Smith W G, Hanning I, Johnston D G, Brown C B
Department of Nephrology, Royal Hallamshire Hospital, Sheffield, UK.
Nephrol Dial Transplant. 1988;3(4):448-52. doi: 10.1093/oxfordjournals.ndt.a091696.
Pancreatic beta-cell function was evaluated in uraemic patients by measuring beta-cell peptides in the peripheral blood after intravenous glucagon (1 mg) stimulation. Patients in chronic renal failure, patients on haemodialysis, and both new and established subjects on continuous ambulatory peritoneal dialysis (CAPD) (10 in each group) were studied and compared to 8 healthy controls. Fasting glucose (3.6-4.4 mmol/l) and insulin concentrations (9.5-11.7 mU/l) were normal and did not differ between the uraemic groups, but c-peptide concentrations were markedly increased in uremia (1.84-2.38 nmol/l) compared to controls (0.48 nmol/l). Following glucagon stimulation an exaggerated blood glucose response with delayed glucose peak was observed, while the peak insulin response to glucagon was normal; however, the return to basal concentrations was delayed in uraemia. The c-peptide response was also exaggerated and peak concentrations in uraemic subjects (3.0-4.3 nmol/l) were significantly greater than controls (1.5 nmol/l). The response of CAPD patients was similar to those on haemodialysis and non-dialysed uraemic patients. The abnormalities seen were due to uraemia, and CAPD treatment had no specific adverse effect on beta-cell function. Thus, from this data there was no evidence that CAPD per se is detrimental to beta-cell integrity.
通过静脉注射胰高血糖素(1毫克)刺激后测量外周血中的β细胞肽,对尿毒症患者的胰腺β细胞功能进行了评估。研究了慢性肾功能衰竭患者、血液透析患者以及持续非卧床腹膜透析(CAPD)的新患者和老患者(每组10例),并与8名健康对照者进行了比较。空腹血糖(3.6 - 4.4毫摩尔/升)和胰岛素浓度(9.5 - 11.7毫国际单位/升)正常,尿毒症组之间无差异,但与对照组(0.48纳摩尔/升)相比,尿毒症患者的C肽浓度显著升高(1.84 - 2.38纳摩尔/升)。注射胰高血糖素后,观察到血糖反应过度且血糖峰值延迟出现,而对胰高血糖素的胰岛素峰值反应正常;然而,尿毒症患者恢复至基础浓度的时间延迟。C肽反应也过度,尿毒症患者的峰值浓度(3.0 - 4.3纳摩尔/升)显著高于对照组(1.5纳摩尔/升)。CAPD患者的反应与血液透析患者和未透析的尿毒症患者相似。观察到的异常是由尿毒症引起的,CAPD治疗对β细胞功能没有特定的不良影响。因此,根据这些数据,没有证据表明CAPD本身会损害β细胞的完整性。