It has recently been suggested that advanced glycosylation end-products (AGEs) are formed in the peritoneum in patients on CAPD. However, the exact location of AGE accumulation, the relation with the duration of CAPD and its pathophysiological role in CAPD remain unclear. If the peritoneum is glycosylated, it could bring about altered peritoneal function. Therefore, the aim of this study is to clarify the localization of AGEs in the peritoneum in accordance with the duration of CAPD and to examine its relation to the peritoneal permeability. Fifteen non-diabetic patients were divided into three groups (each 5 patients) on the basis of the mean duration (D) of CAPD (Group 1, D = 0 month; Group II, D = 34 months; Group III, D = 84 months). The AGE staining by monoclonal anti-AGE antibody in the peritoneum and the four-hour peritoneal equilibration test (PET) were compared among these groups. AGE was absent or found only weakly in Group I. However, in groups II and III, AGE was moderately or strongly positive especially in the vascular walls and it was dominant in group III. PET revealed that peritoneal permeability for glucose, creatinine, beta2-microglobulin and albumin was increased in Group II as compared to Group I, and it was further increased in Group III. The results of this study indicate that AGEs become dominantly accumulated in the vascular wall in accordance with the prolongation of CAPD treatment, and this might play some roles for the increased permeability of the peritoneal membrane in CAPD.

Therapy with human recombinant erythropoietin (EPO) has been accepted as effective for renal anemia in dialysis patients. However, studies in rats have shown that correcting anemia with EPO may affect the progression of renal dysfunction. In humans, however, the effect of EPO on residual renal function is a matter of controversy. We, therefore, investigated whether the long-term administration of EPO to predialysis patients influences residual renal function. Anemic patients at the predialysis stage with a serum creatinine (Cr) concentration ranging from 2 to 4 (average 2.9) mg/dl and a hematocrit (Ht) of less than 30% were randomly assigned to two groups which consisted of anemic patients not treated with EPO (group I, untreated anemic controls, n = 31) and anemic patients treated with EPO (group II, treated anemics, n = 42). Patients with nonsevere or moderate anemia (Ht > 30%) with a Cr ranging from 2 to 4 (average 2.6) mg/dl were also recruited as nonanemic controls (group III, untreated nonanemic controls, n = 35). Blood pressure was controlled to the same degree among the three groups by combined treatment with calcium antagonists and angiotensin-converting enzyme inhibitors. All patients were kept strictly on a low-protein (0.6 g/kg/day) and a low-salt (7 g/day) diet. The degree of control of dietary protein and blood pressure and the frequency of angiotensin-converting enzyme inhibitor administration were comparable among the three groups. The primary end point for each patient was a doubling of the baseline Cr which yielded cumulative renal survival rates which were plotted against time. Ht rose significantly from 27.0 ± 2.3 to 32.1 ± 3.2% in group II (n = 42, p < 0.001) with a rate of increase of 0.4 ± 0.06%/week. However, it declined from 27.9 ± 1.8 to 25.3 ± 1.9% in group I (n = 31, p < 0.001) and from 35.9 ± 3.5 to 32.2 ± 3.9% in group III (n = 35, p < 0.001). Cr doubled in 26 patients (84%) in group I as compared with 22 (52%) in group II and 21 (60%) in group III. The cumulative renal survival rates in groups II and III were significantly better than that in group I: p = 0.0003 (group I vs. group II) and p = 0.0024 (group I vs. group III). However, there was no difference in the renal survival rate between groups II and III (p = 0.3111). The better survival rate obtained in group II was attributable to the better survival rate for the nondiabetic patients in this group. The present study suggests that anemia, per se, is a factor in the progression of end-stage renal failure and that reversal of anemia by EPO can retard the progression of renal failure, especially in nondiabetic patiens, provided that blood pressure control, rate of increase in Ht, and dietary protein restriction are appropriate.

Mandibular lesions develop from both odontogenic and nonodontogenic origins and have varying degrees of destructive potential. Common benign cystic lesions include periapical (radicular) cysts, follicular (dentigerous) cysts, and odontogenic keratocysts. Benign solid tumors represent a broad spectrum of lesions such as ameloblastomas, odontomas, ossifying fibromas, and periapical cemental dysplasia. Malignant tumors that often involve the mandible include squamous cell carcinomas, osteosarcomas, and metastatic tumors. In addition, vascular lesions such as hemangiomas and arteriovenous malformations may develop, further expanding the differential diagnosis. Because mandibular lesions have a wide range of pathologic features but similar imaging appearances, familiarity with embryologic characteristics and secondary findings is crucial. Patient age at manifestation, prevalence, location within the mandible, cystic or solid appearance, border contour, and effect of the lesion on adjacent structures are all considerations in making the diagnosis. Despite this information, however, many lesions are impossible to differentiate without biopsy. In such cases, defining the degree of malignant potential is very helpful. Although imaging will not always provide a specific diagnosis, it should help narrow the differential diagnosis, thereby helping to guide patient treatment.

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