医学
移植
胰岛素
糖尿病
内科学
低血糖
傍晚
无症状的
优势比
胃肠病学
外科
内分泌学
天文
物理
作者
Manfred Hecking,Michael Haidinger,Dominik Döller,Johannes Werzowa,Andrea Tura,Jinyao Zhang,Hilal Tekoglu,Johannes Pleiner,Thomas Wrba,Susanne Rasoul‐Rockenschaub,Ferdinand Mühlbacher,Sabine Schmaldienst,Wilfred Druml,Walter H. Hörl,Michael Krebs,Michael Wolzt,Giovanni Pacini,Friedrich K. Port,Marcus D. Säemann
标识
DOI:10.1681/asn.2011080835
摘要
No effective interventions to reduce risk for new-onset diabetes after transplantation (NODAT), a condition associated with postoperative hyperglycemia and reduced patient and graft survival, have been established. In this 1-year, proof-of-concept clinical trial, we randomly assigned 50 renal transplant recipients to immediate-postoperative isophane insulin for evening blood glucose ≥140 mg/dl (treatment group) or short-acting insulin and/or oral antidiabetic agents for blood glucose ≥180-250 mg/dl (standard-of-care control group). We included only patients without a history of diabetes who received tacrolimus. By the third postoperative evening, all patients in the treatment group had blood glucose ≥140 mg/dl and were subsequently treated with basal insulin; during the first 3 weeks after transplantation, the mean ± SD daily insulin dosage was 17±11 IU/d. Among controls, 23 (92%) of 25 had blood glucose ≥200 mg/dl and 18 (72%) of 25 received standard-of-care antihyperglycemic treatment. Asymptomatic hypoglycemia occurred five times in the treatment group and once in the control group. Throughout follow-up, the treatment group had 73% lower odds of NODAT (odds ratio, 0.27) than the control group, and hemoglobin A1c was on average 0.38% lower in the treatment group than the control group. Twelve months after transplantation, all patients in the treatment group were insulin-independent, whereas 7 (28%) of 25 controls required antidiabetic agents. The groups did not differ for insulin sensitivity, but the treatment group showed better β-cell function throughout the 1-year follow-up. In conclusion, this study suggests regimens that include basal insulin significantly reduce the odds for NODAT after renal transplantation, presumably via insulin-mediated protection of β cells.
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