Serum Guanidino Compound Levels and Clearances in Uremic Patients Treated with Continuous Ambulatory Peritoneal Dialysis

Deyn, Peter Paul De; Marescau, Bart; Swartz, Richard D.; Hogaerth, R.; Possemiers, Ilse; Löwenthal, A.

doi:10.1159/000185885

Cited by 20 publications

(18 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The presented serum G C levels found in uremic chil dren treated by either H D or peritoneal dialysis were comparable to those described in adults [10,42], Essen tially, guanidinosuccinic acid, creatinine, a-N-acetylarginine, argininic acid, guanidine and methylguanidine showed the greatest increases. As in their adult counter part, creatinine levels were slightly lower in C CP Dtreated than in hemodialyzed patients before dialysis, and both guanidine and methylguanidine concentrations were higher in the C C P D group [42], Interestingly, while most G C concentrations in the serum of dialyzed adults and children were in the same range, guanidinosuccinic acid serum levels were consistently much higher (threefold) in children.…”

Section: Discussionsupporting

confidence: 79%

“…As in their adult counter part, creatinine levels were slightly lower in C CP Dtreated than in hemodialyzed patients before dialysis, and both guanidine and methylguanidine concentrations were higher in the C C P D group [42], Interestingly, while most G C concentrations in the serum of dialyzed adults and children were in the same range, guanidinosuccinic acid serum levels were consistently much higher (threefold) in children.…”

Section: Discussionmentioning

confidence: 80%

See 1 more Smart Citation

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

Deyn

Robitaille

Vanasse

et al. 1995

Nephron

Self Cite

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionsupporting

confidence: 79%

Section: Discussionmentioning

confidence: 80%

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

Deyn

Robitaille

Vanasse

et al. 1995

Nephron

Self Cite

View full text Add to dashboard Cite

show abstract

“…Maybe, the latter factor accounts for some of the differences in efficacy of the two dialytic techniques in removing GCs. Indeed, the 10-hour equilibration percen tage of 126.5 ±32.0 (x±S D , n = 14) for creatine in our CAPD group [1] could be in agreement with this hypothe sis. Caution is indicated however: the creatine concentra tion shown to be higher in dialysate than in serum, after a 10-hour dwell period, could also be explained by local synthesis of this GC in the peritoneal cavity.…”

Section: Dear Sirsupporting

confidence: 87%

“…Here, we assessed the interrelationships of parameters for the removal of the GCs and urea by HD [2] and by CAPD [1] by calculating the linear correlation coefficient. The GCs considered were: arginine, homoarginine, N-aacetylarginine, guanidine, guanidinoacetic acid, creati nine, methylguanidine, argininic acid, guanidinosuccinic acid and creatine.…”

Section: Dear Sirmentioning

confidence: 99%

Differential Removal of Guanidinosuccinic Acid and Creatine by Hemodialysis and Continuous Ambulatory Peritoneal Dialysis

Deyn

Marescau

Swartz

et al. 1991

Nephron

Self Cite

View full text Add to dashboard Cite

Dear Sir,In two previous reports, we presented serum guanidino compound (GC) levels and the clearances of GCs by continuous ambulatory peritoneal dialysis (CAPD) and the influence of a single hemodialysis (HD) on serum GC levels in steady-state patients with terminal renal insuffi ciency (I, 2). Highly standardized dialysis procedures were performed. In hemodialyzed patients, guanidino succinic acid, among other GCs, remained markedly elevated and reached toxic levels before a dialysis ses sion. In serum of patients who underwent CAPD, guani dinosuccinic acid, creatinine and methylguanidine reached levels associated with toxic effects in vitro. Se rum creatine levels were lower in peritoneally dialyzed patients than in control subjects. In the peritoneal dialy sis group, significantly different clearances were found for the different GCs ranging from 4.02 ± 1.08 m l/m in for arginine to 7.94±2.76 ml/min for creatine during a 3-hour exchange period. Also in the hemodialyzed group, substantial differences were found in the percent decrease of the different GCs, ranging from 25 ± 13% for arginine to 74±7.5% for guanidinosuccinic acid.Here, we assessed the interrelationships of parameters for the removal of the GCs and urea by HD [2] and by CAPD[1] by calculating the linear correlation coefficient. The GCs considered were: arginine, homoarginine, N-aacetylarginine, guanidine, guanidinoacetic acid, creati nine, methylguanidine, argininic acid, guanidinosuccinic acid and creatine. The 3-hour equilibration percentage and the ratio (serum GC concentration before HD /serum GC concentration after HD) were used as para meters for the removal of ten different GCs and urea by CAPD and HD respectively. A weak, nonsignificant pos itive correlation ( r = 0.105) was found between CAPD equilibrium percentage and the parameter for GC remo val by HD ( fig.

