Heaf J G, Jensen S B, Jensen K, Ali S, von Jessen F
Department of Nephrology, State University Hospital, Copenhagen, Denmark.
Scand J Urol Nephrol. 1998 Sep;32(5):350-5. doi: 10.1080/003655998750015322.
(a) To determine the normalized cellular clearance (Kcn) of urea, creatinine and phosphate in patients undergoing maintenance hemodialysis; (b) To identify the factors, particularly circulatory, which determine Kcn; (c) To evaluate whether intra-dialytic blood sampling can predict the size of the post-dialytic solute concentration rebound.
Kinetic modelling of urea, creatinine and phosphate, using a two-pool variable volume computer simulation, was performed on two occasions on 34 patients undergoing maintenance dialysis. The cellular clearance was determined (a) from the size of the rebound 50 min after the end of dialysis; (b) from a mid-dialytic blood sample. Conventional two-dimensional M-mode echocardiography and Doppler peripheral blood pressure measurement were performed.
The model produced accurate measurements of rebound Kc for urea in 93% of measurements, creatinine in 49% and phosphate in 13%. The corresponding figures for mid-dialysis Kcn were 76%, 39% and 0%. The rebound Kcn was, for urea, 8.31 +/- 4.31 ml/kg/min, and for creatinine 4.07 +/- 2.98. The mid-dialysis Kcn was, for urea, 8.57 +/- 4.25 ml/kg/min, and for creatinine 5.06 +/- 3.36. High post-dialytic rebounds (and low Kcn values) were associated with erythropoietin use (p < 0.05) and occurrence of end-dialytic hypotension (p < 0.02). Patients treated with calcium antagonists had a significantly (p < 0.001) higher Kcn. There was no correlation between mid-dialysis and rebound Kcn. Circulatory indices had no influence on Kcn.
The two-pool cellular clearance model is compatible with urea kinetics, but not creatinine or phosphate. It is therefore unlikely that it is the correct model for small molecule kinetics. The post-dialytic solute rebound may be partly an iatrogenic phenomenon and can be reduced by preventing post-dialytic hypotension and by calcium antagonist treatment, both of which improve regional blood flow. The size of the rebound cannot be predicted by intra-dialytic blood sampling.
(a) 测定维持性血液透析患者尿素、肌酐和磷酸盐的标准化细胞清除率(Kcn);(b) 识别决定Kcn的因素,尤其是循环相关因素;(c) 评估透析中采血能否预测透析后溶质浓度反弹的程度。
对34例维持性透析患者进行了两次尿素、肌酐和磷酸盐的动力学建模,采用双池可变体积计算机模拟。细胞清除率通过以下方式确定:(a) 根据透析结束后50分钟的反弹程度;(b) 通过透析中血样。进行了传统的二维M型超声心动图检查和多普勒外周血压测量。
该模型对尿素反弹Kc的测量准确率为93%,肌酐为49%,磷酸盐为13%。透析中Kcn的相应数字分别为76%、39%和0%。尿素的反弹Kcn为8.31±4.31 ml/kg/min,肌酐为4.07±2.98。透析中尿素的Kcn为8.57±4.25 ml/kg/min,肌酐为5.06±3.36。透析后高反弹(以及低Kcn值)与使用促红细胞生成素(p<0.05)和透析结束时低血压的发生(p<0.02)相关。接受钙拮抗剂治疗的患者Kcn显著更高(p<0.001)。透析中Kcn与反弹Kcn之间无相关性。循环指标对Kcn无影响。
双池细胞清除率模型与尿素动力学相符,但与肌酐或磷酸盐不符。因此,它不太可能是小分子动力学的正确模型。透析后溶质反弹可能部分是医源性现象,可通过预防透析后低血压和钙拮抗剂治疗来减少,这两种方法均可改善局部血流。透析中采血无法预测反弹程度。