Diabetes insipidus lithium-induced

Polydipsia and polyuria are common but reversible concomitants of lithium treatment, occurring at therapeutic serum concentrations. The principal physiologic lesion involved is loss of responsiveness to antidiuretic hormone (nephrogenic diabetes insipidus). Lithium-induced diabetes insipidus is resistant to vasopressin but responds to amiloride. 

Carbamazepine and lithium can elevate each other s serum levels (the mechanism is unknown). Toxicity is possible while blood levels are within the normal range, and is partially associated with pre-existing brain abnormalities. The diuretic effect of lithium outweighs the antidiuretic effect of carbamazepine. Carbamazepine does not protect against lithium-induced diabetes insipidus. Lithium can enhance carbamazepine-induced hyponatremia. 

Stone, K.A. (1999) Lithium-induced nephrogenic diabetes insipidus. J Am Board Earn Pract 12 43—47. 

Both drugs are used in conjunction with other diuretics like thiazide or loop diuretics to augment natriuresis and reduce loss of potassium. Triamterene may be used in the treatment of congestive heart failure, cirrhosis and the edema caused by secondary hyperaldosteronism. Amiloride is also useful in lithium induced diabetes insipidus. 

Billings PR. Amiloride in the treatment of lithium induced diabetes insipidus (letter). N Engl J Med 1985 312 1575-1576. 

Bisphosphate nucleotidase Involved in AMP production inhibited by lithium may be target that results in lithium-induced nephrogenic diabetes insipidus... 

The authors suggested that the sequence of events was lithium-induced nephrogenic diabetes insipidus resulting in hypernatremia followed by the dural sinus thrombosis. 

When a 45-year-old man with severe lithium-induced diabetes insipidus developed hyperosmolar, nonketotic hyperglycemia, it was suggested that poorly controlled diabetes mellitus may have contributed to the polyuria (684). Prior contact with a female patient who had developed hyperosmolar coma secondary to lithium-induced diabetes insipidus (685) allowed physicians 4 years later to treat her safely after a drug overdose and a surgical procedure, by avoiding intravenous replacement fluids with a high dextrose content (despite stopping lithium several years earlier, the patient continued to put out 10 liters of urine daily) (686). 

Azam H, Newton RW, Morris AD, Thompson CJ. Hyperosmolar nonketotic coma precipitated by lithium-induced nephrogenic diabetes insipidus. Postgrad Med J 1998 74(867) 39 11. 

MacGregor DA, Baker AM, Appel RG, Ober KP, Zaloga GP. Hyperosmolar coma due to lithium-induced diabetes insipidus. Lancet 1995 346(8972) 413-7. 

Kidney urine Lithium-induced nephrogenic diabetes insipidus Rat model 1H NMR Acetate, lactate, allantoin, TMA, and creatinine (46)... 

Hypernatremia can occur secondary to dehydration in patients taking lithium and is not uncommon in association with lithium poisoning. Lithium-induced diabetes insipidus is often a contributing factor. 

Dehydration, secondary to lithium-induced nephrogenic diabetes insipidus, was thought to be the cause of a superior sagittal sinus thrombosis in a 30-year-old woman who presented with confusion, papilledema, and a left hemiparesis (336). 

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. 

Mukhopadhyay D, Gokulkrishnan L, Mohanaruban K. Lithium-induced nephrogenic diabetes insipidus in older 402. people. Age Ageing 2001 30(4) 347-50. 

Eustatia-Rutten CF, Tamsma JT, Meinders AE. Lithium- 403. induced nephrogenic diabetes insipidus. Neth J Med 2001 58(3) 137-42. 

Finch CK, Kelley KW, Williams RB. Treatment of lithium-induced diabetes insipidus with amiloride. Pharmacotherapy 2003 23(4) 546-50. 

Sirois F. Lithium-induced neurogenic diabetes insipidus in a surgical patient. Psychosomatics 2004 45 82-3. 

Nephrogenic diabetes insipidus has been described in patients receiving foscarnet, either alone or associated with a distal renal tubular acidosis [66, 67, 68]. In fact, a recent review cited foscarnet as the second most common reported cause of drug-induced diabetes insipidus, second only to lithium [69]. In experiments using toad urinary bladders [70], serosal application of foscarnet enhanced water flow in the presence of submaximal ADH concentrations, but did not affect water transport in the absence of ADH or when maximal concentrations of ADH were used. Mucosal foscarnet did not affect water transport. Further studies are needed to clarify the mechanisms for altered water handling by the kidneys with foscarnet. 

Renal urinary concentration is associated with enhanced expression of rBSCl, a rat sodium cotransporter, in the thick ascending limb of Henle. In two recent studies by Kwon et al [60] and Michimata et al [62] dehydration or high plasma AVP resulted in an enhanced expression of rBSCl in rats with lithium induced nephrogenic diabetes insipidus. rBSCl expression was closely associated with the adverse effects of Li ions on collecting duct function [60, 62]. 

Volume resuscitation is the cornerstone of management of lithium toxicity (Table 3) [124, 125]. Patients with underlying lithium-induced diabetes insipidus may initially present with volume depletion. It must be borne in mind, however, that hypernatremia [125] is a potential complication, especially in those with underlying diabetes insipidus. Forced saline diuresis is expected to increase lithium clearance by decreasing proximal tubular reabsorption. With normal renal function, lithium can be cleared at a rate of 10-40 mL/min [125]. The excretion of lithium can be further increased acutely by using acetazolamide and/or loop diuretics [124,125]. 

Singer I, Rottenberg D, Puschett IB. Lithium-Induced nephrogenic diabetes insipidus in vivo and in vitro studies. J Clin Invest 1972 51 1081-1091. 

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