Fellström B, Backman U, Danielson B G, Johansson G, Ljunghall S, Wikström B
Nephron. 1982;31(1):31-6. doi: 10.1159/000182610.
The renal handling of urate was investigated in 28 recurrent calcium stone formers and 12 healthy controls. 12 patients were hyperuricosuric and 16 patients had incomplete proximal or distal acidification defects. Measurements of the glomerular filtration and the tubular reabsorption of filtered urate were made through the pyrazinamide (PZA)-suppression test of urate secretion. Hyperuricosuria could not be explained by defects in the renal handling of urate. Patients with proximal acidification defects had a higher tubular reabsorption of filtered urate than the other subjects. Tubular reabsorption of filtered urate was inversely correlated, and filtered urate escaping reabsorption positively correlated to the 24-hour excretion of urate. In contrast, the PZA-suppressible fraction of urate excretion, which is the net effect of tubular secretion and post-secretory reabsorption and thought to be the main regulator of urate excretion, was not correlated to the 24-hour excretion of urate. It is concluded that the renal handling of urate is basically normal in calcium stone disease, whereas minor deviations may co-exist with renal tubular acidification dysfunction.
对28例复发性钙结石患者和12名健康对照者的尿酸盐肾脏处理情况进行了研究。12例患者尿酸排泄过多,16例患者存在近端或远端酸化不完全缺陷。通过尿酸盐分泌的吡嗪酰胺(PZA)抑制试验对滤过尿酸盐的肾小球滤过和肾小管重吸收进行了测量。尿酸排泄过多无法用尿酸盐肾脏处理缺陷来解释。近端酸化缺陷患者滤过尿酸盐的肾小管重吸收高于其他受试者。滤过尿酸盐的肾小管重吸收呈负相关,而逃脱重吸收的滤过尿酸盐与尿酸盐24小时排泄呈正相关。相比之下,尿酸盐排泄的PZA可抑制部分,即肾小管分泌和分泌后重吸收的净效应,被认为是尿酸盐排泄的主要调节因子,与尿酸盐24小时排泄无关。得出的结论是,钙结石病中尿酸盐的肾脏处理基本正常,而轻微偏差可能与肾小管酸化功能障碍并存。