Abstract
Because of its existence in man as a sparingly soluble end-product of purine metabolism, the elimination of uric acid from the body has assumed special significance in human physiology and medicine (Sorensen and Levinson, 1975). Urate excretion is normally partitioned between the kidney and intestine. The ratio of renal-to-extra-renal urate elimination is approximately 2:1 in normal persons stabilized on a low dietary purine intake, under steady-state conditions, when uric acid turnover reflects the rate of de novo purine biosynthesis (Sorensen, 1960; Sorensen, 1965). Under conditions of normal dietary purine intake, however, exogenous purine is also metabolized to uric acid (Zöllner, 1973). The extent to which such exogenous purine may alter the ratio of renal-to-intestinal urate elimination has not been characterized in detail. However, based on studies in hypouricemic patients with Wilson’s disease who manifested defective renal urate reabsorption, the available evidence suggests that intestinal uric acid elimination may fall to very low values in hypouricemic states, with the kidney concomitantly excreting a much greater fraction of the urate turnover (Sorensen and Kappas, 1966). This situation can reverse following successful treatment of the renal lesions of Wilson’s disease with penicillamine. Conversely, intestinal elimination assumes a greater role in uric acid elimination in patients with advanced chronic renal insufficiency, in whom the urinary urate excretion may be greatly depressed (Sorensen and Levinson, 1975).
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Steele, T.H. (1978). Urate Excretion in Man, Normal and Gouty. In: Kelley, W.N., Weiner, I.M. (eds) Uric Acid. Handbook of Experimental Pharmacology, vol 51. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-66867-8_10
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