Abstract. Acid-base balance and peritoneal membrane longevity are of utmost relevance for pediatric patients undergoing peritoneal dialysis (PD). PD fluids with neutral pH and reduced glucose degradation product contents are considered more biocompatible, because they preserve peritoneal cell functions in vitro. To investigate the clinical effects of a novel PD fluid buffered with 34 mM pure bicarbonate at neutral pH, a randomized, prospective, crossover comparison with conventional, acidic, 35 mM lactate PD fluid was performed for two consecutive 12-wk periods with 28 children (age, 6 mo to 15 yr) undergoing automated PD (APD). Blood bicarbonate levels and arterial pH were significantly higher after 3 mo of bicarbonate PD (24.6 Ϯ 2.3 mM and 7.43 Ϯ 0.06, respectively), compared with lactate PD (22.8 Ϯ 3.9 mM and 7.38 Ϯ 0.05, respectively; P Ͻ 0.05). This effect was reversible among patients who returned from bicarbonate to lactate fluid. Low initial pH and young patient age independently predicted increased blood pH during bicarbonate APD. Peritoneal equilibration tests revealed subtle changes in solute transport, with a less steep creatinine equilibration curve during bicarbonate dialysis, suggesting reduced peritoneal vasodilation. The peritoneal release of carcinogen antigen-125 increased twofold during bicarbonate APD (29 Ϯ 15 versus 15 Ϯ 8 U/ml per 4 h, P Ͻ 0.01), which is consistent with recovery of the mesothelial cell layer. This effect was fully reversed when the patients returned to lactate fluid. Effluent carcinogen antigen-125 levels were inversely correlated with peritoneal glucose exposure during lactate but not bicarbonate APD, indicating improved in vivo mesothelial cell tolerance of high-dose glucose with the neutral-pH PD fluid with reduced glucose degradation product content. Among children undergoing APD, neutral-pH, bicarbonate-buffered PD fluid provides more effective correction of metabolic acidosis and better preservation of peritoneal cell mass than do conventional, acidic, lactate-based fluids.

The yield pressure and the resistance to distension increased in response to SNS for idiopathic fecal incontinence. This will inevitably increase the resistance to flow through the anal canal, which may contribute to the benefits of sacral nerve stimulation.

IFI seems to be associated with impaired ano-rectal sensory functions in both the afferent fibers to the brain and the cortical processing of anal sensory pathways. This may play a central role for the pathogenesis of IFI.

Cortical potentials evoked from the anal canal are challenged by latency jitter likely related to variability in muscle tone due to the distensions. Using single-sweep analysis, anal CEPs proved to be reproducible and should be used in future evaluation of the anal function.

Patients treated with radiotherapy or chemoradiation for anal cancer have low anal resting and squeeze pressures as well as reduced resistance to distension and flow.