Next to the skin, the peritoneum is the largest human organ, essentially involved
in abdominal health and disease states, but information on peritoneal paracellular
tight junctions and transcellular channels and transporters relative to peritoneal
transmembrane transport is scant. We studied their peritoneal localization and quantity
by immunohistochemistry and confocal microscopy in health, in chronic kidney disease
(CKD) and on peritoneal dialysis (PD), with the latter allowing for functional characterizations,
in a total of 93 individuals (0–75 years). Claudin-1 to -5, and -15, zonula occludens-1,
occludin and tricellulin, SGLT1, PiT1/SLC20A1 and ENaC were consistently detected
in mesothelial and arteriolar endothelial cells, with age dependent differences for
mesothelial claudin-1 and arteriolar claudin-2/3. In CKD mesothelial claudin-1 and
arteriolar claudin-2 and -3 were more abundant. Peritonea from PD patients exhibited
increased mesothelial and arteriolar claudin-1 and mesothelial claudin-2 abundance
and reduced mesothelial and arteriolar claudin-3 and arteriolar ENaC. Transperitoneal
creatinine and glucose transport correlated with pore forming arteriolar claudin-2
and mesothelial claudin-4/-15, and creatinine transport with mesothelial sodium/phosphate
cotransporter PiT1/SLC20A1. In multivariable analysis, claudin-2 independently predicted
the peritoneal transport rates. In conclusion, tight junction, transcellular transporter
and channel proteins are consistently expressed in peritoneal mesothelial and endothelial
cells with minor variations across age groups, specific modifications by CKD and PD
and distinct associations with transperitoneal creatinine and glucose transport rates.
The latter deserve experimental studies to demonstrate mechanistic links.
