Infectious complications are frequent and often lethal in patients with uremia. 
Serious alterations in neutrophil function, e.g., phagocytosis, mononuclear cell 
activation, cytokine production, complement activation, T-cell function, and 
adhesion molecule expression, have been documented in uremic patients. Uremia 
per se is a cause of some of these derangements, but much evidence now exists 
that blood-membrane interaction during dialysis is responsible for many of these 
abnormalities. This is particularly true when bio-incompatible cellulose-based 
membranes are used. In many of these patients, newly described granulocyte 
inhibitory proteins (GIP) can be demonstrated. These two proteins, GIP I and II 
(28 kD and 9.5 kD, respectively, in molecular weight), block effective bacterial 
killing, chemotaxis, and oxygen metabolism. It appears that GIP I is a member of 
the lightchain family, and GIP II is the advanced glycosilation end product of 
beta 2-microglobulin. Another inhibitory protein, degranulation inhibitory 
protein (DIP), has been isolated. This protein is 14 kD in molecular weight, and 
is identical to the angioplastic factor angiogenin. DIP levels are significantly 
elevated in patients undergoing dialysis. Much still needs to be learned about 
the interactions of these inhibitory proteins with other soluble inflammatory 
mediators and, in particular, cytokines. It is clear, however, that profound 
derangements in immune function take place during uremia and dialytic therapy. 
Such derangements are likely to play an important role in determining the rate 
of recovery of renal function and the patient's ability to respond to septic 
insults. Further insights into the pathogenesis of uremic-dialytic immune 
dysfunction are already yielding improved patient management and decreased 
infection rates.