Diabetes insipidus lithium causing

In nephrogenic diabetes insipidus the kidney s ability to respond to AVP is impaired by different causes, such as drugs (e.g. lithium), chronic disorders (e.g. sickle cell disease, kidney failure) or inherited genetic disorders (X-linked or autosomal NDI). This type of diabetes insipidus can not be treated by exogenous administration of AVP or AVP analogues. Instead, diuretics (hydrochlorothiazide combined or not with amiloride) and NSAI (indomethacin) are administrated to ameliorate polyuria. 

The answer is c. (Katzung, p 493.) Lithium treatment frequently causes polyuria and polydipsia. The collecting tubule of the kidney loses the capacity to conserve water via anti diuretic hormone. This results in significant free-water clearance, which is referred to as nephrogenic diabetes insipidus. 

Lithium reduces the kidney s ability to concentrate urine and may cause a nephrogenic diabetes insipidus with low urine specific gravity and low osmolality polyuria (urine volume greater than 3 L/day). This may be treated with loop diuretics, thiazide diuretics, or triamterene. If a thiazide diuretic is used, lithium doses should be decreased by 50% and lithium and potassium levels monitored. 

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. 

If serum Na+ is not monitored closely, ADH antagonists can cause severe hypernatremia and nephrogenic diabetes insipidus. If lithium is being used for a psychiatric disorder, nephrogenic diabetes insipidus can be treated with a thiazide diuretic or amiloride. 

Also known as water diabetes, diabetes insipidus (DI) is a rare chronic disease that causes excessive urination. If not properly treated, it can result in electrolyte imbalance and dehydration. It may be caused by a number of factors, including lithium use (a psychiatric drug used for bipolar disorder), neurological disease, or an inadequate amount of ADH (anti-diuretic hormone, or vasopressin, which is produced by the pituitary gland). DI caused by insufficient ADH is called central diabetes insipidus. 

Lithium also impairs the function of the peripheral nervous system, reducing motor nerve conduction velocity (Faravelli et al., 1999). It causes many metabolic adverse effects, resulting in hypothyroidism, hyperthyroidism (rare), hyperparathyroidism, and diabetes insipidus (Livingston et al., 2006). 

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). 

The authors reviewed the causes and pathophysiological mechanisms of nephrogenic diabetes insipidus. They also discussed the metabolic effects of lithium, including renal and thyroid effects, hypercalcemia, leukocytosis, and weight gain. 

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. 

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... 

In children under 8 years of age, demeclocycline (like other tetracyclines) causes bone and teeth abnormalities. Lithium causes nephrogenic diabetes insipidus as a toxic effect the drug is never used to treat SIADH because of its other toxicities. 

Lithium and only a few other drugs have been reported to cause chronic interstitial nephritis, which is usually a progressive and irreversible lesion (Choudhury and Ahmed 2006 Silva 2004). Several renal tubular lesions have been associated with lithium therapy an impaired ability to concentrate urine (nephrogenic diabetes insipidus) has been seen in up to 87% of patients (Markowitz et al. 2000). Acute... 

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. 

Thyroid storm associated with hypercalcemia and diabetes insipidus followed an episode of lithium toxicity in a 67-year-old man taking long-term lithium [36 ]. The thyroid disorder followed a thyroiditis pattern, in which the patient became hypothyroid before spontaneous normalization. Since this is such an unusual occurrence, hthium may not have played a significant causative role in this man s illness. 

A 24-year-old woman who was 24 weeks pregnant and had pregnancy-related hyponatremia and mood symptoms was given lithium and developed diabetes insipidus, which rapidly corrected her hyponatremia and caused central pontine and extrapontine myehnolysis [48 ]. 

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