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- W2499642731 abstract "Wilson disease is a disorder of copper metabolism due to defective intracellular copper transport in hepatocytes. The mutant gene in Wilson disease encodes a copper-transporting ATPase known as ATP7B that is mainly expressed in hepatocytes. Mutations that cause reduced function or absence of ATP7B reduce hepatic biliary copper excretion and cause hepatic copper accumulation. Nephrolithiasis may be found in some patients with Wilson disease. This is most likely present in patients with tubular defects in acidification or resultant changes in the urinary excretion of substrates that augment stone formation. In the setting of either acute or severe chronic liver failure due to Wilson disease, hepatorenal syndrome may develop. This entity is defined by the development of oliguria in association with reduced renal clearance and a low urine sodium excretion of ‹10 mEq/l that is unresponsive to volume expansion. Patients with acute liver failure due to Wilson disease have a higher incidence of renal dysfunction compared to other etiologies of liver failure. Renal injury may occur not only from copper, but also from some of the treatments for Wilson disease. Most commonly, the copper-chelating drug, d-penicillamine, may cause acute or later-onset renal toxicity. A syndrome with lupus nephritis may occur early on, associated with the appearance of cellular elements in the urinary sediment and renal injury. Proteinuria of varying degrees may occur even years following the initiation of therapy with d-penicillamine. Within the first 2 years of therapy, low-molecular-weight proteins are found in the urine, suggesting tubular injury." @default.
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- W2499642731 date "2009-01-01" @default.
- W2499642731 modified "2023-09-25" @default.
- W2499642731 title "Wilson Disease and the Kidney" @default.
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- W2499642731 doi "https://doi.org/10.1016/b978-0-12-449851-8.00042-5" @default.
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