Lithium (lithium carbonate) toxicity as a cause of nephrogenic diabetes insipidus complicated by acute kidney injury and severe hypernatremia

Lithium (lithium carbonate) toxicity as a cause of nephrogenic diabetes insipidus complicated by acute kidney injury and severe hypernatremia

Lithium is the first-line maintenance therapy in bipolar affective disorder. It is excreted by the kidneys without undergoing metabolism [1]. Several factors can influence its plasma concentration, including sodium levels, fluid intake, and numerous medications, primarily nonsteroidal anti-inflammatory drugs (NSAIDs), angiotensin-converting enzyme inhibitors (ACE inhibitors), diuretics – mainly thiazides – and angiotensin II receptor blockers. Lithium salt toxicity can lead to acute kidney injury and lithium-induced nephrogenic diabetes insipidus (Li-NDI), accompanied by hypernatremic dehydration, which further exacerbates neurological symptoms and can result in patient death [2,3,4]. Chronic lithium therapy may also cause varying degrees of glomerulopathy, predominantly focal segmental glomerulosclerosis (FSGS) and minimal change disease (MCD). The article presents two cases of lithium toxicity, the complications that arose during therapy, and the treatment applied. It discusses recommendations regarding the treatment of lithium salt toxicity and the mechanisms leading to acute and chronic nephropathy.
(POL NEPHROL DIAL 2025; 29: 143-146)

K. Jakucka-Burek, M. Janas