Mathiesen E R, Hommel E, Olsen U B, Parving H H
Hvidøre Hospital, Klampenborg, Denmark.
Diabet Med. 1988 Mar;5(2):145-9. doi: 10.1111/j.1464-5491.1988.tb00961.x.
We investigated whether the glomerular synthesis of prostaglandins modulates the glomerular filtration rate and urinary albumin excretion in incipient diabetic nephropathy (defined as urinary albumin excretion between 30 and 300 mg/24 h (microalbuminuria) in two out of three sterile ketone-free 24-h urine collections in patients having insulin-dependent diabetes mellitus (IDDM) without hypertension or other kidney disease). The urinary excretion of prostaglandin E2 was significantly elevated in 8 insulin-dependent diabetic patients with incipient nephropathy as compared with 9 normoalbuminuric IDDM patients and 11 healthy controls: 317 (182-1273); 95 (67-225); 132 (54-263) pg/min, respectively (2p less than 0.01). Glomerular filtration rate (single bolus 51Cr-EDTA technique) and albuminuria (radioimmunoassay) were measured twice within 2 weeks in 8 females having IDDM with incipient nephropathy. The study design was a randomized double-blind trial with the patients receiving either indomethacin (150 mg/day) or placebo for 3 days prior to the kidney function studies. Indomethacin treatment induced a significant reduction in urinary prostaglandin E2 excretion (73%) (2p less than 0.01), urinary albumin excretion rate diminished from 207 (63-253) to 87 (49-147) mg/24 h (2p less than 0.01), fractional clearance of albumin declined (70%) (2p less than 0.01). Glomerular filtration rate remained stable (108 (88-133) versus 110 (95-142) ml/min). Blood glucose and blood pressure were comparable during the placebo and indomethacin treatment (12.6 +/- 3 versus 13.4 +/- 5 mmol/l and 122/79 +/- 3/9 versus 122/82 +/- 4/10 mmHg, respectively). Our results suggest that enhanced glomerular synthesis of vasodilating prostaglandins may accelerate microalbuminuria in incipient diabetic nephropathy.
我们研究了在初发糖尿病肾病（定义为胰岛素依赖型糖尿病（IDDM）且无高血压或其他肾脏疾病的患者，在三次无酮无菌24小时尿液收集样本中，有两次样本的尿白蛋白排泄量在30至300毫克/24小时之间（微量白蛋白尿））中，前列腺素的肾小球合成是否会调节肾小球滤过率和尿白蛋白排泄。与9名正常白蛋白尿的IDDM患者和11名健康对照相比，8名患有初发肾病的胰岛素依赖型糖尿病患者的前列腺素E2尿排泄量显著升高：分别为317（182 - 1273）；95（67 - 225）；132（54 - 263）皮克/分钟（P<0.01）。对8名患有初发肾病的IDDM女性患者在2周内进行了两次肾小球滤过率（单次推注51Cr - EDTA技术）和蛋白尿（放射免疫测定）测量。研究设计为随机双盲试验，在进行肾功能研究前3天，患者分别接受吲哚美辛（150毫克/天）或安慰剂治疗。吲哚美辛治疗使尿前列腺素E2排泄量显著降低（73%）（P<0.01），尿白蛋白排泄率从207（63 - 253）降至87（49 - 147）毫克/24小时（P<0.01），白蛋白分数清除率下降（70%）（P<0.01）。肾小球滤过率保持稳定（108（88 - 133）对110（95 - 142）毫升/分钟）。在安慰剂和吲哚美辛治疗期间，血糖和血压相当（分别为12.6±3对13.4±5毫摩尔/升和122/79±3/9对122/82±4/10毫米汞柱）。我们的结果表明，在初发糖尿病肾病中，肾小球血管舒张性前列腺素合成增强可能会加速微量白蛋白尿。
