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Long-term hemodialysis (HD) patients complaining of shoulder joint pain were treated by HD and by push/pull HDF using high-flux synthetic membranes with large pores (Asahi PAN 20CX2) for 2 weeks. The results showed no significant difference in Kt/Vurea between HD and push/pull HDF. Nevertheless, reduction of the plasma beta 2-microglobulin was greater during push/pull HDF than during HD. These findings can be explained by far more convective flux in push/pull HDF than in HD: nearly 30 L during push/pull HDF vs. 3 L during HD. In the present study, there was no alleviation of the shoulder joint pain during HD treatment, whereas marked relief of the symptom was found during push/pull HDF treatment. Since the two treatment modalities differ simply in their efficiency in removing larger molecular weight substances, the joint pain alleviation effected by push/pull HDF could well be ascribed to elimination of an unknown larger molecular weight substance causing this symptom. However, a considerable amount of beta 2-microglobulin was removed both by HD and push/pull HDF. Therefore, the substance causing the joint pain might be larger than beta 2-microglobulin.

We analyzed the rebound pattern of plasma β₂-microglobulin (β₂-m) concentration from 4 h after completion of hemodiafiltration until the start of the next treatment according to the one-pool β₂-m kinetic model so as to determine β₂-m generation rate and whole-body β₂-m clearance. Next, we obtained the whole renal β₂-m clearance as the product of renal creatinine clearance and the glomerular sieving coefficient of β₂-m. Then, extrarenal β₂-m clearance was calculated as the difference between whole-body β₂-m clearance and whole renal β₂-m clearance, and renal β₂-m clearance due to tubular absorption was taken to be the difference between whole renal β₂-m clearance and renal β₂-m clearance due to urinary excretion. The results showed that the β₂-m generation rate was virtually the same for all patients and that the higher the patients and that the higher the patients’ plasma β₂-m concentration was, the lower was the whole-body β₂-m clearance. Moreover, in the present study, an inverse correlation was found between the following respective factors: plasma β₂-m concentration and whole renal β₂-m clearance; plasma concentration and renal clearance due to tubular absorption; plasma concentration and renal clearance due to urinary excretion. However, there was no correlation between plasma β₂-m concentration and extrarenal β₂-m clearance. The findings indicate that the variation of plasma β₂-m concentration with the individual patient is solely attributable to the variation in residual renal function in terms of β₂-m elimination.

The present experiment demonstrated that an irreversible glomerulosclerosis could be induced in the rat through repeated intravenous administrations of OX-7 (a monoclonal anti-Thy-1.1 antibody). Rats were injected with 0.2 mg of affinity-purified OX-7 at 1-week intervals for a period of 4 weeks. Glomerular damage was periodically examined at light-microscopic level. Thirty-five days after the initial injection (7 days after the final injection), capillary aneurysms and expansion of the mesangial areas with hypercellularity were frequently observed. Similar glomerular damage was also observed in rats 7 days after they received a single injection of either 1.0 or 0.2 mg of OX-7. After repeated injections, 112 days from the initial administration (84 days after the final injection), approximately 60% of the glomeruli had expanded mesangial areas with an apparent increase in the mesangial matrix. The result contrasts sharply with that obtained from a single injection of OX-7 in that more than 85% of the glomeruli showed no abnormalities 84 days after the injection. This chronic model, as a result of repeated injections of the antibody, could serve as a potential for further investigation of the mechanisms involved in the development of chronic glomerulonephritis.

Blood volume was measured continuously during hemodialysis using the authors' hematocrit continuous measurement system in an attempt to determine any relationship between dialysis-induced hypotension with acute onset and blood volume. Hypotension resulted approximately 3 h into dialysis in the present study. This point in time was that at which blood volume was more than 5% above the minimum level during the dialysis treatment, and in some patients it was more than 10% over the minimum level of blood volume. At the time dialysis-induced hypotension occurred or before, there was no sharp decrease in blood volume nor any change in the plasma refilling rate. This suggested that this hypotension is caused by a sudden breakdown of the blood pressure support mechanism compensating for decreased blood volume.

The beta 2-microglobulin clearance increased as the convective transport was added during hemodialysis to perform hemodiafiltration (HDF), suggesting that a convective transport type artificial kidney is more effective for beta 2-microglobulin removal. Actually, the decrease in the plasma beta 2-microglobulin level per treatment was more pronounced in hemofiltration and push/pull HDF than in hemodialysis. In the present study, no significant fluctuation in the pretreatment level of beta 2-microglobulin was shown by serial treatment by hemodialysis, whereas an obvious decreasing trend of it was indicated in serial treatment of either push/pull HDF or hemofiltration. Moreover, our study indicated that the ratio of posttreatment beta 2-microglobulin level in relation to its pretreatment level increases as the treatment by hemofiltration or push/pull HDF is repeated.

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