show abstract

“…45 Indeed, there are experimental observations showing that the levels of several guanidino compounds are markedly increased in human serum, cerebrospinal fluid, and various brain regions in uremic patients. 18,46,47 An increase in guanidino compounds in uremia is likely to represent a diminished release or effect of NO, and consequently, a decrease of cerebral blood flow in uremic patients is highly conceivable. Indeed, a significant reduction in the middle cerebral artery and basilar blood flow velocity has been observed in uremic patients on dialysis.…”

Section: Discussionmentioning

confidence: 99%

Effects of Some Guanidino Compounds on Human Cerebral Arteries

Segarra

Medina

Ballester

et al. 1999

Stroke

View full text Add to dashboard Cite

Background and Purpose-Accumulation of endogenous guanidino-substituted analogues of L-arginine in chronic renal failure might contribute to some of the vascular and neurological disorders of this pathology. We tested the hypothesis that in human cerebral arteries, some guanidino compounds may increase vascular tone, through nitric oxide (NO) synthase inhibition, and impair endothelium-dependent relaxation. Methods-Rings of human middle cerebral artery were obtained during autopsy of 26 patients who had died 3 to 12 hours before. The rings were suspended in organ baths for isometric recording of tension. We then studied the responses to N G -monomethyl-L-arginine (L-NMMA), N G ,N G -dimethyl-L-arginine (asymmetrical dimethylarginine; ADMA), aminoguanidine (AG), and methylguanidine (MG). Results-L-NMMA (10Ϫ6 to 3ϫ10 Ϫ4 mol/L) and ADMA (10 Ϫ6 to 3ϫ10 Ϫ4 mol/L) caused concentration-and endothelium-dependent contractions (median effective concentrations [EC 50 ]ϭ1.1ϫ10Ϫ5 and 1.6ϫ10 Ϫ5 mol/L, respectively; E max ϭ35.5Ϯ7.9% and 43.9Ϯ5.9% of the response to 100 mmol/L KCl). AG (10 Ϫ5 to 3ϫ10 Ϫ3 mol/L) and MG (10 Ϫ5 to 3ϫ10 Ϫ3 mol/L) produced endothelium-independent contractions (E max ϭ44.3Ϯ8.8% and 45.7Ϯ5.8% of the response to 100 mmol/L KCl, respectively). L-Arginine (10 Ϫ3 mol/L) prevented the contractions by L-NMMA and ADMA but did not change contractions induced by AG and MG. L-NMMA and ADMA inhibited endothelium-dependent relaxation induced by acetylcholine in a concentration-dependent manner; AG and MG were without effect. Conclusions-The results suggest that the contractions induced by L-NMMA and ADMA are due to inhibition of endothelial NO synthase activity, whereas AG and MG do not affect the synthesis of NO. An increase in the plasma concentration of L-NMMA and ADMA associated with uremia is likely to represent a diminished release or effect of NO, and consequently, an increased cerebrovascular tone in uremic patients is highly conceivable. (Stroke. 1999;30:2206-2211.)Key Words: cerebral arteries Ⅲ endothelium Ⅲ nitric oxide N itric oxide (NO) synthesized from L-arginine accounts for the powerful vasodilator effects of endotheliumderived relaxing factor 1,2 and consequently plays a decisive role in determining vasomotor tone in several vascular beds, including the cerebral circulation. [3][4][5][6][7] The synthesis of NO can be specifically and competitively antagonized by arginine analogues such as N G -monomethyl-L-arginine (L-NMMA). 4,8 Histochemical studies have demonstrated the presence of NO synthase immunoreactivity in the adventitia of rat and human cerebral arteries. 9,10 Consistent with these observations, several reports have shown that NO from perivascular nerve endings mediates dilatation in the cerebral arteries through a nonadrenergic, noncholinergic mechanism, 11-13 whereas NO of endothelial origin can modulate contractile responses of isolated human cerebral arteries to sympathetic stimulation. 6 Uremia is an established risk factor for cardiovascular disease and cerebrovascular acciden...

show abstract

Serum Guanidino Compound Levels and Clearances in Uremic Patients Treated with Continuous Ambulatory Peritoneal Dialysis

Cited by 20 publications

References 27 publications

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

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

Differential Removal of Guanidinosuccinic Acid and Creatine by Hemodialysis and Continuous Ambulatory Peritoneal Dialysis

Effects of Some Guanidino Compounds on Human Cerebral Arteries

Contact Info

Product

Resources

About