Clinical and Experimental Pediatrics

The Korean Pediatric Society (대한소아청소년과학회)
권호 표지

Hypernatremia and hyponatremia

고나트륨혈증과 저나트륨혈증

  • Kim, Dong Un (Department of Pediatrics, College of Medicine, The Catholic University of Korea)
  • 김동언 (가톨릭대학교 의과대학 소아과학교실)
  • Received : 2006.03.22
  • Accepted : 2006.03.24
  • Published : 2006.05.15
Download PDF
⟨ Previous Next ⟩

Abstract

Sodium is the major cation of the extracellular fluid and the primary determinant of extracellular osmolality. Therefore, hypernatremia causes water movement out of cells, while hyponatremia causes water movement into cells, resulting in cellular shrinkage and cellular swelling, respectively. Serious central nervous system symptoms may complicate both conditions. Since hypernatremia and hyponatremia are accompanied by abnormalities in water balance, it is essential to understand the mechanisms regulating extracellular osmolality and volume as well as the pathophysiology of hypernatremia and hyponatremia, in order to manage both conditions with swiftness and safety.

Keywords

References

  1. Kuramochi G, Kobayashi I. Regulation of the urine concentration mechanism by the oropharyngeal afferent pathway in man. Am J Nephrol 2000;20:42-7 https://doi.org/10.1159/000013554
  2. Robertson GL, Aycinena P, Zerbe RL. Neurogenic disorders of osmoregulation. Am J Med 1982;72:339-53 https://doi.org/10.1016/0002-9343(82)90825-7
  3. Dunn FL, Brennan TJ, Nelson AE, Robertson GL. The role of blood osmolality and volume in regulating vasopressin secretion in the rat. J Clin Invest 1973;52:3212-9 https://doi.org/10.1172/JCI107521
  4. Holtzman EJ, Harris HW Jr, Kolakowski LF Jr, Guay- Woodford LM, Botelho B, Ausiello DA. Brief report : a molecular defect in the vasopressin V2-receptor gene causing nephrogenic diabetes insipidus. N Engl J Med 1993;328: 1534-7 https://doi.org/10.1056/NEJM199305273282105
  5. Hochberg Z, Van Lieburg A, Even L, Brenner B, Lanir N, Van Oost BA, et al. Autosomal recessive nephrogenic diabetes insipidus caused by an aquaporin-2 mutation. J Clin Endocrinol & Metabol 1997;82:686-9 https://doi.org/10.1210/jc.82.2.686
  6. Deen PM, Croes H, van Aubel RA, Ginsel LA, van Os CH. Water channels encoded by mutant aquaporin-2 genes in nephrogenic diabetes insipidus are impaired in their cellular routing. J Clin Invest 1995;95:2291-6 https://doi.org/10.1172/JCI117920
  7. Gullans SR, Verbalis JG. Control of brain volume during hyperosmolar and hypoosmolar conditions. Annu Rev Med 1993;44:289-301 https://doi.org/10.1146/annurev.me.44.020193.001445
  8. Lein YH, Shapiro JI, Chan L. Effects of hypernatremia on organic brain osmoles. J Clin Invest 1990;85:1427-35 https://doi.org/10.1172/JCI114587
  9. Finberg L. Hypernatremic(hypertonic) dehydration. N Eng J Med 1973;286:196-8
  10. Strange K. Regulation of solute and water balance and cell volume in the central nervous system. J Am Soc Nephrol 1992;3:12-27
  11. Knoers N, Monnens LAH. Amiloride-hydrochlorothiazide versus indomethacin-hydrochlorothiaxide in the treatment of nephrogenic diabetes insipidus. J Pediatr 1990;117:499-502 https://doi.org/10.1016/S0022-3476(05)81106-0
  12. Verbalis JG. Pathogenesis of hyponatremia in an experimental model of the syndrome of inappropriate antidiuresis. Am J Physiol 1994;267:R1617-25
  13. Moritz ML, Ayus JC. Prevention of hospital-acquired hyponatremia : a case for using isotonic saline. Pediatrics 2003; 111:227-30 https://doi.org/10.1542/peds.111.2.227
  14. Kaneko K, Shimojima T, Kaneko K. Risk of exacerbation of hyponatremia with standard maintenance fluid regimens. Pediatr Nephrol 2004;19:1185-6
  15. New MI, Wilson RC. Steroid disorders in children : congenital adrenal hyperplasia and apparent mineralocorticoid excess. Proc Natl Acad Sci USA 1999;96:12790-7 https://doi.org/10.1073/pnas.96.22.12790
  16. Weisberg LS. Pseudohyponatremia : a reappraisal. Am J Med 1989;86:315-8 https://doi.org/10.1016/0002-9343(89)90302-1
  17. Berendes E, Walter M, Cullen P, Prien T, Van Aken H, Horsthemke J, et al. Secretion of brain natriuretic peptide in patients with aneurysmal subarachnoid haemorrhage. Lancet 1997;349:245-9 https://doi.org/10.1016/S0140-6736(96)08093-2
  18. Friedman E, Shadel M, Halkin H, Farfel Z. Thiazideinduced hyponatremia. Reproducibility by single dose rechallenge and an analysis of pathogenesis. Ann Intern Med 1989;110:24-30 https://doi.org/10.7326/0003-4819-110-1-24
  19. Schrier RW, Fassett RG. A critique of the overfill hypothesis of sodium and water retention in the nephrotic syndrome. Kidney Int 1998;53:1111-7 https://doi.org/10.1046/j.1523-1755.1998.00864.x
  20. Arieff AI, Ayus JC, Fraser CL. Hyponatremia and death or permanent brain damage in healthy children. BMJ 1992; 304:1218-22 https://doi.org/10.1136/bmj.304.6836.1218
  21. Verbalis JG, Gullans SR. Hyponatremia causes large sustained reductions in brain content of multiple organic osmolytes in rats. Brain Res 1991;567:274-82 https://doi.org/10.1016/0006-8993(91)90806-7
  22. Laureno R, Karp BI. Myelinolysis after correction of hyponatremia. Ann Intern Med 1997;126:57-62 https://doi.org/10.7326/0003-4819-126-1-199701010-00008
  23. Ellis SJ. Severe hyponatraemia : complications and treatment. QJM 1995;88:905-9