Central pontine myelinolysis secondary to hypokalaemic nephrogenic diabetes insipidus

This version was published on 1 January 2010

Ann Clin Biochem 2010;47:86-89
doi:10.1258/acb.2009.009094
© 2010 Association for Clinical Biochemistry

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Case Reports


C Davenport1,
A Liew1,
P Vic Lau2,
D Smith1,
C J Thompson1,
G Kearns2 and
A Agha1


1 Academic Department of Endocrinology;
2 Department of Rheumatology, Beaumont Hospital, Dublin, Ireland


Corresponding author: Dr Amar Agha, Academic Department of Endocrinology, Endocrine Research Office, 2nd floor, Beaumont Hospital, Dublin 9, Ireland. Email: amaragha{at}beaumont.ie

Central pontine myelinolysis (CPM) has been described in alcoholic patients and in the aftermath of rapid correction of chronic hyponatraemia. We describe a case of CPM occurring secondary to nephrogenic diabetes insipidus (DI), which developed as a consequence of severe hypokalaemia. A 63-year-old man with alcohol dependence was admitted to hospital with severe pulmonary sepsis and type 1 respiratory failure. On admission, he had euvolaemic hyponatraemia of 127 mmol/L, consistent with a syndrome of inappropriate antidiuretic hormone secondary to his pneumonia. Following admission, his plasma potassium dropped from 3.2 to a nadir of 2.3 mmol/L. Mineralocorticoid excess, ectopic adrenocorticotrophic hormone production and other causes of hypokalaemia were excluded. The hypokalaemia provoked significant hypotonic polyuria and a slow rise in plasma sodium to 161 mmol/L over several days. Plasma glucose, calcium and creatinine were normal. The polyuria did not respond to desmopressin, and subsequent correction of his polyuria and hypernatraemia after normalization of plasma potassium confirmed the diagnosis of nephrogenic DI due to hypokalaemia. The patient remained obtunded, and the clinical suspicion of osmotic demyelination was confirmed on magnetic resonance imaging. The patient remained comatose and passed away 10 days later. This is the first reported case of nephrogenic DI resulting in the development of CPM, despite a relatively slow rise in plasma sodium of less than 12 mmol/L/24 h. Coexisting alcohol abuse, hypoxaemia and hypokalaemia may have contributed significantly to the development of CPM in this patient.


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