Steele T H, Manuel M A, Boner G
Nephron. 1975;14(1):49-61.
The uricosuric properties of acetazolamide were investigated in order to elucidate the relationship between changes in proximal tubular sodium reabsorption and urate excretion in man. Acetazolamide produced a modest uricosuric response which was not suppressible by pyrazinamide. Alkalinization of the urine with sodium bicarbonate elicited an even smaller increment in the urate clearance. If urinary alkalinization does play a role in the uricosuric response to acetazolamide, it probably decreases urate reabsorption within the distal nephron. The present studies, when taken together with previous work, suggest that alterations in proximal tubular sodium and water reabsorption probably do not play an important role in the normal control of urate excretion or in the pathogenesis of hyperuricemic states. Diuretic-induced hyperuricemia occurring during extracellular fluid volume depletion probably results from either diminished tubular secretion of urate, accelerated postsecretory urate reabsorption, or both.
为阐明人体近端肾小管钠重吸收变化与尿酸排泄之间的关系，对乙酰唑胺的促尿酸排泄特性进行了研究。乙酰唑胺产生了适度的促尿酸排泄反应，该反应不能被吡嗪酰胺抑制。用碳酸氢钠碱化尿液引起的尿酸清除率增加甚至更小。如果尿液碱化在对乙酰唑胺的促尿酸排泄反应中确实起作用，那么它可能会降低远端肾单位内尿酸的重吸收。本研究与先前的工作一起表明，近端肾小管钠和水重吸收的改变可能在尿酸排泄的正常调节或高尿酸血症状态的发病机制中不起重要作用。细胞外液量减少期间利尿剂引起的高尿酸血症可能是由于尿酸的肾小管分泌减少、分泌后尿酸重吸收加速或两者兼而有之。
