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      Hyponatremia and Inflammation: The Emerging Role of Interleukin-6 in Osmoregulation


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          Although hyponatremia is a recognized complication of several inflammatory diseases, its pathophysiology in this setting has remained elusive until recently. A growing body of evidence now points to an important role for interleukin-6 in the non-osmotic release of vasopressin. Here, we review this evidence by exploring the immuno-neuroendocrine pathways connecting interleukin-6 with vasopressin. The importance of these connections extends to several clinical scenarios of hyponatremia and inflammation, including hospital-acquired hyponatremia, postoperative hyponatremia, exercise-associated hyponatremia, and hyponatremia in the elderly. Besides insights in pathophysiology, the recognition of the propensity for antidiuresis during inflammation is also important with regard to monitoring patients and selecting the appropriate intravenous fluid regimen, for which recommendations are provided.

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          Most cited references28

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          Hyponatremia among runners in the Boston Marathon.

          Hyponatremia has emerged as an important cause of race-related death and life-threatening illness among marathon runners. We studied a cohort of marathon runners to estimate the incidence of hyponatremia and to identify the principal risk factors. Participants in the 2002 Boston Marathon were recruited one or two days before the race. Subjects completed a survey describing demographic information and training history. After the race, runners provided a blood sample and completed a questionnaire detailing their fluid consumption and urine output during the race. Prerace and postrace weights were recorded. Multivariate regression analyses were performed to identify risk factors associated with hyponatremia. Of 766 runners enrolled, 488 runners (64 percent) provided a usable blood sample at the finish line. Thirteen percent had hyponatremia (a serum sodium concentration of 135 mmol per liter or less); 0.6 percent had critical hyponatremia (120 mmol per liter or less). On univariate analyses, hyponatremia was associated with substantial weight gain, consumption of more than 3 liters of fluids during the race, consumption of fluids every mile, a racing time of >4:00 hours, female sex, and low body-mass index. On multivariate analysis, hyponatremia was associated with weight gain (odds ratio, 4.2; 95 percent confidence interval, 2.2 to 8.2), a racing time of >4:00 hours (odds ratio for the comparison with a time of <3:30 hours, 7.4; 95 percent confidence interval, 2.9 to 23.1), and body-mass-index extremes. Hyponatremia occurs in a substantial fraction of nonelite marathon runners and can be severe. Considerable weight gain while running, a long racing time, and body-mass-index extremes were associated with hyponatremia, whereas female sex, composition of fluids ingested, and use of nonsteroidal antiinflammatory drugs were not. Copyright 2005 Massachusetts Medical Society.
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            Interleukin-1 stimulates the secretion of hypothalamic corticotropin-releasing factor

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              Development of severe hyponatraemia in hospitalized patients: treatment-related risk factors and inadequate management.

              Although hyponatraemia [plasma sodium (PNa) 122+/-4 mmol/l). In hospital-acquired hyponatraemia, treatment started significantly later (1.0+/-2.6 vs 9.8+/-10.6 days, P<0.001) and the duration of hospitalization was longer (18.2+/-11.5 vs 30.7+/-23.4 days, P=0.01). The correction of PNa in hospital-acquired hyponatraemia was slower after both 24 h (6+/-4 vs 4+/-4 mmol/l, P=0.009) and 48 h (10+/-6 mmol/l vs 6+/-5 mmol/l, P=0.001) of treatment. Nineteen patients (26%) from both groups were not treated for hyponatraemia and this was associated with a higher mortality rate (seven out of 19 vs seven out of 55, P=0.04). Factors that contributed to hospital-acquired hyponatraemia included: thiazide diuretics (none out of 38 vs eight out of 36, P=0.002), drugs stimulating antidiuretic hormone (two out of 38 vs eight out of 36, P=0.04), surgery (none out of 38 vs 10 out of 36, P<0.001) and hypotonic intravenous fluids (one out of 38 vs eight out of 36, P=0.01). Symptomatic hyponatraemia was present in 27 patients (36%), and 14 patients died (19%). The development of severe hyponatraemia in hospitalized patients was associated with treatment-related factors and inadequate management. Early recognition of risk factors and expedited therapy may make hospital-acquired severe hyponatraemia more preventable.

                Author and article information

                Nephron Physiol
                Nephron Physiology
                S. Karger AG
                May 2011
                22 December 2010
                : 118
                : 2
                : p45-p51
                Department of Internal Medicine – Nephrology, Erasmus Medical Center, Rotterdam, The Netherlands
                Author notes
                *Reinout M. Swart, MD, PO Box 2040, NL–3000 CA Rotterdam (The Netherlands), Tel. +31 6 2428 7308, E-Mail reinoutswart@hotmail.com
                322238 Nephron Physiol 2011;118:p45–p51
                © 2010 S. Karger AG, Basel

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                Page count
                Figures: 3, Tables: 1, Pages: 7

                Cardiovascular Medicine,Nephrology
                Infectious disease,Lipopolysaccharides,Vasopressin,Immuno-neuroendocrinology,Acute phase response


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