Mehta Paulomi, Slatter Tania, Walker Robert
Kidney Injury and Transplant Immunology Group, Centre for Transplant and Renal Research, Westmead Institute for Medical Research, Westmead, New South Wales, Australia.
Department of Medical Laboratory Science, School of Pharmacy, University of Otago, Dunedin, New Zealand.
Physiol Rep. 2025 Sep;13(17):e70552. doi: 10.14814/phy2.70552.
Lithium-induced kidney injury is commonly associated with the development of nephrogenic diabetes insipidus. Longer term lithium exposure is associated with the development of chronic interstitial fibrosis. The mechanisms of lithium-induced kidney injury are multifaceted, affecting many intracellular cell signaling pathways associated with cell cycle regulation, cell proliferation, and subsequent increased extracellular matrix formation and interstitial fibrosis. Amiloride has been demonstrated to have multiple pleiotropic actions, independent of its competitive antagonism of ENaC, in reducing the progressive lithium-induced interstitial fibrosis. Further exploration of these interactions has the potential to expand our knowledge of pathways of tubular cell injury and repair, which in turn will lead to potential new therapeutic targets and drugs.
锂诱导的肾损伤通常与肾性尿崩症的发生有关。长期接触锂与慢性间质纤维化的发生有关。锂诱导肾损伤的机制是多方面的,影响许多与细胞周期调控、细胞增殖以及随后细胞外基质形成增加和间质纤维化相关的细胞内信号通路。已证明氨氯地平在减轻锂诱导的进行性间质纤维化方面具有多种多效性作用,这与其对上皮钠通道(ENaC)的竞争性拮抗作用无关。对这些相互作用的进一步探索有可能扩展我们对肾小管细胞损伤和修复途径的认识,进而带来潜在的新治疗靶点和药物。