The fact that low expression of the klotho gene occurs in tissues other than the kidney and brain, including the pituitary, placenta, skeletal muscle, urinary bladder, aorta, pancreas, testis, ovary, thyroid gland, and colon, does not necessarily negate the concept that the Klotho detected in the peritoneal dialysate originates, at least in part, from several tissues near the peritoneum [1]. Although no data were available regarding the relationship between the peritoneal Klotho and IgG levels among our subjects, the positive relationship between the amount of peritoneal Klotho and the concentrations of total protein and albumin in the effluent

MRT67307 dialysate demonstrated in the present study, and the previous findings that the molecular weight of the soluble form of Klotho is estimated to be 130 kDa [11], seem to support the concept that there might be no local Klotho production in the peritoneum, and that the peritoneal soluble Klotho detected in the present study may therefore have originated

from the serum, thereby modulating the serum level of soluble Klotho in the PD subjects. On the other hand, the urinary excreted Klotho detected in our subjects may not have been of glomerular origin, but rather, may have originated exclusively from the renal tubules, because we failed to confirm any significant associations Selleckchem IWP-2 between the amounts of urinary excreted Klotho and those Amino acid of albumin and total protein, despite the significant correlation between the urinary total protein and albumin. Given that urinary soluble Klotho is of glomerular origin, the renal kinetics of albumin might be comparable to those of urinary soluble Klotho, because the molecular weight of soluble Klotho is approximately twofold that of albumin [11, 24]. There is still insufficient evidence to explain our finding of an undetectable level of

peritoneal Klotho in one PD subject. However, it is reasonable to consider that the presence of an undetermined neutralizing factor or inhibitor of Klotho might have been involved. Otherwise, differences in peritoneal permeability may play a role in the presence or absence of Klotho in the peritoneal dialysate. Indeed, the majority of our patients with detectable peritoneal Klotho were categorized as high average transporters by a peritoneal equilibration test, while the selleck chemical patient with undetectable Klotho was categorized as a low transporter (data not shown). Consequently, the clinical impact of the serum level of soluble Klotho should be evaluated carefully, especially among PD patients. Although the present study provided new information on the kinetics of soluble Klotho among PD subjects, our results should be interpreted within the context of the study limitations.