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J Renal Inj Prev. 2016 Nov 1;6(1):26-29. doi: 10.15171/jrip.2017.05. eCollection 2017.

Severe symptomatic acute hyponatremia in traumatic brain injury responded very rapidly to a single 15 mg dose of oral tolvaptan; a Mayo Clinic Health System hospital experience - need for caution with tolvaptan in younger patients with preserved renal function.

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1
Department of Nephrology, Mayo Clinic Health System, Eau Claire, WI 54702, USA.
2
North East London NHS Foundation Trust, UK.

Abstract

Tolvaptan is now well established as a potent pharmaceutical agent for symptomatic hyponatremia from syndrome of inappropriate antidiuretic hormone secretion (SIADH), congestive heart failure and liver cirrhosis. Previous studies had recruited older (63-65 years) patients with mild renal impairment (serum creatinine, 1.3-1.4 mg/dl). A 2012 report in the Journal of Neurology, Neurosurgery & Psychiatry described tolvaptan as a "lifesaving drug". A major outcome concern in the treatment of chronic hyponatremia is potentially fatal pontine demyelination from over-rapid correction of serum sodium >0.5 mEq/dL/h. The maximum reported correction of serum sodium within 24 hours was 13 mEq/L in a case of SIADH. We recently experienced the dramatic correction of hyponatremia at 1 mEq/dL/h over 18 hours, following 15 mg of oral tolvaptan in a 32-year old male patient with normal kidney function (serum creatinine 0.76 mg/dL), following traumatic brain injury (TBI). Tolvaptan is indeed an effective and life-saving drug for post-TBI hyponatremia. However, we strongly recommend the use of lower doses of tolvaptan (≤15 mg/d) in younger patients with more preserved renal function to avoid the development of life-threatening pontine demyelination.

KEYWORDS:

Renal function; Hyponatremia; Subarachnoid hemorrhage; Syndrome of inappropriate; Tolvaptan; anti- diuretic hormone (SIADH)

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