View clinical trials related to Hypernatremia.
Filter by:Diets containing excessive salt (>12 g/day) have negative effects on kidney and cardiovascular system. Considering this known fact, the investigators aimed to study if the amount of the water taken with excessive salt had any part on these negative effects by testing the blood pressure, serum osmolality, endothelial functions, cardiac function, inflammatory parameters and sympathetic nervous system. Excessive dietary salt raises the serum osmolality, which triggers the protection mechanisms of the body. The first mechanism is the secretion of vasopressin from posterior pituitary and the second one is the polyol mediated aldose reductase enzyme activation in renal tubules. In the beginning, water and a little amount of salt is reabsorbed from the kidneys for keeping the serum osmolality in normal ranges by the elevation of vasopressin. Besides the high levels of vasopressin for long durations may have a role in both developments of hypertension and the progression/development of chronic kidney disease. Polyol mediated aldose reductase enzyme turns glucose into sorbitol, which is turned to fructose by sorbitol dehydrogenase activity. Fructose is degraded by fructokinase activity into toxic substances. With this pathway, the acute energy need is satisfied, yet uric acid, local oxidative stress, and inflammatory mediators rise while nitric oxide levels decreasing. These facts are independent risk factors for both kidney disease progression and hypertension. In addition, excessive salt intake may elevate the transforming growth factor beta-1 (TGF-B1) levels, which activates the sympathetic system, inflammation, and endothelial dysfunction. According to these data, the investigators speculate that if they increase the amount of water intake while eating the high salt diet they may decrease the toxic effect of salt with less increase in serum osmolarity. To test this hypothesis, by regulating the salt and water amount in healthy people's diets, the investigators aimed to evaluate the following these parameters; biochemical parameters that could affect the blood and urine osmolality, blood pressure, vascular endothelial functions with the non-invasive flow-mediated dilatation technique and arterial stiffness, systolic and diastolic functions of the heart by transthoracic echocardiography. In addition, it was planned to evaluate the hormonal effects of arginine vasopressin, a long peptide with 39 amino acids, which is longer and easier to measure than vasopressin levels in serum by measuring the pituitary hormone-derived copeptin. Although, decreasing the salt intake is the first step of the treatment in hypertension, and kidney diseases, the compliance rate to less sodium intake is very low (<20%). The investigators aim is to evaluate the effects of water, which is taken acutely with the excessive salt intake on cardiovascular system and kidney. The findings of the study will important for public health. If the investigators prove their hypothesis, they may recommend increasing high water intake before feeling thirst of which may contribute to decreasing the prevalence of hypertension and kidney disease.
The goal of this study is to find differences between patients who do and do not develop ICU-acquired hypernatremia (IAH). Therefore extended sodium and fluid balances will be performed. Also a couple of other factors that possibly contribute to the development of IAH and/or could give clues about the mechanisms in the development of IAH will be investigated.
The main objective of the trial is to evaluate the risk of hypokalemia following administration of a isotonic solution compared to a hypotonic solution in acutely ill hospitalised children, who need intravenous fluid therapy.
This study investigates the differens in sodium storage in skin between normal subjects, patients after cardiac surgery and septic patients.
The purpose of this study is to estimate the effect of an early induced hypernatremia protocol (150-155 milliequivalent/L) versus normonatremia plus mannitol (135 - 145 milliequivalent/L) in terms of neurologic outcome in patients with severe traumatic brain injury managed at critical care unit.
The patients with severe hypernatremia who received conventional treatment are often undertreated. Continuous venovenous hemofiltration (CVVH) can effectively remove solute or water from circulation system. Several case reports demonstrated that CVVH could effectively decrease serum sodium concentration of the patients with severe hypernatremia. The use of CVVH for acute severe hypernatremia in critically ill patients could improve patient survival by effectively decreasing the serum sodium concentration to a normal level.
Acquired hypernatremia appears to be associated with mortallity in ICU. To reduce hypernatremia and shorten the time of hypernatremia, we investigate the effect of hydrochloorthiazide compared to a placebo
Patients who are on mechanical ventilation in an intensive care unit often require diursis as part of their pre-extubation regimen. The drug of choice for diuresis has traditionally been furosemide. However, this drug cause hypernatremia (a rise in serum sodium) in a significant proportion of patients. Hypernatremia is traditionally treated by providing free water supplementation to the patient. This strategy creates a vicious and unproductive cycle of giving free water, and then diuresing it off. We propose a strategy for breaking this cycle by using a second diuretic-- metolazone-- which has a tendency to rid the body of more sodium, thereby minimizing hypernatremia.
Cerebral edema is seen heterogenous group of neurological disease states that mainly fall under the categories of metabolic, infectious, neoplasia, cerebrovascular, and traumatic brain injury disease states. Regardless of the driving force, cerebral edema is defined as the accumulation of fluid in the brain's intracellular and extracellular spaces. This occurs secondary to alterations in the complex interplay between four distinct fluid compartments within the cranium. In any human cranium; fluid is contained in the blood, the cerebrospinal fluid, interstitial fluid of the brain parenchyma, and the intracellular fluid of the neurons and glia. Fluid movement occurs normally between these compartments and depends on specific concentrations of solutes (such as sodium) and water. In brain-injured states, the normal regulation of this process is disturbed and cerebral edema can develop. Cerebral edema leads to increased intracranial pressure and mortality secondary to brain tissue compression, given the confines of the fixed-volume cranium. Additionally, secondary neuronal dysfunction or death can occur at the cellular level secondary to the disruption of ion gradients that control metabolism and function. While studies utilizing bolus dosing of hyperosmolar therapy to target signs or symptoms of increased intracranial pressure secondary to cerebral edema are numerous, there is a paucity of studies relating to continuous infusion of hyperosmolar therapy for targeted sustained hypernatremia for the prevention and treatment of cerebral edema. The investigators hypothesize that induced, sustained hypernatremia following traumatic brain injury will decrease the rate of cerebral edema formation and improve patient outcomes.
Background: Hypo- and hypernatremia are common in hospitalized patients. The differential diagnosis of dysnatremia is challenging. Osmotically inadequate secretion of antidiuretic hormone (ADH) is the predominant mechanism in most dysnatremic disorders. ADH measurement is cumbersome. It is derived from a larger precursor peptide along with copeptin, which is a more stable peptide directly mirroring the production of ADH. Objective: To evaluate the additional value of copeptin to improve a currently used algorithm in the differential diagnosis of (A) severe hypoosmolar hypo- and (B) severe hypernatremia. Design: Prospective observational study.