Ali M. Sherif

Peritoneal dialysis (PD) is used as renal replacement therapy in patients with end-stage kidney disease. However, peritoneal membrane failure remains problematic and constitutes a critical cause of PD discontinuation. Recent studies have revealed the unique biological action of molecular hydrogen (H2) as an anti-oxidant, which ameliorates tissue injury. In the present study, we aimed to examine the effects of H2 on the peritoneal membrane of experimental PD rats. Eight-week-old male Sprague-Dawley rats were divided into the following groups (n = 8–11 each) receiving different test solutions: control group (no treatment), PD group (commercially available lactate-based neutral 2.5% glucose PD solution), and H2PD group (PD solution with dissolved H2 at 400 ppb). Furthermore, the influence of iron (FeCl3: 5 μM: inducer of oxidative cellular injury) in the respective PD solutions was also examined (Fe-PD and Fe-H2PD groups). The H2PD solution was manufactured by bathing a PD bag in H2-oversaturated water created by electrolysis of the water. Twenty mL of the test solutions were intraperitoneally injected once a day for 10 days. Parietal peritoneum samples and cells collected from the peritoneal surface following treatment with trypsin were subjected to analysis. In the PD group as compared to controls, a mild but significant sub-mesothelial thickening was observed, with increase in the number of cells in the peritoneal surface tissue that were positive for apoptosis, proliferation and vimentin, as seen by immunostaining. There were significantly fewer of such changes in the H2PD group, in which there was a dominant presence of M2 (CD163+) macrophages in the peritoneum. The Fe-PD group showed a significant loss of mesothelial cells with sub-mesothelial thickening, these changes being ameliorated in the Fe-H2PD group. H2-dissolved PD solutions could preserve mesothelial cells and peritoneal membrane integrity in PD rats. Clinical application of H2 in PD could be a novel strategy for protection of peritoneal tissue during PD treatment.

Abstract:  Reports analyzing the histopathological differences between encapsulating peritoneal sclerosis (EPS) and simple peritoneal sclerosis (non‐EPS) and those comparing the pathology of early and late EPS are limited. We present pathological comparisons between EPS and non‐EPS, also between the early and late EPS stages. We compared peritoneal membrane (PM) samples (Group B) of 12 EPS patients (Group A) and 23 non‐EPS cases regarding; mesothelial loss, submesothelial compact zone degenerated layer and compact zone thicknesses, densities of total and diseased vessels, fibrin stain, new membrane formation and degenerative changes. Group A was subdivided into 7 early (group A1) and 8 late (group A2) EPS cases; we compared both subgroups in the same manner and finally compared groups A1, A2, and B. No differences were found between groups A and B in the incidences of mesothelial detachment, new membrane formation and compact zone degenerative changes between the two groups. Furthermore, there were no differences in compact zone thickness, and vascular densities in the compact zone of respective vascular grade. Whereas, fibrin deposition and thickness of the submesothelial degenerated layer were significantly higher in group A than group B (P = 0.01 and 0.05, respectively), and the thickness of the compact zone was less in group A1 than in group A2 (P = 0.03). Positive fibrin stains and thick degenerative compact zone layers are important pathological findings in EPS. Angiogenesis, vasculopathy, new membrane formation, fibrosis and degenerative changes of the compact zone are not unique characteristics for EPS. Larger size studies are recommended to verify this issue.

Background. Peritoneal sclerosis (PS) complicates continuous ambulatory peritoneal dialysis (CAPD). Exploring the peritoneal vascular changes, which are characteristic histological findings in long-term PD, may give new insight into the basic pathological process leading to PS. We present a quantitative analysis of peritoneal vascular density as well as vasculopathy grades in relation to PD duration. Methods. Peritoneal samples from 56 stable CAPD patients were analysed, and cases with membrane failure were excluded. Patients were classified into four groups according to CAPD duration in years: group A (n = 12), 0 year; group B (n = 11), 1–5 years; group C (n = 17), 5–9 years; and group D (n = 16), >9 years. The total density, of microvessels (capillaries, post-capillary venules and venules) and the density of each vasculopathy grade (0 = intact, 1 = mild, 2 = moderate and 3 = severe) in the compact zone were calculated (numbers/mm²) in each sample and the percentage ratio of each grade in relation to the total vessel density was also determined. Results. There was no significant difference in the total vessel density (P-value = 0.64). In the grade of vasculopathy (density and percentage ratio), there were significant differences among groups, with grade 0 highest in group A, grade 1 highest in group C and grade 3 highest in group D. Conclusion. The results of this study indicate that vascular density does not increase, at least in stable uncomplicated PD, and that intact vessels decrease with time on PD, while the severe grades of vasculopathy predominate especially on a long-term basis.

Background: Neuromyopathy was reported to be a problem among live donor familial Mediterranean fever (FMF) amyloid kidney transplant recipients. We aimed to address this issue on a long-term basis. Methods: 14 FMF amyloid live donor kidney transplant recipients with a mean post-transplant follow-up period of 82.43 ± 50.1 months in comparison to a control group of 19 non-amyloid renal transplant patients were subjected to thorough neurological examination, laboratory and electrophysiologic studies. Results: Both groups were comparable with regard to mean serum creatinine levels cyclosporine doses (p > 0.05), however trough cyclosporine levels were significantly lower in the amyloidotics than the controls (p = 0.04). Serum creatine phosphokinase was comparable in both groups (p = 0.59). The amyloid patients showed significantly increased polyphasic motor unit potentials and abnormal interference patterns in the biceps brachii muscle (p = 0.03) and the abductor polices brevis muscle (p = 0.05). Multivariate analysis showed a significant level for biceps myopathy in amyloidotics (p = 0.001). Both groups attained no difference with regard to median nerve conduction velocity. Conclusion: Electrophysiologically evidenced neuromyopathy is more liable to occur in long-term live donor FMF amyloidotic kidney transplant recipients than in the other non-amyloidotic kidney transplant recipients even with no clinical manifestations or high creatine phosphokinase levels.