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PMID:Hyponatremia in the neurosurgical patient: diagnosis and management. 1519 38

Hyponatremia has been recognized as an important postoperative metabolic complication after central nervous system (CNS) operations in children. If not appropriately treated, the postoperative hyponatremia can cause several types of CNS and circulatory disorders such as cerebral edema, increased intracranial pressure. The postoperative hyponatremia after CNS surgery has been considered as one of the underlying causes of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). In some cases, however, the cerebral salt wasting (CSW) syndrome has been detected. CSW syndrome is far less well-known than SIADH and also different from SIADH in diagnosis and treatment. It causes an increase in urine output and urine sodium after a trauma of CNS and dehydration symptoms. The appropriate treatment of CSW syndrome is opposite the usual treatment of hyponatremia caused by SIADH. The latter is treated with fluid restriction because of the increased level of free water and its dilutional effect causing hyponatremia, whereas the former is treated with fluid and sodium resuscitation because of the unusual loss of high urinary sodium. Early diagnosis and treatment of CSW syndrome after CNS surgery are, therefore, essential. We made a diagnosis of CSW syndrome in two craniosynostosis children manifesting postoperative hyponatremia and supplied them an appropriate amount of water and sodium via intravenous route. The hyponatremia or natricuresis of the children improved and neurologic and circulatory sequelae could be prevented.
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PMID:Two cases of cerebral salt wasting syndrome developing after cranial vault remodeling in craniosynostosis children. 1530 62

Disorders of water balance are well recognized after traumatic brain injury (TBI), but there are no reliable data on their true prevalence in post-TBI patients. We aimed to evaluate the prevalence of posterior pituitary dysfunction in a large cohort of survivors of TBI. One hundred two consecutive patients (85 males) who suffered severe or moderate TBI were evaluated for diabetes insipidus (DI) at a median of 17 months (range 6-36 months) after the event, using the 8-h water deprivation test (WDT). Their results were compared against normative data obtained from 27 matched, healthy controls. Patients' medical records were retrospectively reviewed for the presence of abnormalities of salt and water balance in the immediate post-TBI period. Twenty-two patients (21.6%) developed DI in the immediate post-TBI period (acute DI group), of whom five had abnormal WDT on later testing. In total, seven patients (6.9%) had abnormal WDT (permanent DI group), five of whom had partial DI. Patients in the acute and permanent DI groups were more likely to have more severe TBI, compared with the rest of the cohort (P < 0.05). In the immediate post-TBI period, 13 patients (12.9%) had syndrome of inappropriate secretion of antidiuretic hormone, which persisted in one patient, and one other patient developed cerebral salt wasting. Diabetes insipidus and syndrome of inappropriate secretion of antidiuretic hormone were common in the immediate post-TBI period. Permanent DI was present in 6.9% of patients who survived severe or moderate TBI, which is higher than traditionally thought. Identification of patients with partial posttraumatic DI is important because appropriate treatment may reduce morbidity and optimize the potential for recovery.
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PMID:Posterior pituitary dysfunction after traumatic brain injury. 1557 48

