Nephrogenic diabetes insipidus, lithium-induced

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

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

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. 

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

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. 

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

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. 

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]. 

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

Yamaki M, Kusano E, Homma S. Cellular mechanisms of lithium Induced nephrogenic diabetes Insipidus. Am Soc Nephrol 1989 404A. 

Answer C. Neurogenic diabetes insipidus is treated with desmopressin, a drug that is similar to vasopressin (ADH) but a selective activator of V2 receptors in the kidney. Remember that V, receptors are present in smooth muscle, and their activation leads to vasoconstriction and bronchoconstriction. Nephrogenic diabetes insipidus (decreased response of vasopressin receptors) is treated with thiazides except in the case of that induced by lithium, when amiloride is preferred (because thiazides increase blood levels of lithium). 

Use adjunct to K -wasting diuretics, lithium-induced nephrogenic diabetes insipidus (amiloride)... 

B. Chronic intoxication may occur in patients on stable therapeutic doses. Lithium is excreted by the kidney, where it is handled like sodium any state that causes dehydration, sodium depletion, or excessive sodium reabsorption may lead to increased lithium reabsorption, accumulation, and possibly intoxication. Common states causing lithium retention include acute gastroenteritis, diuretic use, use of nonsteroidal anti-inflammatory drugs or angiotensinconverting enzyme (ACE) inhibitors, and lithium-induced nephrogenic diabetes insipidus. 

In dehydrated patients, replace fluid deficits with intravenous crystalloid solutions. Initial treatment should Include repletion of sodium and water with 1-2 L of normal saline (children 10-20 mL/kg). Once fluid deficits are replaced, give hypotonic (eg, half-normal saline) solutions because continued administration of normal saline often leads to hypernatremia, especially in patients with lithium-induced nephrogenic diabetes insipidus. 

Martinez-Maldonado M, TerreU J. Lithium carbonate-induced nephrogenic diabetes insipidus and g ucosemto erancQ. Arch Intern Med (1973) 132, 881-4. 

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