Plasma lipoproteins were selectively removed from familial hypercholesterolemic patients by using two types of plasmapheresis: double-membrane filtration and selective adsorption of very low density lipoproteins (VLDL) and low density lipoproteins (LDL). In both techniques, plasma was separated from blood cells by using hollowfiber filters, and 100% of the VLDL and LDL was recovered in the filtrate. In doublemembrane filtration, the second hollow-fiber filter trapped 84% of LDL + VLDL, 48% of high density lipoprotein ( P lasma low density lipoprotein (LDL) has been recognized as a primary risk factor for developing atherosclerotic vascular lesions, especially in coronary arteries.1 Reduction of the plasma LDL level has been shown to decrease the incidence of ischemic heart attack in hyperlipoproteinemic patients. 2On the other hand, the plasma high density lipoprotein (HDL) level is inversely correlated, in epidemiological studies, 3 to the incidence of coronary heart disease independently of plasma LDL contribution. Thus, the risk of coronary heart disease must be considered from both of these aspects.

Plasma concentrations of immunoreactive (IR)-atrial natriuretic polypeptide (ANP) were measured before and after hemodialysis (HD) as well as isolated ultrafiltration (UF) in 9 patients with end-stage renal disease. There were significant falls in plasma concentrations of IR-ANP during both UF (from 78.6 ± 109.7 to 45.4 ± 56.8 pg/ml; mean ± SD; p < 0.025) and HDs (from 84.7 ± 48.6 to 35.0 ± 28.4 (p < 0.01) on first HD; from 73.7 ± 74.2 to 31.8 ± 21.8 pg/ml (p < 0.01) on later HD). There were distinct positive correlations between blood pressures and plasma concentrations of IR-ANP. These results support the view that ANP is secreted mainly by the expansion of blood volume. The fall in plasma concentrations of IR-ANP after HD seems to be caused by the decrease of blood volume, but not by removal due to dialysis of the peptide. However, the physiological role of ANP in patients with end-stage renal disease remains unknown.

Using urea and inulin as markers, we have developed a simple method to calculate intracellular and extracellular fluid volume in patients before and after hemofiltration therapy. During conventional hemofiltration using substitution fluid with a Na+ concentration of 140 mEq/L, a decrease in extracellular fluid volume was noted whereas the intracellular fluid volume was unaltered. Furthermore, we have developed a computerized mathematical model to analyze transcellular fluid shifts during hemofiltration. This model also indicates a decrease in extracellular fluid volume only, the intracellular fluid volume remaining unchanged. High-Na+ hemofiltration using substitution fluid with an Na+ concentration of 160 mEq/L has enabled us to remove fluid from both intracellular and extracellular compartments. Thus, high-Na+ hemofiltration is expected to normalize the intracellular hydration in uremic patients, and to reduce the decrease in extracellular fluid volume during hemofiltration therapy. Our data therefore suggest that high-Na+ hemofiltration could prevent hypotension due to large decreases in extracellular fluid volume by inducing a transcellular fluid shift out of body cells. Our computerized model can be a useful tool in the prescription of the optimal Na+ concentration in substitution fluid for individualized hemofiltration therapy.

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