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Renal Tubular Dysfunction and Cirrhosis-Reply

Michael F. Michelis, MD; Peter C. Warms, MD; Robert D. Fusco, MD; Bernard B. Davis, MD
Arch Intern Med. 1975;135(5):748. doi:10.1001/archinte.1975.00330050122027.
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To the Editor.  —We are appreciative of and in complete agreement with Eastlund's remarks summarizing the various factors, including the status of the extracellular fluid volume, that may influence the renal tubular handling of uric acid. In this regard, however, it may be well to recall that the patients with noticeable hypouricemia, who were selected by us for special studies, all showed varying degrees of fluid accumulation. These patients, then, were clearly retaining sodium and water, as has been commonly observed in individuals with advanced cirrhosis.1 This abnormality has been suggested to result, at least in part, from increased proximal tubular sodium and water reabsorption,2 and one may have expected that these patients might also evidence renal urate retention. Obviously, this was not the case.We cannot comment on the possible role of estrogen accumulation in relation to the decreased serum uric acid levels observed in our patients,


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