de Vries A, Sperling O
Ciba Found Symp. 1977(48):179-206. doi: 10.1002/9780470720301.ch12.
The spectrum of kidney and urinary tract disorders related to purines comprises acute hyperuricosuric nephropathy, chronic urate nephropathy and urolithiasis. Two factors in the development of acute hyperuricosuric nephropathy are increased uric acid concentration and low pH in the tubular fluid. Chronic urate nephropathy still possess several problems: incidence (although this seems to be decreasing, presumably owing to effective prevention), the source of interstitial urate, the cause of the interstitial deposition of urate, and the role of urate deposits in the pathogenesis of the interstitial nephropathy. The relation of the experimental nephropathy to the pathogenesis of chronic urate nephropathy in the human is not yet clear but a model is proposed according to which interstitial urate derives from two sources: hyperuricaemic plasma and hyperuricosuric tubular fluid. Urolithiasis related to purines leads to uric acid-urate stones, xanthine stones, 2,8-dihydroxyadenine stones, iatrogenic xanthine and oxipurinol stones, and possibly calcium stones. Pathogenetic factors in uric acid lithiasis are hyperuricosuria (whether due to an inborn enzyme abnormality or of unknown aetiology) and low urinary pH; oliguria is a contributory factor. There remain several open questions about uric acid lithiasis: incidence, the shift of its location from lower to upper urinary tract, the interplay of pathogenetic factors, and the role of compounds which inhibit crystallization.
与嘌呤相关的肾脏和尿路疾病谱包括急性高尿酸血症性肾病、慢性尿酸盐肾病和尿石症。急性高尿酸血症性肾病发生的两个因素是尿酸浓度升高和肾小管液pH值降低。慢性尿酸盐肾病仍存在几个问题：发病率（尽管似乎在下降，可能是由于有效的预防措施）、间质尿酸盐的来源、尿酸盐间质沉积的原因以及尿酸盐沉积在间质性肾病发病机制中的作用。实验性肾病与人类慢性尿酸盐肾病发病机制之间的关系尚不清楚，但有人提出了一个模型，根据该模型，间质尿酸盐来自两个来源：高尿酸血症血浆和高尿酸尿性肾小管液。与嘌呤相关的尿石症可导致尿酸-尿酸盐结石、黄嘌呤结石、2,8-二羟基腺嘌呤结石、医源性黄嘌呤和奥昔嘌醇结石，以及可能的钙结石。尿酸结石形成的致病因素是高尿酸尿症（无论是由于先天性酶异常还是病因不明）和低尿pH值；少尿是一个促成因素。关于尿酸结石仍有几个未解决的问题：发病率、其位置从下尿路向上尿路的转移、致病因素的相互作用以及抑制结晶的化合物的作用。
