Donors with a serum sodium concentration of >155 mmol/L are extended criteria donors for liver transplantation (LT). Elevated serum sodium of donors leads to an increased incidence of hepatic dysfunction in the early postoperative period of LT; however, the exact mechanism has not been reported. We constructed a Lewis rat model of 70% hepatic parenchymal area subjected to ischemia-reperfusion (I/R) with hypernatremia and a BRL-3A cell model of hypoxia-reoxygenation (H/R) with high-sodium (HS) culture medium precondition. To determine the degree of injury, biochemical analysis, histological analysis, and oxidative stress and apoptosis detection were performed. We applied specific inhibitors of the epithelial sodium channel (ENaC) and Na⁺/Ca²⁺ exchanger (NCX) in vivo and in vitro to verify their roles in injury. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) levels and the area of hepatic necrosis were significantly elevated in the HS+I/R group. Increased reactive oxygen species (ROS) production, myeloperoxidase (MPO)‍-positive cells, and aggravated cellular apoptosis were detected in the HS+I/R group. The HS+H/R group of BRL-3A cells showed significantly increased cellular apoptosis and ROS production compared to the H/R group. The application of amiloride (Amil), a specific inhibitor of ENaC, reduced ischemia-reperfusion injury (IRI) aggravated by HS both in vivo and in vitro, as evidenced by decreased serum transaminases, inflammatory cytokines, apoptosis, and oxidative stress. SN-6, a specific inhibitor of NCX, had a similar effect to Amil. In summary, hypernatremia aggravates hepatic IRI, which can be attenuated by pharmacological inhibition of ENaC or NCX.
Animals ; Reperfusion Injury/drug therapy* ; Hypernatremia/complications* ; Rats ; Liver/metabolism* ; Rats, Inbred Lew ; Male ; Apoptosis ; Sodium-Calcium Exchanger/antagonists & inhibitors* ; Reactive Oxygen Species/metabolism* ; Oxidative Stress ; Epithelial Sodium Channel Blockers/pharmacology* ; Epithelial Sodium Channels ; Cell Line ; Liver Transplantation

To explore the influence of preventive use of vasopressin tannate on diabetes insipidus and serum sodium at the early postoperation of craniopharyngioma.
 Methods: The data of 83 patients, who underwent unilateral sub-frontal approach resection of craniopharyngioma between 2010 and 2014 by the same senior neurosurgeon, were retrospectively analyzed. The patients were divided into a vasopressin tannate group (used group) and a control group. The diabetes insipidus and serum sodium changes were compared between the two groups.
 Results: Compared with the control group, the incidence of diabetes insipidus decreased at the early postoperation in the vasopressin tannate group (P<0.05). There was high incidence of diabetes insipidus in patients with pituitary stalk excision and tumor close adhesion to the third ventricle floor at the early postoperation (P<0.05). Under such conditions, the incidence of diabetes insipidus in the vasopressin tannate group was decreased compared with the control group (P<0.05). Postoperative hypernatremia occurred in 37 patients (44.6%), and hyponatremia occurred in 60 patients (72.3%), the average time of the occurrence of hpernatremia and hyponatremia was 1.4 and 3.7 days after surgery. Postoperative high serum sodium and low serum sodium appeared alternately in 19 patients (22.9%). There was significant difference in the serum sodium distribution in the first day after surgery in both groups (P<0.05), and the percent of hpernatremia in the vasopressin tannate group was significantly less than that in the control group (P<0.05).
 Conclusion: Preventive use of vasopressin tannate can effectively reduce diabetes insipidus and hypernatremia incidence at the early postoperative stage after microsurgery for craniopharyngioma.
Arginine Vasopressin ; therapeutic use ; Craniopharyngioma ; complications ; surgery ; Diabetes Insipidus ; prevention & control ; Female ; Humans ; Hypernatremia ; epidemiology ; prevention & control ; Hyponatremia ; epidemiology ; Incidence ; Male ; Microsurgery ; adverse effects ; Pituitary Gland ; surgery ; Pituitary Neoplasms ; Postoperative Complications ; prevention & control ; Postoperative Period ; Retrospective Studies

