Objective Peritoneal fibrosis (PF) is one of the most serious causes of failure in continuous ambulatory peritoneal dialysis (PD). Although the underlying mechanism responsible for the genesis of PF is still unknown, transforming growth factor p (TGFβ1) has been shown to be associated with PF. Angiotensin converting enzyme inhibitors have been shown to prevent the stimulating effect of growth factors. The aim of the present study was to investigate the effect of enalapril on peritoneal function and morphology in a rat model of experimental PF. Methods Twenty-one albino Wistar rats were divided into three groups: ( 1 ) the control group (C) received 10 mL isotonic saline intraperitoneally (IP), ( 2 ) the dextrose (Dx) group 10 mL 3.86% dextrose PD solution IP, and ( 3 ) the enalapril-treated group (ENA) 10 cc 3.86% dextrose PD solution IP plus 100 mg/L enalapril in drinking water. After 4 weeks, a 1-hour peritoneal equilibration test was performed with 20 mL 2.27% dextrose PD solution. Dialysate-to-plasma urea ratio (D/P urea), glucose reabsorption (D1/D0 glucose), ultrafiltration (UF) volume, and levels of dialysate protein, TGFβ1, and cancer antigen 125 (CA125) were determined. The parietal peritoneum was evaluated histologically by light microscopy. Results Administration of enalapril resulted in preserved UF (-0.2 ± 0.7 mL vs 1.7 ± 0.3 mL, p < 0.05), protein loss (2.3 ± 0.5 g/L vs 1.6 ± 0.2 g/L, p > 0.05), and peritoneal thickness (77 ± 7 μ vs 38 ± 5 μ, p < 0.001). D/P urea increased significantly in the Dx group ( p < 0.05). Both higher levels of TGFβ1 (undetectable vs 298 ± 43 pg/mL, p < 0.001) and lower levels of CA125 in dialysate effluent (0.94 ± 0.5 U/L vs 0.11 ± 0.1 U/L, p > 0.05) were determined in the Dx group. Conclusion These findings show that peritoneal morphology and function tests were dramatically deranged in the Dx group. The same properties were partially preserved in the ENA group. The production of TGFβ1 was significantly reduced but peritoneal thickness was not completely inhibited. In conclusion, by inhibiting the production of TGFβ1, enalapril can preserve peritoneal histology, peritoneal function, and remodeling of mesothelial cells.

Background Peritoneal sclerosis (PS) is one of the most serious causes of failure in long-term peritoneal dialysis. Angiotensin II is known to promote fibrosis and inflammation in various tissues. We previously showed that ACE inhibitors (ACEIs) have beneficial effects on hypertonic PD solutions (3.86% PD) induced peritoneal alterations. The aim of this study is to compare the effects of an ACEI and a receptor blocker on peritoneal alterations induced by hypertonic PD solutions in rats. Methods Forty-three non-uremic rats were divided into four groups: group I (Sham) rats received no treatment (n=11), group II received hypertonic (3.86%, 10 ml/day) PD solution (n=10) and groups III and IV received hypertonic PD solution (10 ml/day) plus 640 mg/L valsartan (n=11) and 100 mg/L lisinopril in drinking water (n=11). After four weeks, a one-hour peritoneal equilibration test (PET) was performed with 3.86% PD solution. Dialysate-to-plasma urea ratio (D/P urea), glucose reabsorption (D1/D0 glucose), ultrafiltration volume (UF), dialysate protein, TGFß1 and VEGF levels were determined. Results Administration of valsartan or lisinopril resulted in preserved UF (8±0.8 and 6.7±0.7 vs 4.9±0.8 mL), D1/D0 glucose (0.69±0.05 and 0.62±0.05 vs 0.56±0.04) and peritoneal thickness (19.4±2.9 and 28.5±5.2 vs 53±3 μm), respectively. Both higher level of TGF ß1 (206±40 vs 474±120 pg/mL, p<0.05), and VEGF in dialysate effluent (4±0.4 vs 7.9±3 pg/mL, p>0.05), was determined in the dextrose group. Both cytokines are partially inhibited by valsartan or lisinopril (p >0.05) Conclusion Exposure to hypertonic glucose solution resulted in alterations in peritoneal transport manifested by a rapid dissipation of the glucose gradient and resultant impaired UF response. Administration of valsartan or lisinopril led to attenuation of these alterations. We suggest that the equal protection of the peritoneal membrane from the effects of hypertonic glucose was achieved by receptor blockers and ACE inhibitors.

