Title: Endogenous guanidino compounds as uremic neurotoxins
Authors: De Deyn, P.P. ×
D'Hooge, Rudi
Van Bogaert, P.P.
Marescau, B. #
Issue Date: 2001
Publisher: Nature Pub. Group
Series Title: Kidney international vol:59 issue:supplement 78 pages:S77-S83
Abstract: Epileptic and cognitive symptomatologies are among the most typical manifestations of uremic encephalopathy. Several guanidino compounds (GCs) may play an important role in the etiology of uremic encephalopathy. Four GCs appeared to be highly increased as well in serum, cerebrospinal fluid, and brain of uremic patients, whereas the levels of other metabolically relevant GCs were not or only moderately increased and others were even decreased. These highly increased compounds or "uremic" GCs are creatinine (CTN), guanidine (G), guanidinosuccinic acid (GSA), and methylguanidine (MG). All four compounds were shown to be experimental convulsants in brain concentrations similar to those found in uremic brain. We have described a possible mechanism for the contribution of GCs to uremic hyperexcitability, referring to the in vitro effects of uremic GCs on inhibitory and excitatory amino acid receptors. The excitatory effects of uremic GCs on the central nervous system may be explained by the activation of N-methyl-D-aspartate (NMDA) receptors by GSA,concomitant inhibition of GABA(A) receptors by uremic GCs, and other
depolarizing effects. These effects might also indicate the putative contribution of uremic GCs to the etiology of
uremic encephalopathy
ISSN: 0085-2538
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Laboratory for Biological Psychology
× corresponding author
# (joint) last author

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