Clinical and biochemical profile of hyponatremia and the role of vaptans in comparison to other standard modalities of therapy

Jalal Ahmed; Mohammed Fahad Khan; Shashikiran Umakanth; Seema Shetty

doi:10.18203/2320-6012.ijrms20233030

Authors

Jalal Ahmed Department of Nephrology, Manipal Hospitals, Bangalore, Karnataka, India
Mohammed Fahad Khan Department of Nephrology, Manipal Hospitals, Bangalore, Karnataka, India
Shashikiran Umakanth Department of Medicine, TMA Pai Hospital, Udupi, Karnataka, India
Seema Shetty Department of Medicine, TMA Pai Hospital, Udupi, Karnataka, India

DOI:

https://doi.org/10.18203/2320-6012.ijrms20233030

Keywords:

Hyponatremia, Saline, Tolvaptan

Abstract

Background: This study, conducted from August 2014 to August 2015, investigated hyponatremia in 228 in-hospital patients, aiming to discern its clinical and biochemical features and compare the efficacy of vaptans against standard treatments. The null hypothesis assumed no significant disparity in outcomes, while the alternate hypothesis posited otherwise.

Methods: Using an open-label, non-blinded, observational, prospective comparative design, we assessed 228 hyponatremia patients. We scrutinized their clinical and biochemical profiles and made comparisons between moderate and profound hyponatremia cases, along with different treatment approaches.

Results: Our findings revealed that patients aged 61-80, primarily females, dominated the cohort. Moderate hyponatremia occurred in 56.6% of cases, with severe hyponatremia in 43.4%. Common symptoms included drowsiness, nausea, and vomiting. Euvolemic hyponatremia was predominantly due to SIADH, while heart failure led to most hypervolemic cases. Various treatments were employed, with fluid restriction and normal saline being common. Tolvaptan and 1.6% hypertonic saline significantly increased serum sodium levels at 24 and 48 hours. Hospital stay duration didn’t significantly differ, and no osmotic demyelination cases emerged. Mortality stood at 10.5%, notably higher in profound hyponatremia cases.

Conclusions: This study provides insights into hyponatremia’s clinical and biochemical aspects and compares vaptans to standard treatments. Tolvaptan and hypertonic saline displayed promise in raising serum sodium levels. Nevertheless, further research is warranted to validate these findings and explore additional factors impacting hyponatremia treatment outcomes.

Metrics

Metrics Loading ...

References

Simpson FO. Sodium intake, body sodium, and sodium excretion. Lancet. 1988;2(8601):25-9.

King A. Basic concepts of fluid and electrolyte therapy. Clin Med. 2013;13(5):524.

Turner N, Lameire N, Goldsmith DJ, Winearls CG, Himmelfarb J, Remuzzi G, eds. Oxford Textbook of Clinical Nephrology. 4th edn. Oxford University Press; 2016.

Upadhyay A, Jaber BL, Madias NE. Incidence and prevalence of hyponatremia. Am J Med. 2006;119(7 Suppl 1):S30-5.

Hoorn EJ, Lindemans J, Zietse R. Development of severe hyponatraemia inhospitalized patients: treatment-related risk factors and inadequate management. Nephrol Dial Transplant. 2006;21(1):70-6.

Pillai BP, Unnikrishnan AG, Pavithran PV. Syndrome of inappropriate antidiuretic hormone secretion: Revisiting a classical endocrine disorder. Indian J Endocrinol Metab. 2011;15(Suppl3):S208-15.

Tachi T, Yokoi T, Goto C, Umeda M, Noguchi Y, Yasuda M, et al. Hyponatremia and hypokalemia as risk factors for falls. Eur J Clin Nutr. 2015;69(2):205-10.

Taal MW, Alan SL, Luyckx V. Brenner and Rector’s the kidney. Skorecki K, Chertow GM, Marsden PA, eds. Philadelphia, PA: Elsevier; 2016.

Hawkins RC. Age and gender as risk factors for hyponatremia and hypernatremia. Clin Chim Acta. 2003;337(1-2):169-72.

Clayton JA, Le Jeune IR, Hall IP. Severe hyponatraemia in medical in-patients: aetiology, assessment and outcome. QJM. 2006;99(8):505-11.

Rao MY, Sudhir U, Anil Kumar T, Saravanan S, Mahesh E, Punith K. Hospital-based descriptive study of symptomatic hyponatremia in elderly patients. J Assoc Phys India. 2010;58:667-9.

Padhi R, Panda B, Jagati S, Patra S. Hyponatremia in critically ill patients YR- 2014/2/1. Indian J Crit Care Med. 2014;18(2):83.

Sonnenblick M, Friedlander Y, Rosin AJ. Diuretic-induced severe hyponatremia. Review and analysis of 129 reported patients. Chest. 1993;103(2):601-6.

Hoorn EJ, van Wolfswinkel ME, Hesselink DA, de Rijke YB, Koelewijn R, vanHellemond JJ, et al. Hyponatremia in imported malaria: the pathophysiological role of vasopressin. Malar J. 2012;11:26.

Mishra SK, Mohanty S, Mohanty A, Das BS. Management of severe and complicated malaria. J Postgrad Med. 2006;52(4):281-7.

Schrier RW, Gross P, Gheorghiade M, Berl T, Verbalis JG, Czerwiec FS, et al. Tolvaptan, a selective oral vasopressin V2-receptor antagonist, for hyponatremia. N Engl J Med. 2006;355(20):2099-112.

Vilapurathu JK, Rajarajan S. A prospective study to compare the clinical efficacy of Tolvaptan with 3% hypertonic saline solution in hospitalized patients having hyponatremia. J Res Pharm Pract. 2014;3(1):34-6.

Rajan S, Tosh P, Kadapamannil D, Srikumar S, Paul J, Kumar L. Efficacy of vaptans for correction of postoperative hyponatremia: a comparison between single intravenous bolus conivaptan versus oral tolvaptan. J Anaesthesiol Clin Pharmacol. 2018;34(2):193-7.

Tosh P, Rajan S, Kadapamannil D, Joseph N, Kumar L. Efficacy of oral tolvaptan versus 3% hypertonic saline for correction of hyponatraemia in post-operative patients. Indian J Anaesth. 2017;61(12):996-1001.

Chatterjee N, Sengupta N, Das C, Chowdhuri AR, Basu AK, Pal SK. A descriptive study of hyponatremia in a tertiary care hospital of Eastern India. Indian J Endocrinol Metab. 2012;16(2):288-91