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PubMed1983

Hypernatremia induces hyperlipemia and a fatty liver.

Hypernatremic states, often the result of hypothalamic osmoreceptor dysfunction in humans, are sometimes accompanied by hyperlipemia. To investigate whether hypernatremia could cause hyperlipemia we induced hypernatremia in three groups of rats with their respective controls: Group A rats received hypertonic saline alone intragastrically; group B animals were pair-fed and tap water was substituted for hypertonic saline in the treated group; in group C the rats were again fed intragastrically with a liquid diet mixed with hypertonic saline. Rats receiving excess salt had mean serum Na+ concentrations exceeding 159 mmoles/l. While the serum triglyceride values were significantly higher in all hypernatremic rats, hepatic triglyceride content was greater only in group C rats (p less than .01). Serum free fatty acids and ketone bodies were also higher in group C rats (p less than .01) as compared to controls. These data suggest that hypernatremia by itself leads to hyperlipemia and a fatty liver.

Animals↗
PubMed1994

Physiopathology of hypernatremia following relief of urinary tract obstruction.

We report a case of postobstructive hypernatremia, and illustrate its pathogenesis and treatment. Physicians should be aware of this condition, given its high mortality rate (up to 70%), the high prevalence of potentially obstructive prostatic disease in elderly people and the peculiar sensitivity of this age group to disorders of osmotic regulation. Knowledge of the processes involved in osmoregulation has provided insights into the pathogenesis of this condition, which includes at least three factors: (i) decreased efficacy of the thirst mechanism in elderly patients, (ii) water loss in excess of effective solutes, resulting from osmotic diuresis from urea and transient renal tubular unresponsiveness to antidiuretic hormone, and (iii) inadequate fluid administration and failure to induce a positive fluid balance. These insights led to the development of specific strategies aimed at adequate correction of hypernatremia. Initial therapy should be rapid infusion of normal saline (or half-normal saline) coupled to administration of free water to restore euvolemia and correct hypernatremia, relying on repeated calculations of the free water deficit and taking into account ongoing urinary and insensible losses.

Adenocarcinoma↗
PubMed2003

Dural sinus thrombosis with severe hypernatremia developing in a patient on long-term lithium therapy.

Dural sinus thrombosis has not been described in a patient with hypernatremia resulting from lithium-induced nephrogenic diabetes insipidus. A 63-year-old man on chronic lithium therapy for schizoaffective disorder was transferred to the Emergency Department with dehydration and signs of central nervous system dysfunction after a 3-week isolation in a room in a psychiatric hospital due to exacerbation of psychiatric disorder, during which he refused to eat. Laboratory examination revealed hypertonic hypernatremia (osmolality, 359 mOsm/kg and Na, 171 mEq/L) and hyposthenuria (specific gravity, 1.010 and osmolality, 249 mOsm/kg), with normal serum endogenous vasopressin concentration (2.3 pg/mL). The serum lithium concentration was within the therapeutic range (0.94 mEq/L). Cranial computed tomography demonstrated subarachnoid hemorrhage and suggested dural sinus thrombosis. Although treatment with indomethacin (25 mg parenterally at 8-hour intervals) was somewhat effective in restoring renal concentrating capacity, he died of massive hemorrhagic infarction on the sixth hospital day, probably secondary to dural sinus thrombosis. The clinical diagnosis was confirmed by postmortem examination. Physicians should be alert for the possibility of dural sinus thrombosis as a complication of hypernatremia resulting from lithium-induced nephrogenic diabetes insipidus.

Diabetes Insipidus, Nephrogenic↗
PubMed2001

Volume supplementation with iso-sodium solution prevents hypernatremia after head injury.

OBJECTIVE: To evaluate our developed volume supplement protocol in preventing hypernatremia after head injury. METHODS: Iso-sodium solution was infused to keep the 8-hour water balance positive in 20 head-injured patients with hypotonic urine. RESULTS: Serum sodium concentrations moved to within a normal range in 6 patients and were temporarily increased in 12 patients. Seven of the 12 showed a negative cumulative water balance and slightly low creatinine clearance. Mean arterial pressure in the other five patients was lower after supplementation and was positively related to sodium excretion. Hypernatremia could not be prevented in the other two patients and they did not survive. Creatinine clearance was below 40 mL/min/m2 in these two patients before supplementation. CONCLUSION: Our protocol worked effectively in patients in whom renal function was preserved. Decreased creatinine clearance because of preexisting dehydration and lower arterial pressure disturbed increase in urinary sodium excretion and temporarily aggravated the hypernatremia.

