Lithium renal disease

Because lithium is not bound to any plasma or tissue proteins, it is widely distributed throughout the body. Lithium ions are eliminated mainly by the kidneys. There is a direct relationship between the amount of sodium chloride ingested and the fraction of filtered lithium resorbed, in that, the lower the sodium intake, the greater is the lithium retention. The contraindications are significant cardiovascular or renal diseases that would compromise its excretion. 

Braden GL. Lithium-induced renal disease. In Greenberg A, editor. Primer on Kidney Diseases. San Diego Academic Press, 1998 332-4. 

Kincaid-Smith P. Pathogenesis of the renal lesion associated with the abuse of analgesics. Lancet 1967 1 859-862. Kincaid-Smith P, Nanra RS. Lithium-induced and analgesic-induced renal diseases. In Diseases of the kidney, 5 edition. Schrier RW, Gottschalk CW (editors). Little Brown, Boston 1993 p. 1099-1129. 

Chugh S, Yager Li. End stage renal diseases after treatment with lithium. J Clin. Psychopharmacol 1997 17 (6) 495-497. 

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... 

Chronic renal failure as a result of toxic or environmental exposures usually involve progressive chronic interstitial nephropathy, which, in addition to prolonged analgesic abuse, may result from chronic lithium ingestion, heavy metal exposure or treatment with cyclosporine [2]. Exposure to hydrocarbons may accentuate the renal insufficiency in patients with preexisting renal disease or result in the appearance of the nephrotic syndrome or a form a rapidly progressive glomerulonephritis. 

Simon G. Combination angiotensin ccmverting en me inhibitor/lithium ther y contiaindi-cated in renal disease. Am JMed( 9ZZ) 85, 893-4. 

While renal pathology associated with lithium-related end-stage renal disease is generally felt to be characterized by interstitial fibrosis and focal glomerular sclerosis, there is an increasing literature of an association with microcyst formation [48 ]. 

While renal disease is generally viewed as a reason for withdrawing lithium, in some individuals the beneficial response to lithium is unique and patients return to lithium despite kidney failure. In two cases patients were given lithium despite dialysis and end-stage renal disease due to lithium [52, 53 j. While complicated to manage, the belief in such cases is that the damage is done and continuing lithium caimot make the situation worse. 

Knebel RJ, Rosenhcht N, Collins L. Lithium carbonate maintenance therapy in a hemodialysis patient with end-stage renal disease. Am J Psychiatry 2010 167(11) 1409-10. 

Neurogenic DI—inadequate renal response to ADH associated with drug therapy (e.g., lithium), renal damage, or genetic renal disease... 

Other causes include magnesium-containing antacids in patients with renal insufficiency, enteral or parenteral nutrition in patients with multiorgan system failure, magnesium for treatment of eclampsia, lithium therapy, hypothyroidism, and Addison s disease. 

High-risk patients The risk of lithium toxicity is very high in patients with significant renal or cardiovascular disease, severe debilitation, dehydration, or sodium depletion, or in patients receiving diuretics. Undertake treatment with extreme caution. 

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