Lithium-induced nephrogenic diabetes insipidus (Li-NDI) is associated with increased urinary sodium excretion and decreased responsiveness to aldosterone and vasopressin. Dysregulation of the epithelial sodium channel (ENaC) is thought to play an important role in renal sodium wasting. The effect of 7-day aldosterone and spironolactone treatment on regulation of ENaC in rat kidney cortex was investigated in rats with 3 wk of Li-NDI. Aldosterone treatment of rats with Li-NDI decreased fractional excretion of sodium (0.83 +/- 0.02), whereas spironolactone did not change fractional excretion of sodium (1.10 +/- 0.11) compared with rats treated with lithium alone (1.11 +/- 0.05). Plasma lithium concentration was decreased by aldosterone (0.31 +/- 0.03 mmol/l) but unchanged with spironolactone (0.84 +/- 0.18 mmol/l) compared with rats treated with lithium alone (0.54 +/- 0.04 mmol/l). Immunoblotting showed increased protein expression of alpha-ENaC, the 70-kDa form of gamma-ENaC, and the Na-Cl cotransporter (NCC) in kidney cortex in aldosterone-treated rats, whereas spironolactone decreased alpha-ENaC and NCC compared with control rats treated with lithium alone. Immunohistochemistry confirmed increased expression of alpha-ENaC in the late distal convoluted tubule and connecting tubule and also revealed increased apical targeting of all three ENaC subunits (alpha, beta, and gamma) in aldosterone-treated rats compared with rats treated with lithium alone. Aldosterone did not, however, affect alpha-ENaC expression in the cortical collecting duct (CCD), which showed weak and dispersed labeling similar to that in rats treated with lithium alone. Spironolactone did not affect ENaC targeting compared with rats treated with lithium alone. This study shows a segment specific lack of aldosterone-mediated alpha-ENaC regulation in the CCD affecting both alpha-ENaC protein expression and trafficking, which may explain the increased sodium wasting associated with chronic lithium treatment.
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PMID:Lithium-induced NDI in rats is associated with loss of alpha-ENaC regulation by aldosterone in CCD. 1633 30

Pre-operative central diabetes insipidus has been reported in 8-35% of patients affected with craniopharyngioma, and in 70-90% after surgery. The management of postoperative polyuria and polydipsia can be challenging and fluid balance needs to be closely monitored. The classical triphasic pattern of endogenous vasopressin secretion--an initial phase of symptomatic diabetes insipidus occurring 24 hours after surgery; a second phase of inappropriate vasopressin secretion potentially causing hyponatraemia; and a third phase with a return to diabetes insipidus occurring up to 2 weeks later--is often complicated by cerebral salt wasting and thirst disorders. Inadequate adrenal replacement therapy and anticonvulsant agent treatment may increase the risk of life-threatening hyponatraemia in the course of desmopressin (DDAVP) treatment. Appropriate management, in order to avoid life-threatening or disabling electrolyte disturbances, requires a good grasp of the relevant pathophysiology. We review here the pathophysiology and management of the multiple fluid disorders encountered following surgery for craniopharyngiomas.
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PMID:Diabetes insipidus in craniopharyngioma: postoperative management of water and electrolyte disorders. 1670 Mar 19

Acute hyponatremia, following neurosurgery, results from inappropriate antidiuretic hormone secretion (SIADH) or cerebral salt wasting (CSW). CSW is due to abnormally high atrial or brain natriuretic peptides (ANP, BNP), which block all stimulators of zona glomerulosa steroidogenesis, resulting in mineralocorticoid deficiency. A 3 year-old girl presented CSW at day 4, after resection of craniopharyngioma and hypophysectomy. Hyponatremia, hyperkalemia and high natriuresis occurred on day 8, with low renin and aldosterone and elevated BNP 120.3 ng/ml (undetectable before surgery). Fludrocortisone 100 microg/day controlled natriuresis and restored electrolytes within 24 hours. A 5 year-old boy presented CSW at day 6 after partial resection of optic glioma. Fludocortisone 100 microg/day restored electrolytes within 8 hours. ANP was elevated, 60.6 ng/l, aldosterone and renin were low. Fludrocortisone supplementation should be considered in CSW, as excessive natriuresis is controlled, and electrolytes are easily restored, avoiding life-threatening complications of this complex disorder.
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PMID:Mineralocorticoid deficiency in post-operative cerebral salt wasting. 1805 34

The term cerebral salt wasting (CSW) was introduced before the syndrome of inappropriate antidiuretic hormone secretion was described in 1957. Subsequently, CSW virtually vanished, only to reappear a quarter century later in the neurosurgical literature. A valid diagnosis of CSW requires evidence of inappropriate urinary salt losses and reduced "effective arterial blood volume." With no gold standard, the reported measures of volume depletion do not stand scrutiny. We cannot tell the difference between CSW and the syndrome of inappropriate antidiuretic hormone secretion. Furthermore, the distinction does not make a difference; regardless of volume status, hyponatremia complicating intracranial disease should be treated with hypertonic saline.
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PMID:Cerebral salt wasting versus SIADH: what difference? 1821 9


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