Blood Volume↗
PubMed1981

Hypernatremia in the elderly: relation to infection and mortality.

The records of 23 elderly patients admitted to a county hospital with dehydration and hypernatremia were reviewed. One of these patients had the highest serum sodium level (202 mEq/L) reported in an adult. The overall mortality of 48 percent was not related to the degree of hypernatremia. However, two-thirds of the 17 patients with acute bacteria infections died, whereas all 5 noninfected patients survived. Infection was not always apparent at the time of admission to the hospital. It is proposed that early and appropriate antibiotic therapy may reduce the high mortality associated with hypernatremia in the elderly.

Aged↗
PubMed1986

Hypodipsic hypernatremia associated with absence of septum lucidum and olfactory dysfunction.

A case of hypodipsic hypernatremia in a 16-month-old Japanese boy is reported. Partial antidiuretic hormone deficiency was present. Computed tomography of the brain revealed absence of septum lucidum. No ophthalmological abnormality could be found. He had hyposmia, which has not been reported previously in association with hypernatremia due to hypodipsia. Forced fluid administration and nasal 1-deamino-8-d-arginine vasopressin treatment could maintain serum electrolyte levels within normal ranges. However, episodes of hypernatremia could not be completely avoided while he was treated with 1-deamino-8-d-arginine vasopressin and ad libitum oral fluid.

Central Nervous System↗
PubMedDate not supplied

Hypernatremia in calves.

Hypernatremia (sodium chloride intoxication) is described in two calves due to presumed mixing errors of oral electrolyte solutions while undergoing therapy for neonatal diarrhea. The experimental induction of hypernatremia in two clinically normal calves is also reported. Physical findings in diarrheic calves included depression, weakness, dehydration, and diarrhea. Serum sodium concentrations were found to be 171.6 mEq/l and 208.0 mEq/l, respectively. Treatment with intravenous fluids was attempted in both cases, but one calf died after 6 hours and the other calf died after 2 days and exhibited periodic convulsions before death. Experimental induction with oral administration of 1 l of electrolyte concentrate, which contained approximately 2750 mEq sodium revealed that the normal calves would willingly consume the solution as mixed with milk and develop clinical signs of hypernatremia within 6 hours of administration. Serum sodium concentrations of 176.0 and 179.8 were found in the experimental calves and coincided with the onset of overt depression and weakness, at which time they were euthanatized. Cerebrospinal fluid electrolyte analysis paralleled the serum electrolyte alterations.

Administration, Oral↗
PubMed1992

Energy turnover and the production of ammonium by the kidney: effect of hypernatremia.

The purpose of this study was to explore further the relation between the rates of oxygen consumption and ammonium (NH4+) production in the kidney during chronic metabolic acidosis. The experimental model was the dog with chronic metabolic acidosis because of the extensive background literature in this species. Chronic metabolic acidosis was produced by the ingestion of 10 mmol NH4Cl/kg body weight for 5 days. There was a significant increase in the rate of oxygen extraction when hypernatremia was present. Despite this rise in the rate of oxygen consumption, there was no increase in the rate of NH4+ production nor in the rate of glutamine extraction. These data suggest that hypernatremia might prevent a further augmentation in glutamine extraction when the rate of oxygen consumption rises. In addition, a larger proportion of the NH4+ produced was excreted in the urine during hypernatremia. This increase was associated with a rise in the urine flow rate, but not with a fall in urine pH.

Acidosis↗
PubMed2004

Prenatal programming of hypernatremia and hypertension in neonatal lambs.

