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The transperitoneal transport dynamics (removal) of guanidinoacetic acid (GAA) and guanidinosuccinic acid (GSA) has been determined in vitro in the control conditions and after application of furosemide (10(-4) mmol/l) on the mesothelial side of the membrane. GAA peritoneal transfer values, as a rule, were higher than GSA and equaled at mean, in the control series of experiments 0.132 i 0.068 mg x 10(-4) x cm-2 x s-2, respectively. Furosemide decreased GSA passage in 30 min after it addition by about 30%, but GSA transfer diminished later, in 120 min., by about 37%. Therefore, mean GAA transport values before (30-90 min.) and after application of furosemide (120-210 min.) were not statistically significant differentiated, whereas GSA transport parameters were lowered by about 40%. Heterogeneity of the peritoneal GAA and GSA transport dynamics in the control series of the experiments, as well as in the series with furosemide, may be related to the physico-chemical differences (e.g. molecular mass) of the analysed derivates.

Uremic polyneuropathy is a common complication in dialyzed patients (pts). In 37 end stage renal disease (ESRD) pts the electroneurophysiological (ENF) parameters and serum creatinine (Pcr), guanidino compounds (GC) and guanidinosuccinic acid (GSA) levels were studied. There were 21 nondialyzed (ND), 10-hemodialyzed (HD) and 6-intermittently peritoneally dialyzed (IPD) pts. The following ENF parameters on both upper extremities, using method described by Buchtal and Rosenfalck, were performed: sensory nerves (nn.) conduction velocity, amplitude of evoked potential, subjective and objective impulse and motor nerve-conduction velocity. Cr level in serum was measured by enzymatic method, GC-by Rosenberg, Ennor, Morison method, modified by Szczepkowska. GSA isolation was performed by column chromatography. The results indicated disturbances in peripheral nn. function in all studied groups of pts and did not correlate with levels of uremic toxins in serum. However, it does not mean, that sum of the accumulated various toxic metabolites in ESRD pts, does not influence the development of polyneuropathy. The degree of impairment of peripheral nn. conduction in ESRD did not differ significantly between ND and HD or IPD pts. We did not notice, any significant differences in the degree of polyneuropathy in HD or IPD pts.