Dialysis induced hypoxemia.
We investigated the mechanism by which hypoxemia is produced in patients on dialysis by studying changes in neutrophil count, blood gases and pulmonary function in a patient with only trace amounts of circulating C3 associated with Type II mesangiocapillary glomerulonephritis and a control group of 6 patients with normal C3 levels during a 4 hour hemodialysis. Fifteen minutes after the start of dialysis the neutrophil count fell to 13% of pre-dialysis values in the control group while it only fell to 71% in the study patient. A further fall to 47% occurred in the patient at 30 minutes. A drop in PaO2 by 15% of initial values occurred at 15 and 30 minutes in the controls and the patient respectively matching the trend of fall in the neutrophil count. PaCO2 fell sharply across the dialysis membrane with reciprocol changes in the dialysis bath. Alveolar oxygen tension showed a significant reduction starting at 15 minutes correlating with the reduction in PaO2. The A-a O2 gradient was not altered significantly. These data strongly suggest that the principal mechanism leading to hypoxemia during dialysis is hypoventilation resulting from CO2 loss into the dialysis bath. Complement mediated pulmonary leucostasis may play a secondary role in inducing a quicker fall in PaO2 in the early part of dialysis.
D000293:Adolescent; D000328:Adult; D001784:Blood Gas Analysis; D003176:Complement C3 / Q000032:analysis*; D003182:Complement C5 / Q000032:analysis; D005260:Female; D006801:Humans; D000860:Hypoxia / Q000097:blood / Q000209:etiology* / Q000276:immunology; D007958:Leukocyte Count; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000166:cytology; D006435:Renal Dialysis / Q000009:adverse effects*
D003176:Complement C3; D003182:Complement C5