Lithium diabetes insipidus from

The long-term toxic effects of lithium, such as nephrogenic diabetes insipidus, which has been calculated to occur in up to 5% of patients, and the rare possibility of lithium combined with neuroleptics being neurotoxic, has stimulated the research for other drug treatments. However, apart from the neuroleptics, these drugs have not been studied as extensively in the treatment of acute mania, but are worthy of consideration because of their reduced side effects. 

A 76-year-old man developed severe intractable diabetes insipidus which was attributed to lithium (395). He was hospitalized for over 2 weeks and eventually died from intestinal hemorrhage. Vigorous efforts were made to treat his polyuria, electrolyte disturbances, hypernatremia, and dehydration. He had been taking chlorpromazine, lithium, and furosemide, along with other medications, and the diagnosis of lithium-induced nephrogenic diabetes insipidus was considered because of a lack of alternative explanations. 

Overdose is treated by use of i.v. fluid to maintain a good urine output guided by frequent measurement of plasma electrolytes and osmolality. Hyper-natraemia indicates probable diabetes insipidus and isotonic dextrose should then be used until plasma sodium concentration and osmolality become normal. Isotonic saline foriirs part of the fluid regimen (but overuse may result in hypematrae-mia) and potassium supplement will be required. Haemodialysis is effective but may have to be repeated frequently as plasma concentration rises after acute reduction (due to equilibration as lithium leaves cells and also by continued absorption from sustained-release formulahons). 

Many drugs and other chemicals can adversely affect renal function by directly or indirectly affecting the reabsorption of electrolytes and water in the kidney. Chlorpropamide can enhance the secretion of ADH and promote the water conservation actions of the hormone, while lithium use can lead to a nephrogenic diabetes insipidus. NSAIDs block the formation of renal prostaglandins, which can result in hyperkalemia. Hyperkalemia may also result from the use of beta blockers, potassium-sparing diuretics, and cyclosporine. 

In this condition the renal tubules are unresponsive to antidiuretic hormone and, as such, the subject has polyuria. The condition may be congenital or acquired. Acquired nephrogenic diabetes insipidus can result from several causes, such as chronic renal disease, potassium deficiency including primary aldosteronism, drugs such as lithium, systemic diseases such as multiple myeloma, and chronic hypercalcemias, including hyperparathyroidism. The damage to the renal tubules... 

A 54-year-old patient developed nephrogenic diabetes insipidus when she was treated with lithium carbonate. The addition of chlorothiazide reduced her polyuria, but resulted in an elevation in her lithium level from 1.3 to more than 2 mmol/L, with accompanying signs of toxicity. The patient was later successfully treated with chlorothiazide and a reduced dose of lithium. ... 

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