# Persistent Polyuria in Severe Hyponatremia Secondary to Beer Potomania and Hypokalemia: A Case Report

**Authors:** Rimi Tanii, Noboru Tahara, Koichi Hayashi, Shigeki Fujitani

PMC · DOI: 10.7759/cureus.85503 · 2025-06-07

## TL;DR

A man with severe low sodium and potassium levels due to heavy beer drinking had persistent urine output, which improved after correcting the electrolyte imbalances.

## Contribution

This case highlights the complex management of hyponatremia in beer potomania with impaired vasopressin response due to hypokalemia and hypomagnesemia.

## Key findings

- Initial treatment with normal saline caused rapid diuresis and rising sodium levels.
- Correction of hypokalemia and hypomagnesemia restored vasopressin's antidiuretic effect.
- Individualized fluid and electrolyte management is crucial in such cases to prevent overcorrection.

## Abstract

Multiple electrolyte disorders often coexist in patients with beer potomania, including hypotonic hyponatremia caused by excessive beer consumption and poor solute intake. While hyponatremia is well recognized, its management can be complicated by concurrent hypokalemia and hypomagnesemia, and the impact of other electrolyte imbalances on its treatment remains unclarified. Here, we present a case of severe hyponatremia accompanied by persistent polyuria as a consequence of severe hypokalemia and hypomagnesemia. A 46-year-old man with a history of heavy beer consumption was admitted to the hospital with impaired mental status. Laboratory findings revealed multiple electrolyte disorders, including hyponatremia (111 mmol/L), hypokalemia (1.8 mmol/L), and hypomagnesemia (1.4 mg/dL). Initial treatment with normal saline caused massive diuresis (3,500 mL in six hours) and a rapid rise in serum sodium (119 mmol/L). To prevent overcorrection and subsequent osmotic demyelination, 5% dextrose and vasopressin were administered; however, it failed to adequately control diuresis. As severe hypokalemia and hypomagnesemia were corrected, the antidiuretic response of vasopressin was restored, leading to an improvement in urine output. Vasopressin was tapered and discontinued after serum sodium reached 132 mmol/L on hospital day six. In conclusion, this case highlights the importance of individualized fluid and electrolyte management in beer potomania, especially when antidiuretic hormone responsiveness is impaired, possibly due to hypokalemia and hypomagnesemia.

## Linked entities

- **Chemicals:** sodium (PubChem CID 5360545), potassium (PubChem CID 813), magnesium (PubChem CID 5462224), normal saline (PubChem CID 5234), 5% dextrose (PubChem CID 22814120), vasopressin (PubChem CID 8230)
- **Diseases:** hypokalemia (MONDO:0003019), hypomagnesemia (MONDO:0018100)

## Full-text entities

- **Genes:** AVP (arginine vasopressin) [NCBI Gene 551] {aka ADH, ARVP, AVP-NPII, AVRP, VP}
- **Diseases:** impaired mental status (MESH:D001523), Polyuria (MESH:D011141), Hypokalemia (MESH:D007008), Hyponatremia (MESH:D007010), electrolyte disorders (MESH:D014883), hypomagnesemia (OMIM:613882)
- **Chemicals:** dextrose (MESH:D005947), sodium (MESH:D012964)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12231729/full.md

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Source: https://tomesphere.com/paper/PMC12231729