毒鹅膏中毒儿童因肾小管尿酸分泌增加导致低尿酸血症。
Hypouricemia due to increased tubular secretion of urate in children with Amanita phalloides poisoning.
作者信息
Zawadzki J, Jankowska I, Moszczyńska A, Januszewicz P
机构信息
Nephrology Department Child Health Center, Warsaw, Poland.
出版信息
Nephron. 1993;65(3):375-80. doi: 10.1159/000187516.
The tubular transport of urate was studied in 20 children poisoned with Amanita phalloides and in control group. The aim of this study was to investigate the cause of repeatedly observed episodes of hypouricemia in patients after A. phalloides poisoning. A significant negative correlation between serum uric acid concentration and fractional excretion of urate in poisoned and control groups (r = 0.73, p < 0.001) was found. The results of pyrazinamide and probenecid tests performed in patients after A. phalloides poisoning indicated that hyperuricosuria was most likely due to an increment in renal tubular urate secretion, and not due to decreased presecretory and postsecretory reabsorption of uric acid. These findings indicate that hypouricemia found after A. phalloides poisoning in children is of renal origin due to an increase in tubular urate secretion.
在20名因毒鹅膏中毒的儿童及对照组中研究了尿酸盐的肾小管转运。本研究的目的是调查毒鹅膏中毒患者反复出现低尿酸血症的原因。在中毒组和对照组中发现血清尿酸浓度与尿酸盐排泄分数之间存在显著负相关（r = 0.73，p < 0.001）。对毒鹅膏中毒患者进行的吡嗪酰胺和丙磺舒试验结果表明，高尿酸尿症很可能是由于肾小管尿酸盐分泌增加，而非尿酸分泌前和分泌后的重吸收减少所致。这些发现表明，儿童毒鹅膏中毒后出现的低尿酸血症源于肾脏，是由于肾小管尿酸盐分泌增加所致。
Zotero 插件