Lithium And Nephrogenic Diabetes Insipidus

 

                                                                            LIT 

Lit With Lithium

                                             Lithium = Nephrogenic Diabetes Insipidus 

                                                           INCREASED URINATION

 Emergence of Nephrogenic Diabetes Insipidus (NDI) as a Side Effect

• 1960s–1970s: As lithium use increased, nephrologists began reporting cases of polyuria (excessive urination) and polydipsia (excessive thirst) in patients on chronic lithium therapy.

• These symptoms were eventually recognized as nephrogenic diabetes insipidus, a condition where the kidneys become unresponsive to antidiuretic hormone (ADH), leading to impaired water reabsorption.

 Mechanistic Insights

• 1970s–1980s: Research identified that lithium enters the principal cells of the collecting duct in the kidney via epithelial sodium channels (ENaCs).

• Lithium disrupts the cyclic AMP (cAMP) pathway, which is critical for the insertion of aquaporin-2 (AQP2) water channels in the apical membrane. This prevents water reabsorption in response to ADH, leading to NDI.

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