De Deyn P P, Robitaille P, Vanasse M, Qureshi I A, Marescau B
Laboratory of Neurochemistry and Behavior, A.Z. Middelheim, Born-Bunge Foundation, University of Antwerp, Belgium.
Nephron. 1995;69(4):411-7. doi: 10.1159/000188511.
Serum levels of twelve guanidino compounds (GCs) and nerve conduction velocities were determined in a dialyzed renal insufficient pediatric population. Two dialytic groups were considered: one subjected to hemodialysis (HD, 11 patients) and one subjected to continuous cycle peritoneal dialysis (CCPD, 13 patients). Before HD, marked increases were found for guanidino-succinic acid (207 times), methylguanidine (> or = 67 times), argininic acid (24 times), creatinine and alpha-N-acetylarginine (18 times) and guanidine (> or = 14 times) when compared to controls. Important significant increases were still present after an HD session for guanidinosuccinic acid (49 times), methylguanidine (34 times), creatinine (7 times) and alpha-N-acetylarginine and guanidine (6 times). After HD, creatine, arginine and homoarginine were lower than in controls. All GCs, with the exception of creatine, decreased significantly after a single HD session with percentage decrease ranging between 40% (for arginine) and 77% (for guanidinosuccinic acid). Creatine decreased in a statistically nonsignificant manner by 48%. Marked increases were found in the CCPD group for guanidinosuccinic acid (114 times), alpha-N-acetylarginine (12 times), argininic acid (15 times), creatinine (22 times), guanidine (> or = 11 times) and methylguanidine (> or = 48 times). Concentrations of guanidinosuccinic acid before and after HD and in CCPD were comparable to those reported to be toxic in vitro and in vivo. No clinical or electrophysiological indications of polyneuropathy were observed in our population. Sensory and motor nerve conduction studies showed few abnormalities apart from a significant correlation between argininic acid concentration or guanidine levels and the peroneal nerve conduction velocity in the CCPD-treated group.
在一组接受透析的小儿肾功能不全患者中,测定了12种胍基化合物(GCs)的血清水平和神经传导速度。研究了两个透析组:一组接受血液透析(HD,11例患者),另一组接受持续循环腹膜透析(CCPD,13例患者)。与对照组相比,HD前胍基琥珀酸(207倍)、甲基胍(≥67倍)、精氨酸(24倍)、肌酐和α-N-乙酰精氨酸(18倍)以及胍(≥14倍)显著升高。HD治疗后,胍基琥珀酸(49倍)、甲基胍(34倍)、肌酐(7倍)以及α-N-乙酰精氨酸和胍(6倍)仍有显著升高。HD后,肌酸、精氨酸和高精氨酸低于对照组。单次HD治疗后,除肌酸外,所有GCs均显著降低,降低百分比在40%(精氨酸)至77%(胍基琥珀酸)之间。肌酸下降48%,但无统计学意义。CCPD组胍基琥珀酸(114倍)、α-N-乙酰精氨酸(12倍)、精氨酸(15倍)、肌酐(22倍)、胍(≥11倍)和甲基胍(≥48倍)显著升高。HD前后及CCPD组中胍基琥珀酸的浓度与体外和体内报道的毒性浓度相当。在我们的研究人群中未观察到多神经病的临床或电生理指征。感觉和运动神经传导研究显示,除CCPD治疗组精氨酸浓度或胍水平与腓总神经传导速度之间存在显著相关性外,几乎没有异常。