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Lithium is readily absorbed from the gastrointestinal tract. [5] It is distributed to the body with higher levels in the kidney, thyroid, and bone as compared to other tissues. Since lithium is almost exclusively excreted by the kidneys, people with preexisting chronic kidney disease are at high risk of developing lithium intoxication. [13]
Continued use of lithium can lead to more serious kidney damage in an aggravated form of diabetes insipidus. [90] [91] In rare cases, some forms of lithium-caused kidney damage may be progressive and lead to end-stage kidney failure with a reported incidence of 0.2% to 0.7%. [92]
The most obvious cause is a kidney or systemic disorder, including amyloidosis, [2] polycystic kidney disease, [3] electrolyte imbalance, [4] [5] or some other kidney defect. [2] The major causes of acquired nephrogenic diabetes insipidus that produce clinical symptoms (e.g., polyuria) in the adult are lithium toxicity and high blood calcium.
Nephrotoxicity is toxicity in the kidneys. It is a poisonous effect of some substances, both toxic chemicals and medications, on kidney function. [1] There are various forms, [2] and some drugs may affect kidney function in more than one way. Nephrotoxins are substances displaying nephrotoxicity.
Kidney toxicity [5] associated with kidney failure; associated with development of cancer, particularly of the urinary tract, known carcinogen [8] [9] Atractylate Atractylis gummifera: Liver damage, [3] nausea, vomiting, epigastric and abdominal pain, diarrhoea, anxiety, headache and convulsions, often followed by coma [10]
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Excessive levels of lithium can be harmful to the kidneys, and increase the risk of side effects in general. As a result, kidney function and blood levels of lithium are monitored in patients being treated with lithium. [2] Therapeutic plasma levels of lithium range from 0.5 to 1.5 mEq/L, with levels of 0.8 or higher being desirable in acute ...
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