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PMON89 Nephrogenic Diabetes Insipidus in a Patient on Temozolomide

A 54-year-old female admitted for nausea and vomiting found to have hypernatremia. Four months prior to this admission, patient had undergone emergent craniotomy for an intraparenchymal hemorrhage. Found to have a 7.8 cm hemorrhagic and partially necrotic mass. Pathology consistent with anaplastic o...

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Autores principales: Moll, Teresa, Lott, David, Wright, Virginia, Lien, Lillian, Subauste, Jose
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9627386/
http://dx.doi.org/10.1210/jendso/bvac150.1181
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author Moll, Teresa
Lott, David
Wright, Virginia
Lien, Lillian
Subauste, Jose
author_facet Moll, Teresa
Lott, David
Wright, Virginia
Lien, Lillian
Subauste, Jose
author_sort Moll, Teresa
collection PubMed
description A 54-year-old female admitted for nausea and vomiting found to have hypernatremia. Four months prior to this admission, patient had undergone emergent craniotomy for an intraparenchymal hemorrhage. Found to have a 7.8 cm hemorrhagic and partially necrotic mass. Pathology consistent with anaplastic oligodendroglioma. She began radiation and temozolomide 2 months after surgery. On this admission for nausea and vomiting, sodium noted to be elevated at 154 mmol/L (136-145 mmol/L). Initially thought to be due to dehydration and started on intravenous fluids. Urine output noted to increase to 2-3 liters/day with persistently elevated sodium. Urine studies and labs collected while sodium 155 mmol/L significant for urine osmolality 128 mOsm/kg (50-1200 mOsm/kg), serum osmolality 330 mOsm/kg (280-295), and urine sodium 34 mmol/L. Given patient's history of prior craniotomy, radiation, and temozolomide, suspected central diabetes insipidus but DDAVP challenge with 4 mcg did not result in a lower urine output and urine osmolality remained <300 mOsm/kg. Repeat DDAVP challenge produced similar results. Evaluation of other central axis deficiencies revealed normal Free T4 (1.21 ng/dL). Unable to assess for adrenal insufficiency due to patient already on high-dose steroids for malignancy. Workup was turned to potential nephrogenic etiology as patient had been started on pantoprazole during her initial diagnosis 4 months prior. Co-peptin while sodium 148 mmol/L returned at 27.6 pmol/L (<13.1 pmol/L), indicative for nephrogenic diabetes insipidus. Patient was started on amiloride 5 mg twice a day and hydrochlorothiazide 25 mg twice a day with improvement noted in both sodium and urine output. Did discuss renal biopsy to rule-out interstitial nephritis from pantoprazole but given patient was on anti-coagulation for sub-massive pulmonary embolism, biopsy was deferred. Ultimately patient was discharged on amiloride 10 mg and hydrochlorothiazide 25 mg daily with sodium 142 mmol/L. She continued to receive temozolomide but eventually both amiloride and hydrochlorothiazide were held during a subsequent admission about a month later due to hyponatremia from poor oral intake. Sodium remained stable for about 5 months off medication at which time patient was re-started on amiloride for hypernatremia. Unfortunately patient passed due to complications from thrombosis. Review of PubMed revealed only 1 additional case report of a patient on temozolomide who developed nephrogenic diabetes insipidus but that patient was also on sulfamethoxazole-trimethoprim which was most likely the cause. Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m.
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spelling pubmed-96273862022-11-03 PMON89 Nephrogenic Diabetes Insipidus in a Patient on Temozolomide Moll, Teresa Lott, David Wright, Virginia Lien, Lillian Subauste, Jose J Endocr Soc Neuroendocrinology and Pituitary A 54-year-old female admitted for nausea and vomiting found to have hypernatremia. Four months prior to this admission, patient had undergone emergent craniotomy for an intraparenchymal hemorrhage. Found to have a 7.8 cm hemorrhagic and partially necrotic mass. Pathology consistent with anaplastic oligodendroglioma. She began radiation and temozolomide 2 months after surgery. On this admission for nausea and vomiting, sodium noted to be elevated at 154 mmol/L (136-145 mmol/L). Initially thought to be due to dehydration and started on intravenous fluids. Urine output noted to increase to 2-3 liters/day with persistently elevated sodium. Urine studies and labs collected while sodium 155 mmol/L significant for urine osmolality 128 mOsm/kg (50-1200 mOsm/kg), serum osmolality 330 mOsm/kg (280-295), and urine sodium 34 mmol/L. Given patient's history of prior craniotomy, radiation, and temozolomide, suspected central diabetes insipidus but DDAVP challenge with 4 mcg did not result in a lower urine output and urine osmolality remained <300 mOsm/kg. Repeat DDAVP challenge produced similar results. Evaluation of other central axis deficiencies revealed normal Free T4 (1.21 ng/dL). Unable to assess for adrenal insufficiency due to patient already on high-dose steroids for malignancy. Workup was turned to potential nephrogenic etiology as patient had been started on pantoprazole during her initial diagnosis 4 months prior. Co-peptin while sodium 148 mmol/L returned at 27.6 pmol/L (<13.1 pmol/L), indicative for nephrogenic diabetes insipidus. Patient was started on amiloride 5 mg twice a day and hydrochlorothiazide 25 mg twice a day with improvement noted in both sodium and urine output. Did discuss renal biopsy to rule-out interstitial nephritis from pantoprazole but given patient was on anti-coagulation for sub-massive pulmonary embolism, biopsy was deferred. Ultimately patient was discharged on amiloride 10 mg and hydrochlorothiazide 25 mg daily with sodium 142 mmol/L. She continued to receive temozolomide but eventually both amiloride and hydrochlorothiazide were held during a subsequent admission about a month later due to hyponatremia from poor oral intake. Sodium remained stable for about 5 months off medication at which time patient was re-started on amiloride for hypernatremia. Unfortunately patient passed due to complications from thrombosis. Review of PubMed revealed only 1 additional case report of a patient on temozolomide who developed nephrogenic diabetes insipidus but that patient was also on sulfamethoxazole-trimethoprim which was most likely the cause. Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m. Oxford University Press 2022-11-01 /pmc/articles/PMC9627386/ http://dx.doi.org/10.1210/jendso/bvac150.1181 Text en © The Author(s) 2022. Published by Oxford University Press on behalf of the Endocrine Society. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs licence (https://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial reproduction and distribution of the work, in any medium, provided the original work is not altered or transformed in any way, and that the work is properly cited. For commercial re-use, please contact journals.permissions@oup.com
spellingShingle Neuroendocrinology and Pituitary
Moll, Teresa
Lott, David
Wright, Virginia
Lien, Lillian
Subauste, Jose
PMON89 Nephrogenic Diabetes Insipidus in a Patient on Temozolomide
title PMON89 Nephrogenic Diabetes Insipidus in a Patient on Temozolomide
title_full PMON89 Nephrogenic Diabetes Insipidus in a Patient on Temozolomide
title_fullStr PMON89 Nephrogenic Diabetes Insipidus in a Patient on Temozolomide
title_full_unstemmed PMON89 Nephrogenic Diabetes Insipidus in a Patient on Temozolomide
title_short PMON89 Nephrogenic Diabetes Insipidus in a Patient on Temozolomide
title_sort pmon89 nephrogenic diabetes insipidus in a patient on temozolomide
topic Neuroendocrinology and Pituitary
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9627386/
http://dx.doi.org/10.1210/jendso/bvac150.1181
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