Biology and Genetics of Inherited Renal Tubular Disorders (editorial)

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Title: Biology and Genetics of Inherited Renal Tubular Disorders (editorial)
Author: van't Hoff, William G.
Publisher: Experimental Nephrology
Date Published: September 1996 - October 1996
Reference Number: 7
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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)

It has been known since the 1800s that lithium dramatically altered urine output and caused polyuria (excessive urination) and nocturia (sleep being disturbed because of a need to urinate).

Incidence of polyuria in lithium patients varied widely, but in Scandinavia, it was allegedly as high as 40%. Many reports concerning lithium and polyuria have been written since then. Researchers have not always agreed, and there still are questions as to whether lithium-induced complications are reversible.

Towards the end of the 1970s, several cases were reported in which lithium-induced nephrogenic diabetes insipidus (NDI) persisted several months after lithium treatment ceased. It was also reported that lithium-induced defects in urine concentrating ability were not reversible and represented underlying kidney damage. This damage may be aggravated by the concomitant use of neuroleptics (antipsychotic drugs used to treat schizophrenia, paranoia, and other disorders).

An influential report documented a correlation between impaired urine concentrating ability and duration of lithium therapy; it also established a connection between impaired urine concentrating ability and kidney tissue damage. These researchers later asserted that 26% of those on maintenance lithium treatment for more than two years would develop some form of nephritis (inflammation of one or both kidneys) and their ability to concentrate urine would continue to deteriorate.

One researcher has written about psychiatric patients who had not been treated with lithium and who have renal disorders similar to those described in the previous paragraph. She proposes that psychiatric patients as a group may be predisposed to kidney tissue disorders.

This review of the research concerning long-term effects of lithium on the kidneys confirms the fact that lithium is capable of disrupting water balance in the body and this frequently results in polyuria and polydipsia. Effects of long-term lithium use include decreased urine concentrating ability, diminished responsiveness to the antidiuretic hormone (ADH--ADH tells the kidneys to channel water back into the bloodstream rather than passing it into the urine), and an acute lesion on the distal nephron (in the kidney). Most researchers report that these effects seem to be reversible upon cessation of lithium use -- though not always. Diminished urine concentrating ability has not been reversible in many patients with a history of lithium toxicity (poisoning) and those who take neuroleptics simultaneously as lithium.

Lithium patients with polyuria and impaired urine concentrating ability are at increased risk of acute lithium toxicity because their kidneys do not retain enough fluids. These symptoms should be treated with a dosage reduction. Episodes of acute lithium intoxication are largely predictable, and therefore avoidable, provided appropriate precautions are taken.