Sorensen L F
Ann Rheum Dis. 1980 Oct;39(5):424-30. doi: 10.1136/ard.39.5.424.
A report of 20 cases of gout considered to be secondary to chronic renal disease is presented. Studies of renal function and of uric acid metabolism were carried out in 16 patients. The daily production of urate remained within normal limits in the face of progressive renal dysfunction. Renal excretion of uric acid was decreased to a mean of 35.5% of the turnover. The cumulative urinary recovery of intravenously injected 14C-uric acid averaged 32.0%. In 3 patients 14C was successively retrieved in urinary allantoinand urea, in carbon dioxide of expired air, and in faeces. As in normal man, carbon dioxide and ammonia were the principal uricolytic products. The extrarenal excretion of uric acid assumes a greater role in chronic renal disease and eventually becomes the major route of elimination of uric acid. The possibility that gout may be secondary to intrinsic renal disease should be entertained when azotaemia is present.
本文报告了20例被认为继发于慢性肾病的痛风病例。对16例患者进行了肾功能和尿酸代谢研究。尽管肾功能进行性减退，但尿酸盐的日生成量仍保持在正常范围内。尿酸的肾脏排泄减少至周转率的平均35.5%。静脉注射14C-尿酸后，尿中累积回收率平均为32.0%。在3例患者中，14C先后在尿中尿囊素和尿素、呼出气体的二氧化碳以及粪便中被回收。与正常人一样，二氧化碳和氨是主要的尿酸分解产物。在慢性肾病中，尿酸的肾外排泄起更大作用，最终成为尿酸排泄的主要途径。当存在氮质血症时，应考虑痛风可能继发于原发性肾病的可能性。
