Background In continuous ambulatory peritoneal dialysis (CAPD), the peritoneal membrane is continuously exposed to high-glucose-containing dialysis solutions. Abnormally high glucose concentration in the peritoneal cavity may enhance advanced glycosylation end-product (AGE) formation and accumulation in the peritoneum. Increased AGE accumulation in the peritoneum, decreased ultrafiltration volume, and increased peritoneal permeability in long-term dialysis patients have been reported. Aim The purpose of the study was to evaluate the relation between peritoneal membrane permeability and peritoneal accumulation of AGE. Methods Peritoneal membrane permeability was evaluated by peritoneal equilibration test (PET) using dialysis solutions containing 4.25% glucose. Serum, dialysate, and peritoneal tissue levels of AGE were measured by ELISA method using polyclonal anti-AGE antibody. Peritoneal biopsy was performed during peritoneal catheter insertion [new group (group N), n = 18] and removal [long-term group (group LT), n = 10]. Peritoneal catheters were removed due to exit-site infection not extended into the internal cuff ( n = 6) and ultrafiltration failure ( n = 4) after 51.6 ± 31.5 months (13 – 101 months) of dialysis. PET data obtained within 3 months after the initiation of CAPD or before catheter removal were included in this study. Ten patients in group N and 4 patients in group LT were diabetic. Patients in group LT were significantly younger (46.5 ± 11.1 years vs 57.5 ± 1.3 years) and experienced more episodes of peritonitis (3.5 ± 2.1 vs 0.2 ± 0.7) than group N. Results Peritoneal tissue AGE level in group LT was significantly higher than in group N, in both nondiabetic (0.187 ± 0.108 U/mg vs 0.093 ± 0.08 U/mg of hydroxyproline, p < 0.03) and diabetic patients (0.384 ± 0.035 U/mg vs 0.152 ± 0.082 U/mg of hydroxyproline, p < 0.03), while serum and dialysate levels did not differ between the groups in both nondiabetic and diabetic patients. Drain volume (2600 ± 237 mL vs 2766 ± 222 mL, p = 0.07) and D4/D0 glucose (0.229 ± 0.066 vs 0.298 ± 0.081, p < 0.009) were lower, and D4/P4 creatinine (0.807 ± 0.100 vs 0.653 ± 0.144, p < 0.0001) and D1/P1 sodium (0.886 ± 0.040 vs 0.822 ± 0.032, p < 0.0003) were significantly higher in group LT than in group N. On linear regression analysis, AGE level in the peritoneum was directly correlated with duration of CAPD ( r = 0.476, p = 0.012), number of peritonitis episodes ( r = 0.433, p = 0.0215), D4/P4 creatinine ( r = 0.546, p < 0.027), and D1/P1 sodium ( r = 0.422, p = 0.0254), and inversely correlated with drain volume ( r = 0.432, p = 0.022) and D4/D0 glucose ( r = 0.552, p < 0.0023). AGE level in the peritoneal tissue and dialysate were significantly higher in diabetics than in nondiabetics in group LT, while these differences were not found in group N. Serum AGE level did not differ between nondiabetics and diabetics in either group N or group LT. Drain volume and D4/D0 glucose were lower and D4/P4 creatinine and D1/P1 sodium higher in diabetics than in nondiabetics in both groups. Conclusion Peritoneal accumulation of AGE increased with time on CAPD and number of peritonitis episodes, and was directly related with peritoneal permeability. Peritoneal AGE accumulation and peritoneal permeability in diabetic patients were higher than in nondiabetic patients from the beginning of CAPD.

Alzheimer’s disease (AD) is a neurodegenerative disease characterized by the deposition of amyloid-β peptide (Aβ) in diffuse and neuritic plaques. Previous research has suggested that certain vitamins may prevent this process. In the present study, we evaluated the relationship between vitamin intake and cerebral Aβ burden in patients with cognitive impairment. This study included 19 patients with subjective cognitive impairment and 30 patients with mild cognitive impairment. All patients underwent brain MRI and 18F-florbetaben positron emission tomography. The Food Frequency Questionnaire was used to evaluate dietary intake of the 15 vitamins. Intake of vitamin B6 (p = 0.027), vitamin K (p = 0.042), vitamin A (p = 0.063), riboflavin (p = 0.063), β-carotene (p = 0.081), pantothenic acid (p = 0.092), and niacin (p = 0.097) was higher in the Aβ-positive group than in the Aβ-negative group. Multivariate linear regression analysis revealed that pantothenic acid intake was an independent determinant of cerebral Aβ burden (β = 0.287, p = 0.029). No significant correlations were observed between cerebral Aβ burden and the intake of other vitamins. Our findings demonstrated that pantothenic acid intake may be associated with increased cerebral Aβ burden in patients with cognitive impairment. These results may offer insight into potential strategies for AD prevention.