Hyponatraemia: more than just a marker of disease severity?

Abstract

Hyponatraemia--the most common serum electrolyte disorder--has also emerged as an important marker of the severity and prognosis of important diseases such as heart failure and cirrhosis. Acute hyponatraemia can cause severe encephalopathy, but the rapid correction of chronic hyponatraemia can also profoundly impair brain function and even cause death. With the expanding elderly population and the increased prevalence of hyponatraemia in this segment of society, prospective studies are needed to examine whether correcting hyponatraemia in the elderly will diminish cognitive impairment, improve balance and reduce the incidence of falls and fractures. Given that polypharmacy is also common in the elderly population, the various medications that may stimulate arginine vasopressin release and/or enhance the hormone's action to increase water absorption must also be taken into consideration. Whether hyponatraemia in a patient with cancer is merely a marker of poor prognosis or whether its presence may alter the patient's quality of life remains to be examined. In any case, hyponatraemia can no longer be considered as just a biochemical bystander in the ill patient. A systematic diagnostic approach is necessary to determine the specific aetiology of a patient's hyponatraemia. Therapy must then be dictated not only by recognized reversible causes such as advanced hypothyroidism, adrenal insufficiency, diuretics or other medicines, but also by whether the hyponatraemia occurred acutely or chronically. Information is emerging that the vast majority of cases of hyponatraemia are caused by the nonosmotic release of arginine vasopressin. Now that vasopressin V2-receptor blockers are available, a new era of clinical investigation is necessary to examine whether hyponatraemia is just a marker of severe disease or whether correction of hyponatraemia could improve a patient's quality of life. Such an approach must involve prospective randomized studies in different groups of patients with hyponatraemia, including those with advanced heart failure, those with cirrhosis, patients with cancer, and the elderly.

Hyponatremia Is an Independent Predictor of In-Hospital Mortality in Spontaneous Intracerebral Hemorrhage

“…1,3,4 A postulated mechanism of hyponatremia influencing outcome also in neurointensive care could be its relation to an increased nonosmotic release of AVP caused by the overstimulation of the neurohumoral axis or by baroreceptor failure in elderly patients leading to cerebral hypoperfusion. 11,28 After severe neurotrauma such as ICH, increased intracranial pressures and cerebral hypoperfusion may even aggravate secondary brain injury. Assuming that these mechanisms play a role in patients with ICH, increased AVP levels themselves could contribute to a reduced tolerance to cerebral hypoxia.…”

The diagnosis and management of inpatient hyponatraemia and SIADH

“…Whether hyponatraemia in a patient with cancer is merely a marker of poor prognosis or whether its presence may alter the patient's quality of life has not been definitively answered, but there is increasing evidence that hyponatraemia can no longer be considered just a biochemical ‘bystander’ in the ill patient 19. A systematic diagnostic approach is necessary to determine the specific aetiology of a patient's hyponatraemia.…”

Current treatments for acute heart failure: focus on serelaxin

“…20,21 Multiple studies have found an association between hyponatremia in ADHF and adverse effects, including days hospitalized and mortality. 20,22 One major factor in the development of hyponatremia in ADHF is the nonosmotic secretion of arginine vasopressin, which in addition to its vasopressive effects, acts as an antidiuretic in the kidney through stimulation of aquaporin-2 in the renal collecting ducts. Arginine vasopressin acts through three different but related receptors known as V1a, V1b and V2.…”

“…Hemodynamic determinations were taken at baseline and during the infusion period at frequent intervals (0.5, 2, 4, 6, 8, and 20 hours), and during the washout period (21,22, and 24 hours). The peak PCWP decreased rapidly in the serelaxin group, and was significantly lower during the intervals from 0-8 hours.…”