Disease relevance of Hyponatremia

• Pseudohypoaldosteronism, a syndrome characterized by salt wasting and failure to thrive, usually presents in infancy as high urinary levels of sodium despite hyponatremia, hyperkalemia, hyperreninemia, and elevated aldosterone levels [1].
• Severe hyponatremia occurs in some patients with untreated hypopituitarism, but it is not known whether such hyponatremia is caused by the hypersecretion of vasopressin (antidiuretic hormone) [2].
• Use of urea should be considered when symptomatic hyponatremia in SIADH must be quickly corrected [3].
• Therapy of hyponatremia in cirrhosis with a vasopressin receptor antagonist: a randomized double-blind multicenter trial [4].
• Seven patients with persistent hyponatremia but normal or elevated serum arginine vasopressin levels and refractory ascites undergoing peritoneovenous shunting were studied in a Metabolic Unit on a 20 mEq sodium 1200 ml fluid-restricted diet to elucidate the mechanism of this response [5].

Psychiatry related information on Hyponatremia

• This crisis was associated with the following: salt and water depletion, hyponatremia, hypovolemia and hemoconcentration, polydipsia, marked activation of the renin-angiotensin-aldosterone system, increased plasma cortisol concentration, hemolysis, marked impairment in renal function, lethargy, and vomiting.(ABSTRACT TRUNCATED AT 250 WORDS)[6]
• CBZ has led to hyponatremia in patients with epilepsy, neuralgia, mental retardation, and psychiatric disorders with a frequency varying from 4.8 to 40% [7].
• We present a case of a 29-year-old woman with a long history of nocturnal enuresis who developed symptomatic hyponatremia from water intoxication shortly after beginning desmopressin [8].
• Ewes were assigned to receive water deprivation (n = 4) [desamino, D-Arg8]-arginine vasopressin-induced plasma hyponatremia (n = 3), or 4 days of observation (n = 3) [9].
• Five of the 14 older patients had severe hyponatremia (107-117 mEq/l) based on panhypopituitarism, and four of these five patients showed consciousness disturbance as the initial symptom, initiated by physical and/or psychological stress, or occurrence of intratumoral hemorrhage [10].

High impact information on Hyponatremia

• Reboxetine and hyponatremia [11].
• Sertraline and hyponatremia [12].
• The hyponatremia was resolved within a few days after the institution of hydrocortisone therapy, after infusion of normotonic or hypertonic saline had been found to be less effective [2].
• We conclude that both vasoconstrictor (renin-angiotensin) and vasodilator (prostaglandin) mechanisms are operative in patients with heart failure complicated by hyponatremia and that these mechanisms interact to modulate circulatory homeostasis [13].
• Welty and his associated have shown that acute hyponatremia lowered the taurine concentration of rat heart [14].

Chemical compound and disease context of Hyponatremia

• We conclude that psychiatric patients with polydipsia and hyponatremia have unexplained defects in urinary dilution, the osmoregulation of water intake, and the secretion of vasopressin [15].
• We conclude that a nephrotoxic effect of demeclocycline severly limits its usefulness in treating hyponatremia in the cirrhotic patient [16].
• OBJECTIVE: To compare IV sodium chloride with fluid restriction in the treatment of postmenopausal women with chronic symptomatic hyponatremia [17].
• Hyponatremia induced by a combination of amiloride and hydrochlorothiazide [18].
• Tolbutamide-associated hyponatremia [19].

Biological context of Hyponatremia

• The critical role of the adrenal gland in the renal regulation of acid-base equilibrium during chronic hypotonic expansion. Evidence that chronic hyponatremia is a potent stimulus to aldosterone secretion [20].
• Hyponatremia: a prospective analysis of its epidemiology and the pathogenetic role of vasopressin [21].
• These findings indicate that natriuresis and hyponatremia in aneurysmal subarachnoid hemorrhage reflect salt wasting and not inappropriate secretion of antidiuretic hormone and that these changes should be corrected by fluid replacement rather than by fluid restriction [22].
• After 17 weeks, ascites and hyponatremia had developed, and significant decreases in renal plasma flow (-33%), GFR (-30%), and fractional lithium excretion (-44%) were observed [23].
• Following the patient's uneventful recovery from surgery, studies of osmoregulation of vasopressin release and renal water handling were performed to determine the cause of chronic hyponatremia refractory to sodium chloride administration [24].

Anatomical context of Hyponatremia

• It may not be coincidental that two principal markers of an unfavorable prognosis in patients with heart failure, high plasma norepinephrine levels and hyponatremia, share baroreceptor dysfunction as a common theme [25].
• The quantity of AVP peptide in the tumor cell lines was more closely associated with hyponatremia in the patients (P = 0.0026, r2 = 0.28) than was the production of ANF peptide (P = 0.066, r2 = 0.12), although neither association was strong [26].
• Thus, these results show that in the setting of extracellular fluid volume expansion, excessive water retention with hyponatremia can occur in the absence of increases in aquaporin-2 abundance [27].
• In previous studies we developed a rat model in which demyelination is reproducibly produced following rapid correction of chronic hyponatremia and demonstrated that the development of demyelination in this model is strongly associated with NMR indices of blood-brain barrier (BBB) disruption [28].
• Different HE-precipitating factors, such as ammonia, benzodiazepines, inflammatory cytokines and hyponatremia induce or aggravate astrocyte swelling and additionally increase oxidative/nitrosative stress and protein tyrosine nitration [29].

Gene context of Hyponatremia

• Orally active non-peptide-selective V2 receptor antagonists administered to patients with congestive cardiac failure decrease urinary concentrations of aquaporin-2, increase solute-free water clearance, and correct the hyponatremia [30].
• However, urinary aquaporin-2 in hyponatremia was significantly increased when compared with the other two groups [31].
• Thus, non-osmotic release of AVP in CHF upregulates AQP2 water channels, enhances water reabsorption and causes hyponatremia [32].
• Laboratory studies disclosed hyponatremia, low plasma ACTH level (4.2 pmol/L), and a low cortisol level (27.6 nmol/L) [33].
• Asymptomatic hyponatremia occurred in over half of subjects receiving 75 microg or larger doses of GDNF; it was symptomatic in several subjects [34].

Analytical, diagnostic and therapeutic context of Hyponatremia

• To determine the effects of vasodilator and inotropic therapy on hyponatremia in patients with severe heart failure, we measured serum sodium concentration before and after treatment with captopril (70 patients), hydralazine (42 patients), prazosin (22 patients), and amrinone (19 patients), while diuretic dosages were kept constant [35].
• Controlled clinical trials now underway will help elucidate the role of AVP receptor antagonism in the treatment of hyponatremia [36].
• The hyponatremia did not respond to demeclocycline hydrochloride, and antidiuretic hormone (ADH) levels measured by a specific radioimmunoassay were appropriately suppressed [37].
• Grade 3 hyponatremia occurred in two patients, and elevated liver function tests and creatinine occurred but were not dose limiting [38].
• Thus, in animal models, analogous to the hyponatremia forms seen in humans, tolvaptan presents exciting therapeutic implications in the management of patients with severe hyponatremia [39].

References