ACUTE HYPEROXALURIA, RENAL INJURY AND CALCIUM-OXALATE UROLITHIASIS
ACUTE HYPEROXALURIA, RENAL INJURY AND CALCIUM-OXALATE UROLITHIASIS
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DOI：
10.1016/s0022-5347(17)37202-6
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发表时间：
1992-01-01
影响因子：
6.6
通讯作者：
HACKETT, RL
中科院分区：
文献类型：
--
作者：
KHAN, SR;SHEVOCK, PN;HACKETT, RL
单次腹腔注射3、7或10 mg。每100克含草酸钠100克。对雄性Sprague-Dawley大鼠给予大鼠体重。 在注射后的不同时间，分析尿液样本中的草酸盐、尿酶、碱性磷酸酶、亮氨酸氨肽酶、γ-谷氨酰转肽酶和N-乙酰-β-氨基葡萄糖苷酶。 处理肾脏进行光学显微镜检查和肾钙和草酸盐测定。 草酸盐给药导致尿草酸盐增加和肾脏中草酸钙晶体形成。 过量草酸盐的尿排泄量和持续时间以及晶体在肾脏中的保留与给予的草酸钠剂量相关。 在低草酸盐剂量为3毫克/ 100克晶体迅速向下移动到肾单位并清除肾脏。 在较高剂量下，晶体保留在肾脏中，剂量为10 mg/kg。一百克。在注射后七天仍然存在。 晶体滞留与尿酶排泄增强相关，表明肾小管上皮细胞损伤。
Single intraperitoneal injections of three, seven, or 10 mg. of sodium oxalate per 100 gm. of rat body weight were administered to male Sprague-Dawley rats. At various times after the injection, urine samples were analyzed for oxalate, and urinary enzymes, alkaline phosphatase, leucine aminopeptidase, gamma-glutamyl transpeptidase, and N-acetyl-beta-glucosaminidase. The kidneys were processed for light microscopy and renal calcium and oxalate determination. Oxalate administration resulted in an increase in urinary oxalate and formation of calcium oxalate crystals in the kidneys. The amount and duration of urinary excretion of excess oxalate and retention of crystals in the kidneys correlated with the dose of sodium oxalate administered. At a low oxalate dose of three mg./100 gm., crystals moved rapidly down the nephron and cleared the kidneys. At higher doses crystals were retained in kidneys and at a dose of 10 mg./100 gm. were still there seven days post-injection. Crystal retention was associated with enhanced excretion of urinary enzymes indicating renal tubular epithelial injury.