Complement activation during exposure of plasma to cuprophan has been postulated to cause leukopenia and hypoxia in hemodialysis patients. To determine if hypoxia is related to leukopenia and if complement activation leads to a depletion of functional complement components, we dialyzed four patients three times sequentially against each of four types of membranes: cuprophan, regenerated cellulose, cellulose acetate, and polyacrilonitrile. Within 20 min there was a marked leukopenia with cuprophan from 5541 +/- 376 to 1216 +/- 94 (P less than 0.001) and with regenerated cellulose from 5541 +/- 411 to 1533 +/- 203 (P less than 0.001). With cellulose acetate, the change from 5558 +/- 400 to 3783 +/- 341 (P less than 0.001) was less dramatic, and with polyacrilonitrile the fall from 5591 +/- 381 to 464 +/- 401 (P less than 0.02) was minimal. After 2 and 4 hours of dialysis, a rebound leukocytosis was seen with cuprophan, regenerated cellulose, and cellulose acetate, but not with polyacrilonitrile. Transient thrombocytopenia occurred with cuprophan and regenerated cellulose. In spite of the variable degree of leukopenia, all membranes induced a similar and significant hypoxia, which was progressive throughout dialysis, even during the rebound leukocytosis. After 4 hours, the mean PO2 ranged from 91 to 93 mm Hg with all membranes. Functional hemolytic titers of whole complement, C3, C5, and C4 were normal prior to hemodialysis and failed to decrease after 4 hours with any membrane. It is concluded that hemodialysis leukopenia is membrane-dependent and is not the cause of hypoxia. In addition, hemodialysis complement activation does not lead to functional complement depletion and is of no clinical significance.

No abstract

A B S T R A C T 24,25-dihydroxycholecalciferol [24,25-

The dynamics of potassium excretion were examined in normal dogs and dogs with chronic renal insufficiency of at least 4 weeks' duration (remnant model). All animals, in balance on diets providing 15, 50, or 100 mEq of potassium and 100 mEq of sodium, were challenged with 50 mEq of potassium chloride. Immediately thereafter, hourly clearances were obtained for 5 hours. Irrespective of dietary potassium, mean fasting serum potassium and urinary potassium excretion (UKV) were similar in normal and remnant dogs with mean GFR's of 57 +/- 3 and 16 +/- 3 ml/min, respectively. After orogastric administration of 50 mEq potassium, serum potassium rose significantly more in remnant (2.2 to 2.5 mEq/liter) than in normal (0.9 to 1.2 mEq/liter) groups (P less than 0.001). Conversely, UKV increased significantly less, 70 to 96 vs. 151 to 194 micro Eq/min, respectively (P less than 0.001). In 5 hours, normal animals excreted 61 to 67% of the load, but remnant dogs only 30 to 37% (P less than 0.001). In all groups, UKV correlated directly with serum potassium concentration. But this relationship was markedly attenuated in the remnant groups (P less than 0.001) and independent of dietary potassium. In contrast, the same slope describes the relationship between UKV/GRF and serum potassium for all, normal and remnant, animals. The blunted kaliuresis occurred despite the more severe hyperkalemia in remnant than in normal dogs; it was not associated with significant changes in acid-base, diuresis, natriuresis, serum glucose, insulin, and glucagon concentrations and occurred despite prolonged hyperaldosteronism. The results demonstrate a severe limitation of the remnant kidney's ability to rapidly excrete a potassium load. Changes in serum potassium, or a consequence thereof, are important for the urinary excretion of potassium following its acute administration.

No abstract