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C van Guldener

Publications and source records attributed to C van Guldener.

27 records · Page 2Linked to original sources
PubMed1998

No change in impaired endothelial function after long-term folic acid therapy of hyperhomocysteinaemia in haemodialysis patients.

BACKGROUND: Hyperhomocysteinaemia is frequent in chronic haemodialysis patients. Because of its potential role in athero- and thrombogenesis, the effects of long-term homocysteine-lowering treatment on endothelial function are of interest. METHODS: We conducted a randomized, controlled trial in 35 haemodialysis patients. In phase 1, patients were treated with 5 mg folic acid or 5 mg folic acid and 4 g betaine per day for 12 weeks, and in phase 2 with 1 or 5 mg folic acid daily for 40 weeks. In phase 3, all patients received 15 mg folic acid daily for four weeks. Endothelial function was assessed before and after 52 weeks of treatment by determination of flow-mediated vasodilatation of the brachial artery, and by measuring plasma levels of endothelium-derived proteins. RESULTS: Non-fasting predialysis plasma total homocysteine was markedly elevated at baseline (46.9 +/- 6.3 mumol/l) and decreased rapidly after initiation of therapy. Significant differences in plasma homocysteine between the groups were found neither during phase 1 nor phase 2. Plasma total homocysteine had normalized in only two out of 30 patients at the end of phase 2. Increasing the daily folic acid dose to 15 mg did not further reduce plasma total homocysteine. Endothelial function parameters did not improve. CONCLUSIONS: We concluded that betaine is not effective in conjunction with folic acid in the treatment of hyperhomocysteinaemia in haemodialysis patients. Normalization of plasma total homocysteine is seldom achieved with 1, 5 or 15 mg folic acid daily, which may explain why long-term homocysteine-lowering treatment with 1 or 5 mg folic acid does not ameliorate endothelial function.

Adult↗
PubMed1998

Endothelium-dependent vasodilatation is impaired in peritoneal dialysis patients.

BACKGROUND: Peritoneal dialysis (PD) patients have a high risk of cardiovascular mortality, which is not completely explained by conventional risk factors. Other factors related to chronic renal failure and/or dialysis treatment might lead to endothelial dysfunction, which is associated with an adverse cardiovascular outcome. One such factor is hyperhomocysteinaemia, which has a high prevalence in PD patients. METHODS: A vessel wall movement detector system was used to investigate endothelium-dependent, flow-mediated, and endothelium-independent, glyceryl trinitrate-induced, vasodilatation of the brachial artery in 29 PD patients and 29 control subjects. RESULTS: Endothelium-dependent vasodilatation was markedly reduced in the PD group: 5.7 +/- 1.0% vs 10.4 +/- 1.3% in the control group (P = 0.004). Endothelium-independent vasodilatation was not impaired. Plasma total homocysteine was elevated in the PD patients (45.2 +/- 6.2 micromol/l), but was not related to endothelium-dependent vasodilatation. CONCLUSION: Chronic peritoneal dialysis patients have impaired endothelium-dependent vasodilatation, which may reflect an increased susceptibility for the development of atherosclerosis and thrombosis.

Arteriosclerosis↗
PubMed1997

Endothelium-dependent vasodilatation and distensibility of large arteries in chronic haemodialysis patients.

BACKGROUND: Cardiovascular mortality is increased in chronic haemodialysis (HD) patients and is not completely explained by common cardiovascular risk factors. Hyperhomocysteinaemia and chronic HD per se may play a role, because these factors may adversely affect endothelial function and distensibility of conduit arteries, which are important determinants of the risk of atherosclerosis, thrombosis and cardiac hypertrophy. METHODS: A vessel wall movement detector system was used to investigate endothelium-dependent, flow-mediated and endothelium-independent, glyceryl trinitrate-induced vasodilatation in the brachial artery and compliance and distensibility coefficients (CC and DC) in the common carotid artery in 28 chronic HD patients and 28 control subjects. RESULTS: Endothelium-dependent, but not endothelium-independent, vasodilatation was markedly reduced in the HD group (3.7 +/- 1.1 vs. 9.7 +/- 1.2%; P = 0.001). The DC was reduced only in a subgroup of patients aged < 50 years: 16.9 +/- 1.5 vs. 22.4 +/- 2.0 10(-3)/kPa (P = 0.032) and was not related to endothelium-dependent vasodilatation. CC did not differ between the groups. Plasma total homocysteine was elevated in the HD patients, but was neither related to endothelium-dependent vasodilatation, nor to DC. CONCLUSION: Chronic renal failure and (or) chronic haemodialysis are associated with impaired endothelium-dependent vasodilatation, which may reflect an increased susceptibility for the development of atherosclerosis and thrombosis.

