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前列腺素 E_2(PGE_2)在肾脏血液动力学的调节方面占有重要的地位。动物实验研究指出,使肾血流量降低可引起肾脏合成前列腺素类似物质的增加。临床上发现 Bartter 综合征、肝硬化导致的肾功能衰竭、充血性心力衰竭引起的肾前性氮质血症以及肾血管性高血压患者的前列腺素产物增加。似乎每当肾血流受阻时,肾脏产生的前列腺素就增加。肾脏合成的PGE_2是尿内前列腺素的主要来源.作者研究20例慢性肾脏病患者(慢性肾小球肾炎、慢性间质性肾炎)在疾病不同阶段的前列腺素排泄率,按照肾功能不全的程度将患者分成3组:①“轻度”肾功能不全者7例,肌酐清除率高于60ml/min,平均肌酐清除率为106ml/min±14.1;②“中度”肾功能不全者7例,肌酐清除率范围20～59ml/min 之间,平均肌酐清除率36ml/min±4.82;③“重度”肾功能不全者6例,肌酐清除率低于20ml/min,平均肌酐清除率11.8ml/min±0.42。前列腺素测量前1周应停止服药。尿 PGE_2的浓度以放射免疫法测定。结果①健康者29人,尿 PGE_2排泄量为765±
Prostaglandin E2 (PGE2) plays an important role in the regulation of renal hemodynamics. Animal experimental studies indicate that reducing renal blood flow can cause the synthesis of prostaglandins in the kidney to increase. Bartter syndrome is clinically found, renal failure due to cirrhosis, prerenal azotemia due to congestive heart failure, and prostaglandin production increase in patients with renovascular hypertension. It seems that whenever the renal blood flow is blocked, the amount of prostaglandins produced by the kidneys increases. The synthesis of PGE 2 in the kidneys is the main source of prostaglandins in the urine.The authors studied the prostaglandin excretion rate in 20 patients with chronic kidney disease (chronic glomerulonephritis, chronic interstitial nephritis) at different stages of the disease, according to the degree of renal insufficiency The patients were divided into three groups: ① 7 cases with “mild” renal dysfunction, creatinine clearance rate higher than 60ml / min and average creatinine clearance rate 106ml / min ± 14.1; ② “moderate” renal insufficiency in 7 cases, The creatinine clearance rate ranged from 20 to 59ml / min and the mean creatinine clearance rate was 36ml / min ± 4.82. 6 patients with “severe” renal insufficiency had a creatinine clearance rate of less than 20ml / min and an average creatinine clearance rate of 11.8ml / min ± 0.42. One week before prostaglandin measurement should stop taking the drug. The concentration of urinary PGE 2 was determined by radioimmunoassay. Results ① There were 29 healthy people, urinary PGE 2 excretion was 765 ±