Maternal water restriction and the accompanying dehydration-induced anorexia may induce long-term physiological changes in offspring. We determined the impact of prenatal hypertonicity (Pre-Dehy) on offspring cardiovascular and osmoregulatory function. Pre-Dehy lambs were exposed to in utero hypernatremia (8- to 10-meq increase; 110-150 days of gestation) induced by maternal water restriction. Control lambs were born to ewes provided ad libitum water and food throughout gestation. After delivery, all ewes were provided ad libitum water and all newborns were allowed ad libitum nursing. Lambs were prepared with vascular and bladder catheters at 15 +/- 2 days of age and studied at 21 +/- 2 days. After a 2-h basal period, lambs received an infusion of hypotonic (0.075 M) NaCl (0.15 ml.kg(-1).h(-1) iv) for 2 h. Lamb arterial blood pressure was monitored, and blood samples were obtained before, during, and after infusion. During the neonatal basal period, Pre-Dehy lambs had significantly increased plasma osmolality (302 +/- 1 vs. 294 +/- 1 mosmol/kgH(2)O, P < 0.01), sodium levels (144 +/- 1 vs. 140 +/- 1 meq/l, P < 0.01), hematocrit (28 +/- 1% vs. 25 +/- 1%, P < 0.05), and mean arterial blood pressure (79 +/- 2 vs. 68 +/- 1 mmHg, P < 0.001) compared with control lambs. Despite the infusion of hypotonic saline, Pre-Dehy lambs maintained relative hypertonicity, hypernatremia, and hypertension. However, plasma arginine vasopressin, glomerular filtration rate, and urinary osmolar and sodium excretion and clearance (per kg body wt) were similar in the groups. Offspring of prenatally water-restricted ewes exhibit hypernatremia, hypertonicity, and hypertension, which persist despite hypotonic saline infusion. In utero hypertonicity and perhaps maternal nutrient stress may program offspring osmoregulation and systemic arterial hypertension.

Animals↗
PubMed1989

Brain ion and volume regulation during acute hypernatremia in Brattleboro rats.

Regulation of brain ions and volume in response to 30 min of hypernatremia has been studied in two strains of anesthetized rats, the vasopressin-deficient Brattleboro and its vasopressin-competent parent strain, the Long-Evans. Plasma [Na] was increased by intraperitoneal injection of hyperosmolal NaCl. Brain volume was regulated during hypernatremia associated with tissue uptake of Na and Cl in both strains, but osmotically stimulated uptake of Na was 61% less in the Brattleboro. Blood-to-brain transfer constants for 22Na, measured as a function of plasma osmolality, were similar in the two strains. In contrast, bulk flow of cerebrospinal fluid (CSF) into brain, induced by osmotic dehydration of brain, was 55% less in the Brattleboro. CSF secretion in unstressed animals was also reduced, by 34%, in the Brattleboro compared with the Long-Evans. Reduced Na uptake by the brain of the Brattleboro rat during hypernatremia can be explained on the basis of a three-compartment model of brain volume regulation. Results support a function for vasopressin in brain ion homeostasis.

Acute Disease↗
PubMed2003

Peripheral venous thrombosis in children and adolescents with adipsic hypernatremia secondary to hypothalamic tumors.

OBJECTIVE: To determine the clinical presentation and laboratory follow-up in patients with the syndrome of adipsic hypernatremia complicated with a peripheral thrombosis event. METHODS: Report of 3 patients (6-19 years old) with chronic hypernatremia with sustained difficulties to normalize their serum osmolality levels. RESULTS: During post-surgical management the 3 patients developed a peripheral venous thrombotic event as a complication of their chronic hyperosmolality. CONCLUSIONS: Chronic hypernatremia in patients with prolonged immobilization is associated with an increased risk for development of deep venous thrombosis.

Adult↗
PubMed1987

Increased renal sensitivity to vasopressin in two patients with essential hypernatremia.

Patients with essential hypernatremia maintain urinary concentrating ability despite plasma hyperosmolality and low plasma vasopressin concentrations. We investigated renal sensitivity to ultralow dose vasopressin infusions in two patients with a syndrome of hypodipsia, hypernatremia with selective osmoreceptor dysfunction, early puberty, and aggressive behavior. The patients were water loaded until a hypotonic diuresis was established. Vasopressin was infused in stepwise increments from 0.4-12 fmol/kg X min. Both patients had increased renal sensitivity to vasopressin, achieving negative free water clearance at infusion rates of 0.4 and 4 fmol/kg X min (normal greater than or equal to 6). Treatment for 3 months with 1-desamino-8-D-arginine vasopressin (DDAVP) led to an improvement in behavior and the reporting, for the first time, of a sensation of thirst. After DDAVP therapy both patients had a reduction of their renal sensitivity to infused vasopressin. We conclude that untreated patients with essential hypernatremia have increased renal sensitivity to vasopressin which is reduced by DDAVP administration.

