Does hypernatraemia promote thrombosis?

Grant, P. J.; Tate, G. M.; Hughes, J.; Davies, J. A.; Prentice, C. R. M.

doi:10.1016/0049-3848(85)90274-9

Cited by 40 publications

(25 citation statements)

References 10 publications

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“…1). In addition, the therapeutic use of DDAVP involves much greater antidiuretic hormone activity than the maximal level reached during dehydration (17,45,46). Furthermore, DDAVP produces only a transient increase of vWF in blood because it causes release of preexisting intracellular stores of vWF, whereas we observe a prolonged transcriptionally regulated increase in mice.…”

Section: Discussioncontrasting

confidence: 42%

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Secretion of von Willebrand factor by endothelial cells links sodium to hypercoagulability and thrombosis

Dmitrieva

Burg

2014

Proc. Natl. Acad. Sci. U.S.A.

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Hypercoagulability increases risk of thrombi that cause cardiovascular events. Here we identify plasma sodium concentration as a factor that modulates blood coagulability by affecting the production of von Willebrand factor (vWF), a key initiator of the clotting cascade. We find that elevation of salt over a range from the lower end of what is normal in blood to the level of severe hypernatremia reversibly increases vWF mRNA in endothelial cells in culture and the rate of vWF secretion from them. The high NaCl increases expression of tonicity-regulated transcription factor NFAT5 and its binding to promoter of vWF gene, suggesting involvement of hypertonic signaling in vWF up-regulation. To elevate NaCl in vivo, we modeled mild dehydration, subjecting mice to water restriction (WR) by feeding them with gel food containing 30% water. Such WR elevates blood sodium from 145.1 ± 0.5 to 150.2 ± 1.3 mmol/L and activates hypertonic signaling, evidenced from increased expression of NFAT5 in tissues. WR increases vWF mRNA in liver and lung and raises vWF protein in blood. Immunostaining of liver revealed increased production of vWF protein by endothelium and increased number of microthrombi inside capillaries. WR also increases blood level of D-dimer, indicative of ongoing coagulation and thrombolysis. Multivariate regression analysis of clinical data from the Atherosclerosis Risk in Communities Study demonstrated that serum sodium significantly contributes to prediction of plasma vWF and risk of stroke. The results indicate that elevation of extracellular sodium within the physiological range raises vWF sufficiently to increase coagulability and risk of thrombosis.blood clotting | HUVEC | osmotic stress

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Section: Discussioncontrasting

confidence: 42%

“…Increased sodium concentration is a common feature of the thrombosis in these studies. This led to recognition that hypernatremia might contribute to the thrombosis observed in such cases, but the mechanism had not been identified (17).…”

mentioning

confidence: 99%

Secretion of von Willebrand factor by endothelial cells links sodium to hypercoagulability and thrombosis

Dmitrieva

Burg

2014

Proc. Natl. Acad. Sci. U.S.A.

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“…If severe hypernatremia develops acutely, the brain may not be able to increase its intracellular solute sufficiently to preserve its volume, and the resulting cellular shrinkage can cause structural changes. Cerebral dehydration from hypernatremia can result in a physical separation of the brain from the meninges, leading to a rupture of the delicate bridging veins and intracranial or intracerebral hemorrhages [75,76] and venous sinus thrombosis leading to infarction [77]. Acute hypernatremia has also been shown to cause cerebral demyelinating lesions in both animals and humans [44,78,79,80].…”

Section: Morbidity and Mortalitymentioning

confidence: 99%

Preventing neurological complications from dysnatremias in children

2005

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Dysnatremias are among the most common electrolyte abnormalities encountered in hospitalized patients. In most cases, a dysnatremia results from improper fluid management. Dysnatremias can occasionally result in death or permanent neurological damage, a tragic complication that is usually preventable. In this manuscript, we discuss the epidemiology, pathogenesis and prevention and treatment of dysnatremias in children. We report on over 50 patients who have suffered death or neurological injury from hospital-acquired hyponatremia. The main factor contributing to hyponatremic encephalopathy in children is the routine use of hypotonic fluids in patients who have an impaired ability to excrete free-water, due to such causes as the postoperative state, volume depletion and pulmonary and central nervous system diseases. The appropriate use of 0.9% sodium chloride in parenteral fluids would likely prevent most cases of hospital-acquired hyponatremic encephalopathy. We report on 15 prospective studies in over 500 surgical patients that demonstrate that normal saline effectively prevents postoperative hyponatremia, and hypotonic fluids consistently result in a fall in serum sodium. Hyponatremic encephalopathy is a medical emergency that should be treated with hypertonic saline, and should never be managed with fluid restriction alone. Hospital-acquired hypernatremia occurs in patients who have restricted access to fluids in combination with ongoing free-water losses. Hypernatremia could largely be prevented by providing adequate free-water to patients who have ongoing free-water losses or when mild hypernatremia (Na>145 mE/l) develops. A group at high-risk for neurological damage from hypernatremia in the outpatient setting is that of the breastfed infant. Breastfed infants must be monitored closely for insufficient lactation and receive lactation support. Judicious use of infant formula supplementation may be called for until problems with lactation can be corrected.

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“…9 Hypernatremia and increasing plasma arginine vasopressin (AVP) concentrations produce changes in hemostatic function consistent with a hypercoagulable state (Increase in factor VIII coagulant acitivity, the ristocetin co-factor, von Willebrand antigen, plasminogen activator activity and fi brinopeptide A concentration with shortening of the activated partial thromboplastin time). 10 The mechanisms of the effect are unclear. These changes in hemostatic function might contribute to the thromboembolic complications of conditions such as hyperosmolar coma in diabetes mellitus or severe heatstroke in which degrees of hypernatremia occur.…”

Section: Discussionmentioning

confidence: 98%

Deep vein thrombosis complicating severe hypernatremia, rhabdomyolysis, and acute renal failure in a patient with untreated seizure disorder

et al. 2007

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We report a 22-year-old male patient with untreated seizure disorder, presenting with increased frequency of seizures followed by encephalopathy. Laboratory evaluation showed severe hypernatremia (175 meq/l sodium), rhabdomyolysis, and acute renal failure (ARF). Excessive insensible water loss in hot and humid weather, associated with an inability to obtain adequate water replacement, led to a hyperosmolar state (plasma osmolality, 398 mOsm/kg). He was vigorously treated with hypotonic fluid supplement and, further, needed dialysis therapy (peritoneal dialysis followed by hemodialysis) for acute renal insufficiency. The patient survived without any neurological sequelae, but the clinical course was complicated by acute deep vein thrombosis. This case represents what we believe is a unique report in the literature of severe hypernatremia developing via the pathogenic mechanism outlined above and the complication of acute peripheral venous thrombosis, which has not been reported in adults. The purpose of this report is to emphasize hyperosmolarity as a newly described cause of rhabdomyolysis, ARF, and a hypercoagulable state.

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Does hypernatraemia promote thrombosis?

Cited by 40 publications

References 10 publications

Secretion of von Willebrand factor by endothelial cells links sodium to hypercoagulability and thrombosis

Secretion of von Willebrand factor by endothelial cells links sodium to hypercoagulability and thrombosis

Preventing neurological complications from dysnatremias in children

Deep vein thrombosis complicating severe hypernatremia, rhabdomyolysis, and acute renal failure in a patient with untreated seizure disorder

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