A high blood flow of 400 ml/min induces leukocytosis after 2 hr of dialysis with leukocyte concentrations of 110-150% of predialysis values. The leukocytosis occurs with both low and high biocompatible membranes, such as Cuprophan, Hemophan, and Polyamide. Cuprophan induces the most profound leukopenia, and also induces the most pronounced leukocytosis. For treatments with a given membrane there was, however, no correlation between leukopenia and leukocytosis. Leukopenia was independent of blood flow, while leukocytosis was strongly influenced by this factor. These observations indicate that different factors cause leukopenia and leukocytosis. Although a larger area induced more leukopenia, the effect was small. Membrane area had no effect on leukocytosis. There were no acute clinical side effects during dialysis that could be related to the leukocyte overshoot. The cause and chronic clinical consequences of leukocyte overshoot are unknown.

The clinical importance of biocompatibility of hemodialysis membranes is a matter of controversy. The authors studied the relationship between biocompatibility and acute symptoms during hemodialysis (HD). Twenty-three patients underwent 12 different bicarbonate HD using Cuprophan, Hemophan, or Polyamide membranes for short (2 hr) and long (4 hr) treatments, with small or large membrane areas. Subjective and objective symptoms were registered during HD and 12 and 36 hours thereafter. Type of membrane, membrane area, or Kt/V were of no importance for the occurrence of subjective or objective symptoms. The patients registered fewer symptoms during 2 hr HD with high blood flow than during 4 hr HD with slow blood flow (p = 0.04). Headache was particularly more frequent during the 4 hr HD. Blood pressure, and to some extent subjective symptoms, were influenced by ultrafiltration volume but not by type of membrane. Biocompatibility is not a determinant of acute side effects of hemodialysis.

Twenty patients with type II diabetes mellitus and hypertension (WHO stages I and II) participated in a 3-month double-blind cross-over study to evaluate the effects of clonidine (75-300 micrograms daily) on blood pressure, glycemic control and plasma lipoproteins. Already after 1 month's treatment with clonidine the systolic and diastolic blood pressures had decreased, from 168/103 to 161/98 mmHg (p less than 0.01). Fasting blood glucose and HbA1c concentrations were unaffected by 3 months' treatment. Similarly, plasma lipid and lipoprotein concentrations remained unchanged throughout the study (i.e. mean high and low density lipoprotein cholesterol concentrations were 0.89 and 3.87 mmol/l on placebo vs. 0.90 and 3.98 mmol/l on clonidine). Adverse effects were mild and tolerable, and consisted mainly of dryness of the mouth. We conclude that clonidine lowers the blood pressure in patients with type II diabetes without any adverse effects on glycemic control or plasma lipoproteins.

Serum lipoproteins were determined in 15 patients before and during antihypertensive treatment with atenolol 0.1–0.2 g/day for a mean of 8 months. The mean blood pressure fell from 171/103 to 154/93 mm Hg (p<0.05). Significant lipoprotein changes were an increase in very low density triglycerides (VLDL-TG) from 1.21±0.95 (SD) to 1.62±1.24 mmol/l (p<0.01) and in low density (LDL) TG from 0.46±0.12 to 0.51±0.12 mmol/l (p<0.05). Together, these TG increases resulted in development of hypertriglyceridaemia in 7/15 patients during atenolol treatment. No effect on whole serum cholesterol or on the high density lipoprotein cholesterol concentrations were found. Thus, some patients on long term treatment with atenolol seem to receive the benefit of normotension at the cost of hypertriglyceridaemia. This may have practical implications, since hypertriglyceridaemia constitutes an important risk factor for atherosclerosis.

A bedside method of measurement of the whole-blood thrombin time for the determination of heparin activity was used in 300 dialyses. It was easily performed by the whole staff despite the absence of previous training in laboratory work. This test, using a clot timer with an automatic pipette device, gives a minimum risk of exposure to hepatitis virus. An increase of the thrombin time of 50-100 per cent above the starting value (3.7-6.6 sec) was aimed at during the heparin infusion. Bleeding complications, which were minor, were seen only on 18 and fibrin formation only on 26 occasions out of 1500 observations. Within the 50-100 per cent limits bleeding complications were observed on 2 and fibrin formation on only 13 occasions. No protamine was given.