Adolescent↗
PubMedDate not supplied

Idiopathic hypothalamic dysfunction with precocious puberty and adipsic hypernatremia first presenting in adolescence.

BACKGROUND: Idiopathic hypothalamic dysfunction is a rare syndrome that has been described in young children. This syndrome is characterized by a disturbance of thirst regulation with hypernatremia, hyperosmolarity, and altered hypothalamic function. PATIENT REPORT: At age 6 years the reported patients presented with precocious puberty, by age 12 years she had hypernatremia presumed secondary to central diabetes insipidus and was treated with DDAVP, and at age 14 was identified to have hyperprolactinemia. At age 19 she presented with serum sodium of 185 mg/dl during an episode of illness associated with dehydration. After hydration, her sodium remained elevated. Arginine vasopressin was measurable but inappropriate to serum sodium, while urinary cyclic AMP response to vasopressin was appropriate. CONCLUSIONS: This is the first case of precocious puberty identified in association with the more classic features of idiopathic hypothalamic dysfunction, including later-onset hypernatremia, poor thermoregulatory function, obesity, and hyperprolactinemia.

Arginine Vasopressin↗
PubMed2006

Risk factors for excess weight loss and hypernatremia in exclusively breast-fed infants.

Data were prospectively obtained from exclusively breast-fed healthy term neonates at birth and from healthy mothers with no obstetric complication to determine risk factors for excess weight loss and hypernatremia in exclusively breast-fed infants. Thirty-four neonates with a weight loss > or = 10% were diagnosed between April 2001 and January 2005. Six of 18 infants who were eligible for the study had hypernatremia. Breast conditions associated with breast-feeding difficulties (P < 0.05), primiparity (P < 0.005), less than four stools (P < 0.001), pink diaper (P < 0.001), delay at initiation of first breast giving (P < 0.01), birth by cesarean section (P < 0.05), extra heater usage (P < 0.005), extra heater usage among mothers who had appropriate conditions associated with breast-feeding (P < 0.001), mean weight loss in neonates with pink diaper (P < 0.05), mean uric acid concentration in neonates with pink diaper (P < 0.0001), fever in hypernatremic neonates (P < 0.02), and the correlation of weight loss with both serum sodium and uric acid concentrations (P < 0.02) were determined. Excessive weight loss occurs in exclusively breast-fed infants and can be complicated by hypernatremia and other morbidities. Prompt initiation of breast-feeding after delivery and prompt intervention if problems occur with breast-feeding, in particular poor breast attachment, breast engorgement, delayed breast milk "coming in", and nipple problems will help promote successful breast-feeding. Careful follow-up of breast-feeding dyads after discharge from hospital, especially regarding infant weight, is important to help detect inadequate breast-feeding. Environmental factors such as heaters may exacerbate infant dehydration.

Breast Feeding↗
PubMed1979

Hypothalamic hypernatremia due to volume--dependent ADH release, and its treatment with carbamazepine and clofibrate.

A 23-year-old man, diagnosed as having a pituitary adenoma at the age of 17 and received an operation 1 month ago showed a fluctuating hypernatremia and hypodipsia. The water deprivation, water load and hypertonic saline infusion tests were carried out. After a 14-hr water deprivation test, plasma osmolality was 310 mOsm/kg, plasma ADH was 1.5 microunits/ml, and urine osmolality was 591 mOsm/kg. On the water load test subsequently performed, the plasma osmolality decreased to 297 mOsm/kg, but the urine was still hypertonic. Infusion of 2.5% saline solution elicited paradoxically a marked diuresis and dilution of urine despite the elevàtion of plasma osmolality. On the treatment with carbamazepine and clofibrate, the urinary osmolality increased, the hypernatremia was normalized, and a marked natriuresis was elicited with a gain in body weight. These results suggested that the secretion of ADH is regulated by changes in blood volume rather than by the plasma osmolality in this patient. The hypernatremia may be explained as a disturbance or lack of osmoreceptor function for ADH release and the loss of thirst sensation, though the volume receptor still remains functioning for ADH secretion. Depletion of the extracellular fluid volume may be another contributing factor to the elevation of serum sodium level by enhancing the reabsorption of sodium from renal tubules.

