Comparison of four methods of cleaning hollow-fiber dialyzers for reuse.

Four methods of cleaning hollow-fiber artificial kidneys (HFAKs) for reuse were compared in a prospective study. Each cleaning method was randomly assigned and HFAKs were reused until volume loss was greater than or equal to 15 ml, unless discarded for other reasons. HFAKs cleaned with 0.3 M sodium hydroxide averaged 14.5 uses, significantly better (p less than 0.01) than reverse ultrafiltration (6.4 uses), 3% hydrogen peroxide (5.7 uses), or water flush (4.7 uses). Only 1 of 10 HFAKs cleaned with NaOH was discarded owing to volume loss, whereas 25 of 30 HFAKs cleaned by the other methods were rejected for this reason. To relate changes in solute clearance to volume loss, urea and creatinine clearances were determined on HFAKs cleaned by water flush. By the fifth use the average volume had declined to 86.3% of original, but creatinine and urea clearances were reduced, respectively, to 97 and 95% of the original values.

Acetate and bicarbonate fluctuations and acetate intolerance during dialysis.

Plasma bicarbonate losses during acetate dialysis were prevented by using a combination of acetate and bicarbonate in the dialysate. In 21 patients who were treated with combination dialysate, the fall in mean blood pressure (MBP), and frequency of symptoms, and post-dialysis task performance were all similar to that observed during dialysis with acetate alone. Furthermore, dialysis performed with bicarbonate dialysate resulted in significantly smaller MBP drops, fewer symptoms, and an improved task performance compared to either an acetate or a combination dialysis. These findings indicate that the presence of acetate, rather than a bicarbonate loss, was responsible for the patients' intolerance to acetate dialysis. Patients symptomatic on acetate dialysis had a similar ultrafiltration rate, weight loss, MBP drops, and postdialysis serum acetate levels; they were similar in age and weight to symptom-free patients. Thus, the toxic effect of acetate was not related to serum acetate level. There was no difference in bicarbonate dialysis between patients with symptoms on acetate and the symptom-free patients in reference to MBP drops and task performance. This finding suggests that symptomatic patients were not simply less tolerant to the process of dialysis, but differed from symptom-free patients in their response to the presence of acetate.

Effects of oxygen administration on the manifestation of acetate intolerance in dialysis patients.

In a prospective double-blind study. 12 patients were dialyzed four times each with nasal oxygen (O2) and 4 times each with air throughout acetate dialysis. Fewer symptoms (p less than 0.01), improved postdialysis task performance (p less than 0.04) and a tendency for less mean blood pressure drop (p less than 0.07 two-sided) were noted on O2 dialyses than on air dialyses. The rate of acetate metabolism was increased during O2 dialyses since serum acetate levels were significantly lower at 2, 3 and 4 h. Significant hypoxemia was demonstrated in 10 of these patients on acetate dialysis without O2. These results clearly demonstrate that: (1) prevention Of hypoxemia during dialysis reduces acetate intolerance, and (2) compromised tissue O2 availability may be partly responsible for dialysis morbidity.

The influence of acetate versus bicarbonate on patient symptomatology during dialysis.

The effect of large-surface area dialysis (LS) using dialysate containing both acetate and bicarbonate (LS-C) on a patient's symptomatology was compared with that noted with acetate (LS-A) or bicarbonate (LS-B) in the dialysis fluid. Patients experienced significantly more symptoms and deterioration of objective performance test scores with both LS-A and LS-C than LS-B. Furthermore, a correlation was seen between plasma acetate level at the end of dialysis and decrement in the performance test scores. The results suggest that accumulation of acetate rather than acute alteration in acid-base status is primarily responsible for the morbidity.

Less dialysis-induced morbidity and vascular instability with bicarbonate in dialysate.

We devised three protocols to test the postulate that increased morbidity during high-efficiency dialysis with large-surface-area units (LS) might be due in part to the increased flux of bicarbonate out and acetate into the patient inherent is LS dialysis. The first protocol showed that with LS-acetate dialysis there was a marked fall in plasma bicarbonate and Pco2 during the first 3 to 4 h, followed by a rapid rise in bicarbonate above normal and return to control in Pco2. With LS-bicarbonate dialysis, these oscillations were largely eliminated. A second double-blind protocol showed that central nervous system-type symptoms noted during and after LS-acetate dialysis were reduced significantly by switching to LS-bicarbonate dialysis. The third protocol showed that with LS-carbonate the tolerable rate of ultrafiltration could be increased 67% compared with LS-acetate dialysis.

Clinical use of a totally heparin grafted hemodialysis system in uremic patients.

1. A totally heparin grafted dialysis system shows great promise in the treatment of chronic uremia associated with bleeding risk. 2. Long-term treatment of chronic uremia with this system has to await: a) Further studies of the chronic toxicity of CPC. b) Evaluation of performance which may be achieved by using a more homogeneous heparin with higher bioactivity. 3. Detailed studies of platelet factor 4 release with subsequent heparin neutralization to determine the importance of this variable in its effect on system performance.

Successful use of a totally heparin grafted hemodialysis system in sheep.

A total of 33 totally heparin-grafted dialysis systems using HFAK Cordis Dow Models 3 and 4 have been compared to a total of 23 nongrafted systems. The comparison of deltap, flow rate, FBVL and macroscopic inspection showed highly significant differences in favor of the heparin-grafted systems. The antithrombogenic performance of the totally heparin-grafted systems is mainly due to a small leakage of heparin during the experiments. A minimum of 1.35 X 10(-8) Gm/cm2/min of heparin is sufficient to prevent clotting at the blood-polymer interface.