Lithium Nephrotoxicity
| Title: | Lithium Nephrotoxicity |
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| Author: | Walker, Rowan G. |
| Publisher: | Kidney International (Supplement) |
| Date Published: | July 01, 1993 |
| Reference Number: | 129 |
After nearly two decades of concern and controversy surrounding the long-term effects of lithium on the kidney, the fact that lithium is capable of causing a major disturbance in water balance, manifest as polyuria and secondary polydipsia, remains undisputed. A decreased urinary concentrating ability (nephrogenic diabetes insipidus) with a disturbed responsiveness of the distal nephron to the action of ADH (vasopressin) is demonstrable, and the symptoms are largely reversible on cessation of lithium or reduction of the dose. An acute histological lesion of the distal nephron, corresponding to the site of lithium inhibition of the action of ADH, and consisting of epithelial cellular swelling and glycogen deposition, also appears to be readily reversible. Of greater concern is the development of a progressive impairment of urinary concentrating ability in patients on long-term maintenance therapy--especially those with a history of acute lithium toxicity and those additionally treated with neuroleptics. This functional lesion is not always reversible, and the underlying renal histology is a chronic focal interstitial nephropathy. Interestingly, some psychiatric patients never exposed to lithium have demonstrated similar renal histology. There is very little evidence that stable maintenance lithium therapy, without episodes of acute intoxication, is associated with a reduction of glomerular filtration rate. Episodes of acute lithium intoxication are largely predictable, and therefore avoidable, provided appropriate precautions are taken. Patients with polyuria and impaired urinary concentrating ability are at increased risk of acute lithium toxicity because of excessive renal losses of fluid, and these symptoms should be treated in the first instance with dosage reduction. (ABSTRACT TRUNCATED AT 250 WORDS)
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This translation by the NDI Foundation is to assist the lay reader. To provide a clear, accessible interpretation of the original article, we eliminated or simplified some technical detail and complicated scientific language. We concentrated our translation on those aspects of the article dealing directly with NDI. The NDI Foundation thanks the researchers for their work toward understanding and more effectively treating this disorder.
© Copyright NDI Foundation 2007 (JC)
One of the most common side-effects of long-term lithium use is the development of nephrogenic diabetes insipidus (NDI), a kidney disorder characterized by a reduced ability to concentrate urine. One of NDI's primary symptoms is polyuria -- the chronic passage of large amounts of urine. The incidence of polyuria in patients on lithium vary, but have been reported to be as high as 40% in Scandinavian studies. Fortunately, discontinuing lithium use often results in reversal of NDI symptoms, though some research indicates that the long-term use of lithium makes reversibility less likely and can lead to underlying kidney damage.
However, long-term lithium therapy, especially in those with a history of acute lithium toxicity and those treated concurrently with a class of drugs called neuroleptics, can result in the development of a progressive impairment of urinary concentrating ability. Several studies showed significant correlation between impaired urinary concentrating ability and duration of lithium therapy or total lithium dose. This highlighted a possible link between chronic lithium administration, impaired urinary concentrating ability and progressive kidney damage. Additionally, the underlying damage to the kidneys that leads to impaired urinary concentration is not always reversible. Interestingly, one study revealed that some psychiatric patients with manic depression and other, similar bipolar affective disorders who have never been treated with lithium showed kidney damage similar to those observed in patients taking maintenance doses of lithium. This suggests the possibility that psychiatric patients with these sorts of affective disorders may, as a group, be predisposed to the development of chronic kidney disease.
Walker notes that stable lithium therapy does not adversely affect all parts of the kidney. For example, the kidneys' ability to filter body fluid does not seem to be affected, unless the patient has had episodes of acute lithium intoxication. But patients with polyuria and impaired urinary concentrating ability can have excessive loss of fluid from the kidneys and this increases their risk of lithium toxicity. Thus, Walker cautions that, though the risk of chronic kidney damage seems to be small, patients on lithium should be monitored, especially to prevent acute lithium toxicity. For it is such toxicity that can most readily compromise kidney structure and function.