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In the first part with on-line HDF, starting from HDF 60 ml/min a significantly higher beta2-M reduction ratio and clearance vs HD is noted. In HDF100 (i.e. with 241 replacement volume per 4-h treatment) vs HD, a beta2-M reduction ratio of 72.7% vs 49.7% (P= 0.0000) and a beta2-M clearance of 116.8 vs 63.8 ml/min (P=0.0000) was obtained. Comparing HDF120 with HDF100, there is a significantly higher beta2-M clearance with the former (P<0.005), although the beta2-M reduction ratio was not significantly better. In the HDF120 session the amount of beta2-M in the total dialysate was 292 mg per session. If one adds the known 17% adsorption on the polysulfone membrane, a total of 341.6 mg beta2-M per session is removed, which adds up to 1024.8 mg a week. Concerning the small molecules, our results with HDF100 also show a higher creatinine and especially P clearance vs HD. In the second part with 16 patients with more than 10 years of dialysis treatment (mean 14 years 1 month), the mean time on HDF amounted to 39.5% of the total treatment time. In four patients only biocompatible and highly permeable membranes were used, AN69 and mainly polysulfone, and in four other patients these membranes were used for more than 95% of the treatment time. Therefore, it is not surprising that the prevalence of carpal tunnel syndrome was only 12.5% in the patients after 10 years of dialysis. Twenty-five percent of these patients met the criteria for diagnosis of beta2-M bone-amyloidosis, proposed by van Ypersele de Strihou et al., but without a retrospective X-ray analysis. The mean predialysis beta2-M value was 29.6 mg/l. The mean values for serum albumin, serum total cholesterol, HDL and LDL cholesterol were within normal limits. For the parathyroid hormone a mean of 287.5 pg/ml was found. Subtotal parathyroidectomy was performed in five patients. The mean dose of 43 U erythropoietin/kg per session is comparable with those reported in the literature. Conclusions. Like Canaud, in our renal unit, treatment with on-line HDF with a highly permeable and biocompatible membrane has proven to be an efficient, well-tolerated and safe technique. Furthermore it leads to a low prevalence of dialysis amyloidosis and a superior P clearance. However, continuous attention must be paid to an on-line sterile and apyrogenic dialysate. Although on-line HDF is undoubtedly a more optimal approach of chronic dialytic treatment, it also carries a higher cost, which is currently evaluated to be nearly US$11 per session.

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Eight chronic, anuric hemodialysis patients were randomly treated with a high-flux polysulphone dialyzer (F80), using 6 different modes: conventional bicarbonate hemodialysis (HD), hemodiafiltration (HDF) with a replacement solution at 40, 60, 80 or 100 ml/min in postdilution and 80 ml/min in predilution. The differences in β₂-microglobulin (β2M) reduction ratio and clearance were evaluated statistically by analysis of variance (ANOVA). Both studies revealed no significant difference between HD and HDF40 in postdilution, but an increasing significant difference from HDF60 to HDF100 in postdilution and with HDF80 in predilution. The mean reduction ratio ranged from 49.7 (HD) to 72.7% (HDF 100 ml/min), showing an overall statistically significant difference (p = 0.0000). For the clearance, the range was between 63.8 (HD) and 116.8 ml/min (HDF 100 ml/min) (p = 0.0000). β2M in the effluent dialysate with HDF100 ml/min reached up to a mean of 258 mg/session. Concerning small molecules (BUN, creatinine and P), there was a statistically significant different clearance for creatinine and especially for P with HDF 100 ml/min. Conclusion: HDF with an on-line replacement solution at 100 ml/min and a high-flux and biocompatible polysulphone membrane represents a new tool for enhanced removal of β2M. Besides a significant increase in creatinine and especially in phosphorus clearance is noted.

Guanidino compounds are increased in uremia and are highly suspected to be uremic toxins. The serum levels of 11 guanidino compounds and the influence of a single hemodialysis were evaluated in 30 steady-state uremic patients undergoing maintenance hemodialysis. Guanidino compound levels were detected using liquid cation exchange chromatography with a highly sensitive fluorescence detection method. Highly standardized dialysis procedures were performed. Before hemodialysis, high levels were found for guanidinosuccinic acid, N-α-acetylarginine, argininic acid, creatinine, γ-guanidinobutyric acid, guanidine and methylguanidine. Guanidinosuccinic acid reached levels associated with toxic effects in vitro. After hemodialysis, although lowered, guanidinosuccinic acid, creatinine, guanidine and methylguanidine were still markedly increased. No differences in the percent decrease, during a single hemodialysis, of the studied compounds were found using different membranes such as cellulose acetate, cuprophane and polyacrylonitrile membranes. Substantial differences, however, in the percent decrease of the different guanidino compounds were found, ranging from 25 ± 13% for arginine to 74 ± 7.5% for guanidinosuccinic acid. Data reported here show that guanidino compounds are raised in serum of uremic patients undergoing maintenance hemodialysis, before as well as after a single hemodialysis, while substantial differences in the percent decrease of the different guanidino compounds are found.

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We investigated the pharmacokinetics of desferrioxamine and its chelated compounds aluminoxamine and ferrioxamine in normal volunteers and haemodialysis patients with and without iron overload. Desferrioxamine was administered in a single dose of 30 mg per kg body-weight was a 30-min infusion to five healthy volunteers and to 20 haemodialysis patients (five patients without haemosiderosis and 15 patients with haemosiderosis). The interdialytic half-life of ferrioxamine was 2.2 h in normal volunteers, 13.3 h in dialysis patients without haemosiderosis, and 24.6 h in patients with haemosiderosis. There was no interdialytic elimination of aluminoxamine. In a second study, seven dialysis patients received 5, 10, and 20 mg per kg body-weight desferrioxamine in a random order with a time interval of 2 weeks. The peak serum concentrations after these doses were 4.1 +/- 2.9, 6.4 +/- 2.9, and 10.7 +/- 7.1 mumol/l for ferrioxamine and 2.8 +/- 1.5, 3.1 +/- 1.5, and 4.2 +/- 1.7 mumol/l for aluminoxamine. Thus, a 4-fold increase in desferrioxamine dosage resulted in a 2.7-fold increase in peak ferrioxamine levels and in only a 1.5-fold increase in peak aluminoxamine levels. We conclude that dialysis patients, especially those with haemosiderosis, are exposed to persistently elevated ferrioxamine levels. Weekly doses of 5-10 mg/kg of desferrioxamine would be sufficient for aluminium chelation therapy.

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