Finally, this leads to proximal tubular reabsorption, quantified at 80% of that secreted. Subsequently, a tubular secretory phase is produced, with 50% of the urate initially filtered remaining in the tubular lumen. The proportion of filtered urate reabsorbed in the proximal tubule was 99%-100%, leaving 0%-2% of filtered urate in the tubular lumen. 10 The 3-component hypothesis had thus become 4. 9 In the early 70s, Diamond and Paolino, through the sequential combination of various uricosuric medications (sulphinpyrazone, probenecid and salicylates at high doses) and pyrazinamide in healthy subjects, reported the existence of a reabsorption of urate in an area distal to secretion (postsecretory reabsorption). It is later actively reabsorbed in the proximal tubule and then secreted into the tubular lumen. Uric acid circulating in the blood is passively filtered at the glomerulus. 8 Four years later, those same authors published their 3-component theory. The existence of a tubular secretion phase for uric acid was again proposed in 1957 when Gutman and Yu studied 300 patients with gout and concluded that a reduction in the tubular secretion of uric acid could explain the reduction of uricosuria found. It was the first reported case of renal tubular hypouricemia. This led them to assume that this individual’s kidney secreted uric acid. 6 That same year, Praetorius and Kirk described the case of a patient with a severe hypouricemia in which the clearance of uric acid was higher than creatinine. Studying the clearances of inulin and urate, they came to the conclusion that “urate is excreted by glomerular filtration and active tubular reabsorption”. To explain this “incomprehensible phenomenon”, the authors induced hyperuricemia in a group of healthy subjects by an overload of lithium carbonate. tried to find an explanation for the finding that uric acid clearance was lower than that of creatinine. In the early twentieth century, it was assumed that uric acid was filtered by the kidney, and thus excreted in the urine. PHYSIOLOGICAL AND HISTORICAL BACKGROUND OF RENAL TUBULAR HANDLING OF URIC ACID. 1,2 Urate elimination is best studied as an excretion index (normal: 0.40☐.09mg/100ml) 3 or preferably as fractional excretion (normal: 7.25☒.98%). Normal uricosuria values in adults are 620☗5mg/day. Urate excreted in the urine accounts for approximately 70% of that produced daily, with the rest excreted in the faeces. Thus, hyperuricemia is defined as the existence of values above 7mg/dl in men and higher than 6mg/dl in women. Serum urate concentrations are higher in men than in women. NORMAL uric acid Plasma values and urinary excretion Therefore, new therapies to block or stimulate these transport mechanisms may become available in the coming years. Moreover, from a physiological standpoint, there have been new contributions on the mechanisms of uric acid transport in the renal proximal tubule. However, hypouricemia is now increasingly common in nephrology consultations, as a greater number of patients with diabetic nephropathy are seen, and because it is increasingly common to see patients from different races and countries. Traditionally, hypouricemia has not been given the same importance as hyperuricemia, perhaps because of its lower incidence rate. However, it is a biochemical finding that deserves attention since it may be associated with primary or secondary tubulopathies and other underlying conditions. Hypouricemia has no recognisable symptoms, and therefore requires no treatment.
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