Kadono K, Yamaguchi T, Tetsutani T, Yasunaga K
First Department of Internal Medicine, Kansai Medical University.
Nihon Jinzo Gakkai Shi. 1992 Nov;34(11):1183-7.
Since urinary guanidinoacetic acid (GAA) derives from the kidneys, its detection is suggested to be associated with renal disease. We have been making a practice of investigating renal GAA production in diabetic patients, using a citrulline/creatine loading test. We noted a marked increase in urinary GAA excretion in 1 patient. Since GAA-synthesis is hormonally regulated, we made a through investigation of endocrine function in this patient. She was a 58-year-old woman with a 15-year history of diabetes mellitus, proliferative diabetic retinopathy, and negative microalbuminuria. There was a high plasma GH level and urinary 17-KS analysis revealed an increase in the adrenal androgen-derived fractions. Based on the X-ray finding of ballooning of the sella turcica and the MRI data, empty sella syndrome was diagnosed. It was suggested that stimulated anabolic hormone release had accelerated renal nitrogen metabolism and induced aggravation of her retinopathy. The findings in this patient implied the involvement of hormones in the development of diabetic complications.
由于尿胍基乙酸（GAA）来源于肾脏，其检测结果提示与肾脏疾病有关。我们一直通过使用瓜氨酸/肌酸负荷试验来研究糖尿病患者肾脏GAA的产生情况。我们注意到1例患者的尿GAA排泄量显著增加。由于GAA的合成受激素调节，我们对该患者的内分泌功能进行了全面调查。她是一名58岁女性，有15年糖尿病病史，患有增殖性糖尿病视网膜病变，微量白蛋白尿呈阴性。血浆生长激素水平较高，尿17 -酮类固醇分析显示肾上腺雄激素衍生部分增加。根据蝶鞍膨隆的X线检查结果和MRI数据，诊断为空蝶鞍综合征。提示促合成激素释放加速了肾脏氮代谢并导致其视网膜病变加重。该患者的研究结果表明激素参与了糖尿病并发症的发生发展。