Adult↗
PubMed2000

Hyperglycemia, hypernatremia, and hyperosmolarity in 6 neonatal llamas and alpacas.

Neonatal camelids can develop hyperglycemia, hypernatremia, and hyperosmolarity in response to a combination of stress and inadequate water intake. Clinical signs of this syndrome include a fine head tremor, ataxia, and a base-wide stance of the hind limbs, but biochemical analyses are necessary to confirm the diagnosis. Camelids appear to be susceptible to this syndrome because of a poor insulin response to hyperglycemia; hypernatremia results from free water loss associated with glucose diuresis. Water loss associated with glucose diuresis may necessitate a higher rate of fluid administration in camelids with this syndrome than is typically used for treatment of hypernatremia in calves.

Animals↗
PubMed2006

Transient ventriculomegaly in a child presenting with hypernatremia. Case report.

The authors present the case of a 3-year-old girl with a history of myelomeningocele repair, ventriculoperitoneal (VP) shunt placement for hydrocephalus, and shaken baby syndrome who presented in a hypernatremic state as a result of dehydration. At the time of presentation, the patient had experienced a 1-week-long history of diarrhea associated with antibiotic agents used to treat a coexisting pyelonephritis. On admission, the patient exhibited signs and symptoms of dehydration and was discovered to have profound hypernatremia with a serum sodium level of 180 mmol/L. A computerized tomography (CT) scan of the head revealed ventricular enlargement compared with previous imaging findings. A shunt tap revealed intracranial hypotension with good proximal flow. The child was treated for her hypernatremic state, and her neurological condition returned to baseline level. Subsequent CT scans of the head demonstrated a return of the ventricular system to its premorbid size. On the basis of the initial radiographic presentation and subsequent evaluation, the authors hypothesize that the ventricular enlargement was a result of hypernatremia. The signs and symptoms were similar to those found in patients with a VP shunt obstruction; however, a shunt tap revealed intracranial hypotension and excellent proximal flow. To the authors' knowledge, there has not been a radiographically documented case of reversible ventricular enlargement associated with hypernatremia.

Brain Diseases↗
PubMed1996

beta-Alanine protects against taurine and NaCl--induced hypernatremia in the rat.

Rats drinking a combination of taurine and hypertonic saline solution rapidly develop hypernatremia, but rats drinking either solution alone do not. The mechanism by which taurine disrupts the ability to deal with a salt load is not clear. Rats housed in metabolism cages were studied. Food intake, fluid intake, plasma sodium concentration, urine output, sodium balance, visible water balance, and urine osmolality were determined over a period of 8 days. Rats drinking 0.1 M taurine plus 1.8% NaCl developed a mean plasma sodium concentration of 160 +/- 18 mM by Day 6, compared with 137 +/- 1.6 mM in water drinking controls. Ingestion of 1.8% saline alone produced only a mild, transient rise in plasma sodium (<150 mM), which returned to control levels by Day 8. Ingestion by neither 0.1 M taurine alone nor 0.1 M beta-alanine, a taurine transport antagonist, produced any evidence of hypernatremia throughout the experiment. When beta-alanine was added to the taurine + saline regimen, mean plasma sodium reached only 149 +/- 16 mM (Day 6). Inspection of the ratio of cumulative sodium balance to cumulative water balance revealed a rapid increase until Day 2, followed by a virtual plateau thereafter in the taurine + saline group. Rats drinking saline alone showed an equally rapid rise in the ratio, but to a lower plateau level, suggesting that taurine exerts a much more pronounced disturbance of sodium balance than of water balance. The addition of beta-alanine to the regimens of taurine + saline or saline alone produced ratios of cumulative sodium to cumulative water balance significantly lower than that of either regimen without beta-alanine. These findings suggest that taurine induces hypernatremia by interfering with normal homeostatic control mechanisms and that beta-alanine counteracts that action of taurine. The effect of beta-alanine in rats drinking saline alone is consistent with a role for endogenous taurine in normal electrolyte homeostasis.

Animals↗