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      Serum Guanidino Compound Levels in Uremic Pediatric Patients Treated with Hemodialysis or Continuous Cycle Peritoneal Dialysis

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          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 guanidinosuccinic acid (207 times), methylguanidine ( > 67 times), argininic acid (24 times), creatinine and α-N-acetylarginine (18 times) and guanidine ( > 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 α-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), α-N-acetylarginine (12 times), argininic acid (15 times), creatinine (22 times), guanidine ( > 11 times) and methylguanidine ( ≥ 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.

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          Author and article information

          S. Karger AG
          17 December 2008
          : 69
          : 4
          : 411-417
          aLaboratory of Neurochemistry and Behavior and Department of Neurology, A.Z. Middelheim, Born-Bunge Foundation, University of Antwerp, Belgium; bDepartments of Nephrology, Neurology and Endocrinology, Hôpital Sainte-Justine, Montréal, Québec, Canada
          188511 Nephron 1995;69:411–417
          © 1995 S. Karger AG, Basel

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          Pages: 7
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