Tofuku Y, Kuroda M, Takeda R
Nephron. 1982;30(1):39-44. doi: 10.1159/000182430.
We present 2 patients associated with hypouricemia. Serum uric acid levels were 1.6 and 1.3 mg/100 ml, and the ratios of urate clearance to creatinine clearance were 34.1 and 39.4%, respectively, while glomerular filtration rates (GFR) were normal. In the pyrazinamide (PZA) suppression test these 2 patients showed a different response of urate excretion. In the first patient urate excretion showed only a slight decrease following PZA. The load of benzbromarone did not increase urate excretion significantly. This patient is considered to have a defect of urate reabsorption in the proximal tubule, resulting in renal uricosuria. The second patient, on the contrary, showed nearly complete suppression of urate excretion after PZA. Uricosuric response to benzbromarone was far less than in the normal subjects. The suppression rate of urate excretion following PZA in benzbromarone-induced uricosuria was similar to the value of the normals. These results suggest that the latter had a defect of postsecretory reabsorption of urate in the tubule.
我们报告了2例低尿酸血症患者。血清尿酸水平分别为1.6和1.3mg/100ml,尿酸清除率与肌酐清除率之比分别为34.1%和39.4%,而肾小球滤过率(GFR)正常。在吡嗪酰胺(PZA)抑制试验中,这2例患者尿酸排泄的反应不同。在第1例患者中,PZA后尿酸排泄仅略有下降。苯溴马隆负荷并未显著增加尿酸排泄。该患者被认为近端小管尿酸重吸收存在缺陷,导致肾性尿酸尿。相反,第2例患者PZA后尿酸排泄几乎完全被抑制。对苯溴马隆的尿酸排泄反应远低于正常受试者。苯溴马隆诱导的尿酸尿中PZA后尿酸排泄的抑制率与正常受试者的值相似。这些结果表明,后者存在肾小管尿酸分泌后重吸收缺陷。