Abstract
Hyponatraemia is the most common electrolyte disorder in hospitalized patients. Its epidemiology depends on the serum sodium used to define hyponatraemia, which varies from study to study. It can be an early or even first sign of important underlying disease. It can be complicated by two types of neurological disorders cerebral oedema and osmotic demyelination syndrome. It is associated with increased morbidity and mortality rates in hospitalized patients, although it remains unclear whether these associations are mainly due to the underlying disease, direct effects of hyponatraemia, or a combination of both. Aims and Objectives - to study clinical profile of hyponatremia in hospitalized subjects. To study the aetiology of hyponatremia in hospitalized subjects. To assess morbidity and mortality due to hyponatremia. Materials and Methods - 100 patients with hyponatremia were studied. Most common symptoms were Lethargy and tremors, followed by headache, nausea, altered sensorium, convulsion and coma, in order. Hypervolemic hyponatremia is most common followed by euvolemic hyponatremia and hypovolemic hyponatremia. Euvolemic subjects had propensity to develop more severe and symptomatic hyponatremia. Dilutional hyponatremia is the most prevalent underlying pathophysiology of hyponatremia followed by diuretic use, SIADH, GI loss, Hypothyroidism, extra renal/GI loss and Cerebral salt wasting in order. Congestive cardiac failure was the most common cause of hypervolemic hyponatremia, followed by cirrhosis of liver and renal failure. Acute gastroenteritis was most common cause of hypovolemic hyponatremia. SIADH was the most common cause of euvolemic hyponatremia, followed by thiazide diuretics and hypothyroidism, in order.
References
- Oxford Textbook of Clinical Nephrology; 4th Edition; 2016; Oxford University Press
- Harrison’s Principles of Internal Medicine; 19th Edition; 2015; McGraw Hill Edu.
- Schrier’s Manual of Nephrology; 8th Edition; 2015; Wolters Kluwer
- Acute Nephrology for the Critical Care Physician; 2015; Springer
- Comprehensive Clinical Nephrology; 5th Edition; 2015; Elsevier Saunders]
- Hawkins RC. Age and gender as risk factors for hyponatremia and hypernatremia. Clin Chim Acta 2003;337:169-72.
- Shapiro DS, Sonnenblick M, Galperin I, Melkonyan L, Munter G. Severe hyponatremia in elderly hospitalized patients: prevalence, aetiology and outcome. Intern Med J 2010; 40:574-80.
- Janicic N, Verbalis JG. Evaluation and management of hypoosmolality hypoosmolality in hospitalized patients. Endocrinol Metab Clin North A 2003; 32:459– 481.
- Schrier R. The patient with hyponatremia or hypernatremia. In: Schrier RW, ed. Manual of Nephrology. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2000:21–36.
- Ecelbarger, C. A., Kim, G. H., Terris, J., et al. (2000). Vasopressin-mediated regulation of epithelial sodium channel abundance in rat kidney. Am J Physiol Renal Physiol, 279, F46–53.
- Pedersen, N. B., Hofmeister, M. V., Rosenbaek, L. L., et al. (2010). Vasopressin induces phosphorylation of the thiazide-sensitive sodium chloride cotransporter in the distal convoluted tubule. Kiney Int, 78, 160–9.
- Bostanjoglo, M., Reeves, W. B., Reilly, R. F., et al. (1998). 11Beta-hydroxysteroid dehydrogenase, mineralocorticoid receptor, and thiazide-sensitive Na-Cl cotransporter expression by distal tubules. J Am Soc Nephrol, 9, 1347–58.
- Bachmann, S., Bostanjoglo, M., Schmitt, R., et al. (1999). Sodium transport-related proteins in the mammalian distal nephron—distribution, ontogeny and functional aspects. Anat Embryol (Berl), 200, 447–68.
- Mutig, K., Paliege, A., Kahl, T., et al. (2007). Vasopressin V2 receptor expression along rat, mouse, and human renal epithelia with focus on TAL. Am J Physiol Renal Physiol, 293, F1166
- Hoorn, E. J., Lindemans, J., and Zietse, R. (2006). Development of severe hyponatraemia in hospitalized patients: treatment-related risk factors and inadequate management. Nephrol Dial Transplant, 21, 70–6.
- Upadhyay, A., Jaber, B. L., and Madias, N. E. (2006). Incidence and prevalence of hyponatremia. Am J Med, 119, S30–5.
- Anderson, R. J., Chung, H. M., Kluge, R., et al. (1985). Hyponatremia: a prospective analysis of its epidemiology and the pathogenetic role of vasopressin. Ann Intern Med, 102, 164–8.
- Chung, H. M., Kluge, R., Schrier, R. W., et al. (1986). Postoperative hyponatremia. A prospective study. Arch Intern Med, 146, 333–6.
- Feldman, B. J., Rosenthal, S. M., Vargas, G. A., et al. (2005). Nephrogenic syndrome of inappropriate antidiuresis. N Engl J Med, 352, 1884–90.
- Tian, W., Fu, Y., Garcia-Elias, A., et al. (2009). A loss-of-function nonsynonymous polymorphism in the osmoregulatory TRPV4 gene is associated with human hyponatremia. Proc Natl Acad Sci U S A, 106, 14034–9.
- Almond, C. S., Shin, A. Y., Fortescue, E. B., et al. (2005). Hyponatremia among runners in the Boston Marathon. N Engl J Med, 352, 1550–6.
Corresponding Author
Dr Sellakannu
Department – General Medicine, Government Medical College, Bhavnagar
DOI: https://dx.doi.org/10.18535/jmscr/v12i03.07
