Cuprophan reuse and intradialytic changes of lung diffusion capacity and blood gasses

Abstract

The changes in arterial blood gas, pulmonary function tests, leukocyte counts and complement activation were evaluated during first use and subsequent reuse of cuprophan dialyzers. The dialysate buffer was bicarbonate. Reuse of cuprophan dialyzers significantly attenuated the fall in leukocyte counts and the rise in C3a des Arg seen during first use dialysis. First use dialysis also caused a drop in arterial paO2 from 93.0 +/- 12.4 mm Hg to a nadir of 82.8 +/- 12.6 mm Hg at 60 minutes (P less than 0.01). PaO2 levels did not change when reused dialyzers were employed (93.7 +/- 12.2 before dialysis and 96.4 +/- 15.2 mm Hg at 60 minutes, P greater than 0.05). Intradialytic paO2 curves obtained during first use and reuse were significantly different by variance analysis (P less than 0.001). There was also a significant decline in lung diffusion capacity (DLCO, from 30.70 +/- 8.89 to 23.77 +/- 7.76 ml/min X mm Hg, P less than 0.01) and transfer factor (KCO, from 6.07 +/- 1.97 to 5.65 +/- 2.13 ml/min X mm Hg, P less than 0.01), during first use at one hour after initiation of dialysis. This decrease was entirely prevented during reuse, (P less than 0.001 vs. first use by variance analysis). Percentual changes in leukocyte counts and C3a des Arg concentration on one hand, and in paO2, DLCO and KCO on the other were significantly correlated to each other. Other factors with a possible influence on intradialytic pulmonary function such as ultrafiltration volume, dialysate buffer composition, evolution of intradialytic blood pH and cardiac output, were all identical under both experimental conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Complications of Hemodialysis

“…The biocompatibility of the membrane used is one of the most frequently blamed factors in hypoxemia (Graf et al,1980). Especially the use of an acetate-containing dialysate together with a Cuprophan membrane increases hypoxemia (Vanholder et al,1987). Hypocapnia associated with intradialytic loss of CO 2 and adaptation to chronic metabolic acidosis lead to periodic shortness of breath and a tendency to sleep apnea syndrome (De Broe & De Backer, 1989).…”

Dietary Fatty Acid Supplementation Modulates the Urinary Excretion of Calcium and Oxalate in the Rat

“…In contrast, inhibitory effects on both parameters were observed after the incorporation of oleic and eicosapentaenoic (EPA) acids [2]. This observation is interesting in the light of previous findings that: (1) band 3 and band-3-related proteins represent the major transport pathways for oxalate in erythrocytes and the kidney, respectively [9]; (2) band 3 phosphorylation is an important regulatory step of the oxalate flux in erythrocytes [10, 11]; (3) an oxalate transport pathway present in red blood cells [12]might also be found in other cells, in particular renal tubular cells as suggested by the observation of a correlation between erythrocyte oxalate flux rate and renal oxalate clearance rate [13]. …”

Depressed Phagocytosis in Hemodialyzed Patients: In vivo and in vitro Mechanisms

“…In infection, this effect is attributed to complement activation products [33], which are also abundant during cuprophane dialysis [34][35][36]. Neutrophils preexposed to high concentra tions o f activated complement are inhibited in their subse quent migratory responses [37], However, this deactivation is mainly related to locomotion and not to NADPH oxidase activity [38].…”