Prostaglandin-mediated loss of proteins during peritonitis in continuous ambulatory peritoneal dialysis

Steinhauer, Hjalmar B.; Schollmeyer, Peter
February 1986
Kidney International;Feb1986, Vol. 29 Issue 2, p584
Academic Journal
The loss of proteins into the dialysate and the peritoneal generation of the immunoreactive prostanoids PGE2, 6-keto-PGF1α PGF2α, and TXB2; were studied in 12 patients undergoing continuous ambulatory peritoneal dialysis (CAPD) during 16 episodes of peritonitis and in inflammation-free periods. Protein permeability, defined as the ratio of dialysate/plasma protein (D/P), decreased with increasing molecular weight, independent of the condition of the peritoneum. With peritonitis a general rise of permeability was noticed for total protein (TP) and the individual proteins β2-microglobulin (βMG), albumin (Alb), immunoglobulin G (IgG), and α2-macroglobulin (αMG) (P < 0.001). Simultaneously, an increase of dialysate prostanoids occurred with predominance of the vasodilative acting prostaglandins PGI2, determined as its metabolite 6-keto-PGF1α, and PGE2 by factors of 8.4 and 9.7, respectively (P < 0.001), in comparison to peritonitis-free control. In the early phase of peritonitis (0 to 12 hr after the onset of therapy) the augumented peritoneal prostaglandin synthesis correlated positively with the increased permeability of TP (r ≧ 0.7446, P < 0.01) and the individual proteins βMG, Alb, IgG, and αMG (r ≧ 0.5970, P < 0.05), Inhibition of cyclo-oxigenase activity by local administration of indomethacin inhibited both the generation of 6-keto-PGF1α and PGE2 by 39 and 42%, respectively (P < 0.05), and the peritoneal loss of TP by 34% (P < 0.05). In the absence of peritonitis indomethacin only diminished the synthesis of PGE2 whereas the generation of the other prostanoids remained unchanged. No effect occurred on peritoneal protein loss. The present data suggest that vasoactive prostaglandins are involved in the pathophysiology of increased peritoneal protein tosses in the early phase of CAPD-associated peritonitis.


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