Diagnosis and Treatment > Medication > Vaptans

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Raku Son Department of Nephrology, St. Luke’s International Hospital, Tokyo, Japan

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Masahiko Nagahama Department of Nephrology, St. Luke’s International Hospital, Tokyo, Japan

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Fumiaki Tanemoto Department of Nephrology, St. Luke’s International Hospital, Tokyo, Japan

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Yugo Ito Department of Nephrology, St. Luke’s International Hospital, Tokyo, Japan

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Fumika Taki Department of Nephrology, St. Luke’s International Hospital, Tokyo, Japan

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Ryosuke Tsugitomi Department of Pulmonary Medicine, Thoracic Center, St. Luke’s International Hospital, Tokyo, Japan

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Masaaki Nakayama Department of Nephrology, St. Luke’s International Hospital, Tokyo, Japan

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Summary

The etiology of hyponatremia is assessed based on urine osmolality and sodium. We herein describe a 35-year-old Asian man with pulmonary tuberculosis and perforated duodenal ulcer who presented with hyponatremia with hourly fluctuating urine osmolality ranging from 100 to 600 mosmol/kg, which resembled urine osmolality observed in typical polydipsia and SIADH simultaneously. Further review revealed correlation of body temperature and urine osmolality. Since fever is a known non-osmotic stimulus of ADH secretion, we theorized that hyponatremia in this patient was due to transient ADH secretion due to fever. In our case, empiric exogenous glucocorticoid suppressed transient non-osmotic ADH secretion and urine osmolality showed highly variable concentrations. Transient ADH secretion-related hyponatremia may be underrecognized due to occasional empiric glucocorticoid administration in patients with critical illnesses. Repeatedly monitoring of urine chemistries and interpretation of urine chemistries with careful review of non-osmotic stimuli of ADH including fever is crucial in recognition of this etiology.

Learning points:

  • Hourly fluctuations in urine osmolality can be observed in patients with fever, which is a non-osmotic stimulant of ADH secretion.

  • Repeated monitoring of urine chemistries aids in the diagnosis of the etiology underlying hyponatremia, including fever, in patients with transient ADH secretion.

  • Glucocorticoid administration suppresses ADH secretion and improves hyponatremia even in the absence of adrenal insufficiency; the etiology of hyponatremia should be determined carefully in these patients.

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Ruben H Willemsen Department of Paediatric Endocrinology, University of Cambridge, Cambridge, UK

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Violeta Delgado-Carballar Department of Paediatric Endocrinology, University of Cambridge, Cambridge, UK

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Daniela Elleri Department of Paediatric Endocrinology, University of Cambridge, Cambridge, UK

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Ajay Thankamony Department of Paediatric Endocrinology, University of Cambridge, Cambridge, UK

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G A Amos Burke Department of Paediatric Haematology and Oncology, Addenbrooke’s Hospital, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK

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James C Nicholson Department of Paediatric Haematology and Oncology, Addenbrooke’s Hospital, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK

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David B Dunger Department of Paediatric Endocrinology, University of Cambridge, Cambridge, UK

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Summary

An 11-year-old boy developed severe syndrome of inappropriate antidiuretic hormone secretion (SIADH) after diagnosis of an intracranial B-cell lymphoma. His sodium levels dropped to 118–120 mmol/L despite 70% fluid restriction. For chemotherapy, he required hyperhydration, which posed a challenge because of severe hyponatraemia. Tolvaptan is an oral, highly selective arginine vasopressin V2-receptor antagonist, which has been licensed in adults for the management of SIADH and has been used in treating paediatric heart failure. Tolvaptan gradually increased sodium levels and allowed liberalisation of fluid intake and hyperhydration. Tolvaptan had profound effects on urinary output in our patient with increases up to 8 mL/kg/h and required close monitoring of fluid balance, frequent sodium measurements and adjustments to intake. After hyperhydration, tolvaptan was stopped, and the lymphoma went into remission with reversal of SIADH. We report one of the first uses of tolvaptan in a child with SIADH, and it was an effective and safe treatment to manage severe SIADH when fluid restriction was not possible or effective. However, meticulous monitoring of fluid balance and sodium levels and adjustments of fluid intake are required to prevent rapid sodium changes.

Learning points:

  • Tolvaptan can be used in paediatric patients with SIADH to allow hyperhydration during chemotherapy.

  • Tolvaptan has profound effects on urinary output and meticulous monitoring of fluid balance and sodium 
levels is therefore warranted.

  • Tolvaptan was well tolerated without significant side effects.

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