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Acute adverse side-effects of hemodialysis such as hypotension, muscle cramps, osmotic imbalance and thirst are induced by the interference with fluid and electrolyte balance occurring during treatment. Changes in osmolarity due to alterations of plasma sodium concentration during hemodialysis strongly influence fluid distribution between extracellular and intracellular fluid volume. Increased sodium dialysate concentration induces fluid shift from the intracellular to the extracellular compartment. This shift leads to a more efficient ultrafiltration by increasing plasma refilling volume but also to an increased thirst. Treatment of hypotension, cramps and nausea with hypertonic saline solution leads also to a considerable retention of sodium. Profiling hemodialysis consists in deliberately changing ultrafiltration and dialysate. sodium in order to combine an efficient ultrafiltration with a balanced sodium handling and to prevent side-effects during treatment. Continuous measurement and control of blood volume seems to be the best method to prevent hypotensive episodes. Profiling of sodium should not be the cause of a positive sodium balance. The clinical benefits of sodium profiling to the patients have still to be proven.

In patients on chronic hemodialysis hypotensive episodes are frequently encountered during the course of treatment and the prevalence of atherosclerosis is increased. Endothelin-1 (ET-1), an endothelium-derived peptide with vasoconstrictive and mitogenic effects on smooth muscles, is involved in vascular tone regulation and in the pathogenesis of atherosclerosis. The aim of the present study was to investigate plasma ET-1 during hemodialysis treatment and to explore the probable influence of pre-existing hypertension. Forty-seven hemodialysis patients (21 females, mean age 62 +/- 12 years) were evaluated and hypertensive patients (n = 33) were compared to normotensive patients (n = 14). Relative blood volume changes (hemoglobinometry) and blood pressure were measured. Samples were taken before, every hour during and after hemodialysis. Plasma ET-1 was measured by enzyme-linked immunosorbent assay and results were corrected according to hemoconcentration. Hemodialysis with an ultrafiltration rate of 2224 +/- 933 mL was performed. Total blood volume at the end of hemodialysis was 89.4 +/- 8.2% of the pretreatment volume. The fall in blood pressure (137/74 +/- 22/11 mmHg vs 127/73 +/- 30/14 mmHg) correlated with the decrease in blood volume (mean blood pressure: r = 0.33). Plasma ET-1 increased from 1.29 +/- 0.47 pg/mL before to 1.46 +/- 0.56 pg/mL (reference range 0.3-0.9) at the end of hemodialysis (P < 0.05). This rise was more pronounced in patients with hypertension than in normotensive individuals (P < 0.05). The change in blood volume (r = 0.41) and blood pressure (mean blood pressure: r = 0.34) correlated with plasma ET-1 at the end of hemodialysis (P < 0.05). Plasma ET-1 was enhanced in hemodialysis patients compared to normal subjects. During the hemodialysis session an increase in ET-1 was encountered, which was more pronounced in hypertensive than in normotensive patients and paralleled the hemodynamic changes. Apart from pre-existing hypertension, further factors potentially influencing ET-1 include local endothelial injury (arteriovenous fistula) and generalized bioincompatibility reactions (e.g. foreign surface contact) occurring during hemodialysis.

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