Barry Blackwell: The lithium controversy. A historical autopsy
Hector Warnes’ comment on Janos Radó’s additional final comment:
Calcitonin in lithium-induced nephrogenic diabetes insipidus

            About 10% of patients on long-term lithium prophylaxis (more than 10 years) may develop a “Lithium induced nephrogenic diabetes insipidus” (Khanna 2006). I had two cases in my clinical praxis of bipolar patients who had severe polydipsia and polyuria. They woke up four or five times at night to urinate large volumes (more than 3 L/24 hrs;less 300 osmolality). I consulted a nephrologist who wisely advised me to change the medication because of the abnormal creatinine clearance and the glomerular filtrationrate. The condition is caused by complete or partial resistance of the kidneys to arginine vasopressin, the antidiuretic hormone. It is considered a serious adverse effect, because of the risk of developing dehydration (sodium may decreaseto less than 170 mmol/L). It has also been observed during treatment with clozapine, in patients with hypokalemia andhypercalcemia, and it has beenidentifiedas a rare genetic cause of the disorder.
            I am not sure that lithium is the first line of treatment in bipolar disorder even though there is a group of bipolar patients (approximately 40%) who are responsive to lithium prophylaxis.

I would not take it lightly if the patient developed nephrogenic diabetes insipidus because of the kidney risks involved unless lithium has been the only mood stabilizing drug that kept the patient symptom free for many years. We are also aware that an important percentage of patients suffering  from medical, neurological or psychiatric disorders are not compliant with the instructions given by their doctors.

Reference:

Khanna A. Acquired nephrogenic diabetes insipidus. Semin Nephrol 2006;26: 244-8.

January 17, 2019