Abstract

Aquaporin-1 (AQP-1) dysfunction is one of the valid theories for decreased free water transport (FWT) in long-term peritoneal dialysis (PD) ultrafiltration failure (UFF). We questioned whether apoptosis of peritoneal cells could be reflected in an increased release of cellular (CR) K(+) and explain AQP-1 dysfunction. If so, negative relationships between CR-K(+) and FWT would be expected. Therefore, we analysed CR-K(+) to total peritoneal K(+) removal, for possible relationships with FWT, the duration of PD, the presence of late UFF and effluent cancer antigen (CA) 125. Standard peritoneal permeability analyses done with 3.86% glucose were investigated cross-sectionally in three extreme groups: group I: 19 patients <1 year on PD; group II: 20 patients >4 years on PD without UFF; group III: 19 patients >4 years on PD with UFF. Group III had the lowest values of FWT and CR-K(+) (P < 0.01). CR-K(+) had a positive correlation with FWT in groups I and II, but not in group III. These correlations were also present using much simpler methodologies: replacement of CR-K(+) by mass transfer area coefficient (MTAC)-K(+)/MTAC-creatinine ratio or dialysate over plasma (D/P)-K(+)/D/P-creatinine ratio and replacement of FWT by Na(+)-sieving. No relationship with CA125 was present. This study shows that other than diffusive and convectional, K(+) transport is not excluded in patients treated with conventional glucose-based PD solutions. We found evidence for release of K(+) from cells. In general, CR-K(+) was related to parameters of FWT, except for long-term patients with UFF. This suggests glucose-induced hypertonic cell shrinkage as a basic physiological phenomenon during PD. The absence of this relationship in long-term PD patients with UFF either suggests a reduction or inhibition of K(+)-channels and may be due to another mechanism than AQP-1 dysfunction. Most likely, CR-K(+) in UFF does not reflect apoptosis. However, the D/P-K(+)/D/P-creatinine ratio may be useful in detecting peritoneal changes.

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