Mejías E, Navas J, Lluberes R, Martínez-Maldonado M
Department of Internal Medicine, San Juan Veterans Administration Medical Center, Puerto Rico.
Am J Med Sci. 1989 Mar;297(3):145-8. doi: 10.1097/00000441-198903000-00002.
The relationship between hyperuricemia, gout, and autosomal dominant polycystic kidney disease (ADPKD) is not widely recognized. In an attempt to further clarify this relationship, the authors have studied 17 patients with ADPKD, 9 controls, 9 patients with proven gout and chronic renal failure, 11 patients with gout and normal renal function, and 11 patients with chronic renal failure. The mean serum uric acid concentration was higher in patients with ADPKD as a group than in controls (8.0 +/- 1.7 mg/dl vs. 6.4 +/- 1.6 mg/dl, p less than .02). Clinical gout was identified in 24% of patients with ADPKD; none of the patients with chronic renal failure of other etiologies had gout. Fractional excretion of uric acid and the activity of the enzyme hypoxanthine guanine phosphoribosyl transferase (HGPRT) were not different among the groups studied. From this study the authors conclude that ADPKD should be included among those diseases associated with hyperuricemia and gout. A partial deficiency in HGPRT or abnormal renal handling of uric acid do not appear to be responsible for the increased incidence of gout in patients with ADPKD.
高尿酸血症、痛风与常染色体显性遗传性多囊肾病（ADPKD）之间的关系尚未得到广泛认可。为进一步阐明这种关系，作者对17例ADPKD患者、9例对照者、9例已证实患有痛风和慢性肾衰竭的患者、11例患有痛风且肾功能正常的患者以及11例慢性肾衰竭患者进行了研究。ADPKD患者组的平均血清尿酸浓度高于对照组（8.0±1.7mg/dl对6.4±1.6mg/dl，p＜0.02）。24%的ADPKD患者确诊患有临床痛风；其他病因导致慢性肾衰竭的患者均无痛风。所研究的各组间尿酸排泄分数及次黄嘌呤鸟嘌呤磷酸核糖转移酶（HGPRT）的活性无差异。作者从这项研究得出结论，ADPKD应被列入与高尿酸血症和痛风相关的疾病之中。HGPRT部分缺乏或肾脏对尿酸的处理异常似乎并非ADPKD患者痛风发病率增加的原因。
