Severe lithium-induced nephrogenic diabetes insipidus: The diuresis paradox

We report a case of profound nephrogenic diabetes insipidus (NDI) in which renal resistance to antidiuretic hormone results in dilute polyuria despite normal circulating concentrations. A 28-year-old man with bipolar mood disorder presented to his local clinic with symptoms suggestive of lithium toxicity. Plasma lithium concentrations and thyroid-stimulating hormone (TSH) were taken, but results were not acted upon. One week later, he presented obtunded, severely dehydrated and in renal failure. His plasma lithium concentration was 4.3 mmol/L (toxic threshold >1.5 mmol/L) and TSH >100 mIU/L. After admission to the intensive care unit, including haemodialysis and 12 days of ventilation, he developed profound polyuria, with a peak output of 15 L/day. Amiloride with hydrochlorothiazide adequately reduced the polyuria. Management of lithium-induced NDI remains complex, and includes diuretics, which paradoxically reduce polyuria in this setting. Failure to follow up critical results led to profound morbidity, and is a crucial learning point in this case.

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Publication Details

Journal
South African Medical Journal
Published
2025-04-01
DOI
https://doi.org/10.7196/samj.2025.v115i3.2651
Citations
1
Primary Topic
Bipolar Disorder and Treatment
Type
article
Field-Weighted Citation Impact
1.47
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article

Severe lithium-induced nephrogenic diabetes insipidus: The diuresis paradox

Gayle Tatz, Joel A. Dave, Ian Louis Ross, Marc Blockman
1 citations
South African Medical Journal
Bipolar Disorder and Treatment
1.47
article

Severe lithium-induced nephrogenic diabetes insipidus: The diuresis paradox

Gayle Tatz, Joel A. Dave, Ian Louis Ross, Marc Blockman
article en
1 citations

Abstract

We report a case of profound nephrogenic diabetes insipidus (NDI) in which renal resistance to antidiuretic hormone results in dilute polyuria despite normal circulating concentrations. A 28-year-old man with bipolar mood disorder presented to his local clinic with symptoms suggestive of lithium toxicity. Plasma lithium concentrations and thyroid-stimulating hormone (TSH) were taken, but results were not acted upon. One week later, he presented obtunded, severely dehydrated and in renal failure. His plasma lithium concentration was 4.3 mmol/L (toxic threshold >1.5 mmol/L) and TSH >100 mIU/L. After admission to the intensive care unit, including haemodialysis and 12 days of ventilation, he developed profound polyuria, with a peak output of 15 L/day. Amiloride with hydrochlorothiazide adequately reduced the polyuria. Management of lithium-induced NDI remains complex, and includes diuretics, which paradoxically reduce polyuria in this setting. Failure to follow up critical results led to profound morbidity, and is a crucial learning point in this case.

South African Medical JournalVol. 115(3)
University of Cape Town (ZA)
Openalex Percentile: Top 21%
Bipolar Disorder and Treatment
1.47
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