Severe Hyponatremia From Lupus-Related Syndrome of Inappropriate Antidiuresis (SIADH): A Diagnostic Challenge

Severe hypotonic hyponatremia can complicate systemic lupus erythematosus (SLE) via inflammation-driven non-osmotic vasopressin release, leading to the syndrome of inappropriate antidiuresis (SIADH). We report a 24-year-old woman with active SLE who presented with headache, emesis, and confusion. She was clinically euvolemic, with a serum sodium level of 112 mmol/L, a measured serum osmolality of 254 mOsm/kg, a urine osmolality of 620 mOsm/kg, and a urine sodium level of 64 mmol/L; thyroid and adrenal tests were normal. Neuroimaging was unremarkable. Given severe symptoms, we administered guideline-based 3% hypertonic saline boluses while implementing a proactive desmopressin (DDAVP) clamp to prevent aquaresis-driven overcorrection; targets were an initial rise of 4-6 mmol/L and ≤8-10 mmol/L per 24 hours. Fractional excretion of urate (FEurate) decreased to 5% after partial correction, supporting SIADH over cerebral/renal salt wasting. Sodium was corrected safely with frequent monitoring and a standing re-lowering protocol available if limits were exceeded. This case underscores lupus-related SIADH as an important cause of profound hyponatremia and highlights a practical algorithm - hypertonic saline plus DDAVP clamp, FEurate reassessment, and conservative correction goals - to achieve safety while definitive lupus therapy proceeds.

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Journal
Cureus
Published
2025-11-11
DOI
https://doi.org/10.7759/cureus.96577
Primary Topic
Electrolyte and hormonal disorders
Type
article
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article

Severe Hyponatremia From Lupus-Related Syndrome of Inappropriate Antidiuresis (SIADH): A Diagnostic Challenge

Fahad S Alrashidi
Cureus
Electrolyte and hormonal disorders
article

Severe Hyponatremia From Lupus-Related Syndrome of Inappropriate Antidiuresis (SIADH): A Diagnostic Challenge

Fahad S Alrashidi
article en

Abstract

Severe hypotonic hyponatremia can complicate systemic lupus erythematosus (SLE) via inflammation-driven non-osmotic vasopressin release, leading to the syndrome of inappropriate antidiuresis (SIADH). We report a 24-year-old woman with active SLE who presented with headache, emesis, and confusion. She was clinically euvolemic, with a serum sodium level of 112 mmol/L, a measured serum osmolality of 254 mOsm/kg, a urine osmolality of 620 mOsm/kg, and a urine sodium level of 64 mmol/L; thyroid and adrenal tests were normal. Neuroimaging was unremarkable. Given severe symptoms, we administered guideline-based 3% hypertonic saline boluses while implementing a proactive desmopressin (DDAVP) clamp to prevent aquaresis-driven overcorrection; targets were an initial rise of 4-6 mmol/L and ≤8-10 mmol/L per 24 hours. Fractional excretion of urate (FEurate) decreased to 5% after partial correction, supporting SIADH over cerebral/renal salt wasting. Sodium was corrected safely with frequent monitoring and a standing re-lowering protocol available if limits were exceeded. This case underscores lupus-related SIADH as an important cause of profound hyponatremia and highlights a practical algorithm - hypertonic saline plus DDAVP clamp, FEurate reassessment, and conservative correction goals - to achieve safety while definitive lupus therapy proceeds.

CureusVol. 17(11)
Riyadh Armed Forces Hospital (SA)
Openalex Percentile: Top 52%
Electrolyte and hormonal disorders
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