Lithium and Nephrogenic Diabetes Insipidus: Mechanism
Within the collecting duct of the kidney, Aquaporin water channels (AQP2) under the regulation of anti diuretic hormone (ADH) control the movement of water into principal cells.
Principal cells: Manage the Na+/K+ exchange in the collecting duct.
Long term lithium ingestion can manifest with polyuria/ polydipisa due to ADH resistance.
The proposed thought is principal cells uptake Lithium (cation) via the epithelial sodium channels (ENac) located on the luminal side of the principal cells.
The lithium accumulates in the principal cells, interfering with the ability of ADH to increase water permeability.
- M.J. Godinich, D.C. BatlleRenal tubular effects of lithium. Kidney Int, 37 (Suppl 28) (1990), pp. S52-S57.
- J.N.J. Forrest, A.D. Cohen, J. Torretti, M. Himmelhoch, F.H. Epstein. On the mechanism of lithium-induced diabetes insipidus in man and the rat. J Clin Invest, 53 (1974), pp. 1115-1123.
- Trepiccione F., Christensen BM. Lithium-induced nephrogenic diabetes insipidus: new clinical and experimental findings. J Nephrol. 2010 Nov-Dec;23 Suppl 16:S43-8.
- Ecelbarger CA. Lithium treatment and remodeling of the collecting duct. Am J Physiol Renal Physiol. 2006 Jul;291(1):F37-8. Epub 2006 Mar 28.
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