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  • Hypokalaemic paralysis as the initial clinical presentation of Sjogren’s syndrome induced distal renal tubular acidosis

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Case report
Hypokalaemic paralysis as the initial clinical presentation of Sjogren’s syndrome induced distal renal tubular acidosis
  1. Jennifer M Kielty1,
  2. Paul Ryan2,
  3. Donal Sexton3,4 and
  4. Yvelynne P Kelly5
  1. 1Anaesthesiology and Intensive Care Medicine, Saint James's Hospital, Dublin, Ireland
  2. 2Medicine, Saint James's Hospital, Dublin, Ireland
  3. 3Nephrology, Saint James's Hospital, Dublin, Ireland
  4. 4Trinity Health Kidney Centre, Trinity College Dublin School of Medicine, Dublin, Ireland
  5. 5Intensive Care Medicine, Saint James's Hospital, Dublin, Ireland
  1. Correspondence to Dr Jennifer M Kielty; jenniferkielty{at}msn.com

Abstract

A 41-year-old woman presented by ambulance with a 1-day history of new-onset paralysis and nausea and vomiting ongoing for 48 hours. She had no history of any similar episodes. Biochemical analysis showed profound hypokalaemia with a non-anion gap metabolic acidosis. Her initial serum chloride was within the normal range. She had significant electrocardiographic changes on admission with ST depression, U waves and a prolonged QT interval. Urinary anion gap supported the diagnosis of a distal renal tubular acidosis. Subsequent connective tissue disease serology confirmed previously undiagnosed Sjogren’s syndrome. Successful recovery for this patient required multidisciplinary input from the intensive care, nephrology and neurology teams.

  • fluid electrolyte and acid–base disturbances
  • Sjogren's syndrome

https://doi.org/10.1136/bcr-2020-241300

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    Footnotes

    • Twitter @YvelynneKelly

    • Contributors JK: planning, literature search, conduct, reporting, conception and design, acquisition of data, analysis and interpretation. PR: planning, literature search, reporting and acquisition of data. DS: conception and design, analysis and interpretation of data. YPK: conception and design, analysis and interpretation of data.

    • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

    • Competing interests None declared.

    • Provenance and peer review Not commissioned; externally peer reviewed.