Type 1 myotonic dystrophy (DM1) is an autosomal-dominant inherited disorder with a multisystem involvement, caused by an abnormal expansion of the CTG sequence of the dystrophic myotonia protein kinase (DMPK) gene. DM1 is a variable multisystem disorder with muscular and nonmuscular abnormalities. Increasingly, endocrine abnormalities, such as gonadal, pancreatic, and adrenal dysfunction are being reported. But, Electrolytes imbalance is a very rare condition in patients with DM1 yet. Herein we present a 42-yr-old Korean male of DM1 with abnormally elevated serum sodium and potassium. The patient had minimum volume of maximally concentrated urine without water loss. It was only cured by normal saline hydration. The cause of hypernatremia was considered by primary hypodipsia. Hyperkalemic conditions such as renal failure, pseudohyperkalemia, cortisol deficiency and hyperkalemic periodic paralysis were excluded. Further endocrine evaluation suggested selective hyperreninemic hypoaldosteronism as a cause of hyperkalemia.
Adult ; Humans ; Hyperkalemia/complications/*diagnosis ; Hypernatremia/complications/*diagnosis ; Hypoaldosteronism/complications/diagnosis ; Kidney Concentrating Ability ; Male ; Myotonic Dystrophy/complications/*diagnosis/*genetics ; Potassium/blood ; Protein-Serine-Threonine Kinases/*genetics ; Sodium/blood

Central diabetes insipidus (DI), characterized by unexpected fatal hypernatremia, is a rare complication after successful cardiopulmonary resuscitation with therapeutic hypothermia, but may be potentially fatal if recognition is delayed. We describe here a patient who experienced cardiac arrest due to a pulmonary embolism, followed by successful resuscitation after induction of therapeutic hypothermia. The patient, however, suddenly developed unexpected hypernatremia with increased urine output and was diagnosed with central DI as a complication of cerebral edema, and eventually died. Our findings suggest that central DI should be considered as a possible complication following unexpected hypernatremia with increased urine output during therapeutic hypothermia and that desmopressin acetate should be used to treat central DI.
Adult ; Cardiopulmonary Resuscitation/*adverse effects ; Diabetes Insipidus, Neurogenic/diagnosis/etiology ; Fatal Outcome ; Female ; Heart Arrest/complications/therapy ; Humans ; Hypernatremia/*etiology ; Hypothermia, Induced/*adverse effects ; Pulmonary Embolism/complications

OBJECTIVETo explore the pathogenesis and the management of hypernatremia in burn patients.

METHODSTwenty eight burn patients with hypernatremia were enrolled in the study and were divided into infection and non-infection groups. The pathogenesis, clinical features, biochemical indices in blood, the therapeutic results and the prognosis were compared between the two groups.

RESULTSIn non-infection group, the hypernatremia was mainly induced by improper fluid resuscitation and occurred on the 3.1 postburn day (PBD), while that in the infected group, on 7.2 PBD. The patients in non-infected group exhibited much more excited and the blood levels of glucose and urea nitrogen (BUN) were obviously decreased when compared with those in the infected group (P < 0.01). The survival rate in non-infected and infected group were 94.12% and 9.09%, respectively.

CONCLUSIONThe mortality rate of the patients with hypernatremia could be lowered by means of taking optimal measures according to the different patterns of hypernatremia.

Adult ; Blood Glucose ; metabolism ; Blood Urea Nitrogen ; Burns ; blood ; complications ; mortality ; Female ; Humans ; Hypernatremia ; etiology ; mortality ; therapy ; Infection ; complications ; Male ; Middle Aged ; Survival Rate ; Treatment Outcome