Endocrine Abstracts

Introduction: Nephrogenic diabetes insipidus is caused by a deficiency in the action of anti-diuretic hormone, and can be life threatening if not treated appropriately. Lithium is a commonly used mood stabiliser in psychiatry and is known to cause NDI in around 12% of patients. It has been reported in the literature that severe hyperglycemic state may trigger symptomatic lithium-induced NDI in patients who had been on prolonged lithium therapy.

Case: We report the case of a 57-year-old male with a background of bipolar disorder (on lithium for almost 30 years) and type 2 diabetes on OHAs, who presented to A&E following collapse at home. blood test: sodium 148 mmol/L (133–146), blood glucose level of 44 mmol/L (3–6), K 5.1 mmol/L (3.5–5.3), Urea 41.2 mmol/L (2.5–7.8), Creatinine 444 micromol/L (60–110). He was treated for HHS with adequate fluid resuscitation with 0.9% normal saline and intravenous insulin. His sodium level, however, continued to rise reaching 177 mmol/L in 3 days. His urine output ranged from 4 to 9.0 L/day, serum osmolality 366 mosmol/Kg, urine osmolality 206 mmol/L, urine sodium 87 mmol/L, suggesting DI. He received a trial of desmopressin. This failed to reduce his urine output (day 5: 4522 ml, day 6: 4685 ml). Pituitary function test showed hypogonadtrophic hypogonadism, LH 2.3 iu/L (2–9), FSH 0.9 iu/L (2–12), Testosterone 1.2 nmol/L (9–29), normal Thyroid and HPA axis.An MRI pituitary showed no abnormalities. The lack of response to Desmopressin with the normal pituitary morphology and function apart from secondary hypogonadism (which is likely to be functional due to systemic illness) lead us to believe that this is the case of NDI. His lithium level at presentation was 1.04 mmol/L (0.5–1.2). However, lithium serum levels and clinical findings do not always overlap. The clinical situation was complicated by the initial presentation of HHS and AKI, which are normally managed with large volumes of fluids. Through accurate titration of fluids to sodium levels and careful monitoring of hydration status, the sodium level normalised in a gradual progressive manner from 174 to 144 mmol/L over two weeks. Proper glycemic control was achieved with the addition of regular insulin and his acute kidney injury resolved.

Conclusion: Hyperglycemic state with large losses of body water may aggravate and unmask lithium-induced nephrogenic diabetes insipidus (NDI) which had been asymptomatic previously. This case highlights the importance of strict fluid and electrolyte balance in the management of NDI.