Adult↗
PubMed1996

Folic acid treatment of hyperhomocysteinemia in dialysis patients.

We measured fasting total plasma homocysteine (Hcy) in 10 chronic hemodialysis (HD) and 10 chronic peritoneal dialysis (PD) patients. Mean (+/- SEM) Hcy was 55.7 +/- 10.1 and 50.5 +/- 14.3 mumol/l, respectively (normal range 6-19 mumol/l). Hemodialysis treatment lowered Hcy by about 30%. Daytime Hcy concentrations were stable in the PD patients. Six weeks of treatment with folic acid (FA) significantly lowered Hcy in HD and PD patients to 24.0 +/- 1.8 and 21.0 +/- 3.6 mumol/l, respectively. After withdrawal, Hcy rose slowly, in parallel with the gradually decreasing plasma FA concentrations, which were greatly elevated during treatment. Chronic treatment with FA of another group of patients showed a similar effect on Hcy. Preliminary results of oral methionine loading in chronic dialysis patients were compatible with delayed homocysteine metabolism via the transsulfuration pathway. Further studies on the optimal treatment of hyperhomocysteinemia in chronic dialysis patients are needed.

Adult↗
PubMed1995

Constant infusion clearance is an inappropriate method for accurate assessment of an impaired glomerular filtration rate.

Recently renewed interest has been focused on constant infusion clearance to assess GFR accurately. In this study we compared GFR and ERPF calculated from the constant infusion method (CIM = I x V/P) with that calculated from the standard method (StM = U x V/P), in 100 patients with renal disease who were subdivided in four groups according to their GFR-StM (< 30; 30-60; 60-90; > 90 ml/min). After a priming dose, a constant infusion of 125I-iothalamate (= GFR) and 131I-hippurate (= ERPF) was started at 9 a.m. The infusion rates were individually adjusted to the GFR which was approximated from the serum creatinine concentration. After a 90-min equilibration period, GFR-StM and ERPF-StM were determined for two 2-h periods. These values were compared with GFR-CIM and ERPF-CIM calculated from the plasma concentration of the respective tracers at the end of each 2-h period (= 210 and 330 min). In the patient group with GFR-StM < 30 ml/min, the 125I-iothalamate plasma concentration increased progressively over time. Consequently, average GFR-CIM at 210 min (34.2, SE +/- 2.1 ml/min) was higher than the GFR-CIM at 330 min (31.9, SE +/- 2.0 ml/min; P < 0.001). In addition both values were significantly higher than the corresponding GFR-StM values (18.1 +/- 2.4 and 15.3 +/- 1.6 ml/min respectively). In the two patient groups with GFR-StM > 60 ml/min, the 125I-iothalamate plasma concentration decreased progressively over time.(ABSTRACT TRUNCATED AT 250 WORDS)

Glomerular Filtration Rate↗
PubMedDate not supplied

Folic acid treatment of hyperhomocysteinemia in peritoneal dialysis patients: no change in endothelial function after long-term therapy.

BACKGROUND: Hyperhomocysteinemia occurs in renal failure and may increase the risk for cardiovascular disease, possibly by damaging the endothelium. Folic acid and betaine are required in two separate homocysteine conversion pathways and may therefore lower plasma homocysteine. OBJECTIVE: To study the therapeutic role of betaine and the effect on endothelial function of long-term homocysteine-lowering therapy with folic acid, in peritoneal dialysis (PD) patients. PATIENTS AND DESIGN: Thirty PD patients were randomized to a 12-week treatment with 5 mg folic acid and 4 g betaine daily, or to 5 mg folic acid alone daily. They were then rerandomized to treatment with 1 or 5 mg folic acid daily for 40 weeks. MEASUREMENTS: At baseline and after 52 weeks, endothelial function was assessed by determination of endothelium-dependent vasodilatation and biochemical markers. RESULTS: Plasma total homocysteine (tHcy) was elevated at baseline: 42.6 (5.8) micromol/L. Only 1 patient (3%) had a normal plasma homocysteine (i.e., < or = 15 micromol/L) before therapy. Normalization of plasma homocysteine occurred in 39% of the patients at 12 weeks. Betaine had no additional homocysteine-lowering effect. Plasma tHcy levels were similar during treatment with 1 or 5 mg folic acid daily. Endothelial function was impaired at baseline and had not improved after 52 weeks of treatment. CONCLUSIONS: Peritoneal dialysis patients have hyperhomocysteinemia, which can be normalized with folic acid alone in about 40% of patients. Betaine does not further lower plasma homocysteine. A maintenance dose of 1 or 5 mg folic acid daily results in equivalent plasma homocysteine levels. Long-term reduction in plasma homocysteine did not result in improvement of endothelial function as assessed by our methods.

Betaine↗