The new proposed classification system for non-invasive urothelial neoplasms does not increase the reproducibility. There is still a need for uniformity in grading in order to compare the different studies and therapies and to provide more accurate information for management.

Introduction. Acute kidney injury (AKI) pathogenesis is complex. Findings of gentamicin nephrotoxicity are seen in 30% of the AKI patients. Vitamin D has proven to be effective on renin expression, inflammatory response, oxidative stress, apoptosis, and atherosclerosis. We aimed to investigate the effect of vitamin D in an experimental rat model of gentamicin-induced AKI. Methods. Thirty nonuremic Wistar albino rats were divided into 3 groups: Control group, 1 mL saline intramuscular (im) daily; Genta group, gentamicin 100 mg/kg/day (im); Genta + vitamin D, gentamicin 100 mg/kg/day (im) in addition to 1α, 25 (OH)2D3 0.4 mcg/kg/day subcutaneously for 8 days. Blood pressures and 24-hour urine were measured. Blood urea and creatinine levels and urine tubular injury markers were measured. Renal histology was semiquantitatively assessed. Results. Urea, creatinine and urine neutrophil gelatinase-associated lipocalin, and kidney injury molecule-1 were all increased in Genta group indicating AKI model. Systolic blood pressure decreased, but urine volume and glutathione increased in Genta + Vit D group compared to Control group. Histological scores indicating tubular injury increased in Genta and Genta + Vit D groups. Conclusions. Vitamin D does not seem to be effective on histological findings although it has some beneficial effects via RAS system and a promising effect on antioxidant system.

The role of p53 mutation has been shown in different human malignancies, including various skin cancers. In this study, we examined p53 protein expression in 25 eccrine poromas and 11 porocarcinomas by immunohistochemistry. P53 expression was observed in 88% (22 of 25) of eccrine poromas and 73% (8 of 11) of porocarcinomas. In eccrine poromas, percentage of cells reactive for p53 was less than 5% (low expresser) in 6 cases, 5 to 50% (moderate expresser) in 14 and greater than 50% (high expresser) in 2 cases. In terms of intensity, 13 cases showed weak staining, 8 moderate, and 1 case showed strong reactivity. On the other hand, 2 cases of porocarcinoma were low expresser, 2 were moderate and 4 were high expresser. All of the high expressers had also strong staining. This study has demonstrated that eccrine poromas showed significant p53 expression as much as porocarcinomas and, therefore, p53 positivity cannot be accepted as a valuable parameter for malignancy. P53 gene may involve in the carcinogenetic pathway of porocarcinoma but it is likely that other oncogenes may also have a role.

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Early diagnosis and classification of amyloid deposition and differentiation from other glomerular fibrillar deposits relies on routine Congo red (CR) histochemistry. Congo red fluorescence (CRF) is an alternative method based on examination of the CR-stained section by ultraviolet (UV) light. The aim of this study is to investigate the usefulness of CRF, especially when applied to frozen kidney sections. Congo red fluorescence was applied to sections of frozen kidney biopsies prospectively and to paraffin sections retrospectively. The findings of CRF were compared to CR staining in bright light. Prospectively, 15 cases of amyloidosis were diagnosed on frozen sections and identical CR staining was found in all of the paraffin-stained sections. There were no false positives or negatives. Retrospectively, 146 renal biopsies previously stained with CR were re-evaluated with CRF. Eighty-seven CR positive cases were confirmed by CRF, and one new case was identified. Congo red fluorescence is simple to perform and more pronounced, therefore easier to evaluate than CR in bright light. Congo red, when combined with immunohistochemistry, is still visible under UV whereas CR is masked in bright light. Although not widely used, the CRF method for detecting amyloid is simple to use with a high specificity and sensitivity, and may be applied successfully to frozen sections.

Encapsulating peritoneal sclerosis (EPS) is a clinical syndrome associated with ileus symptoms and irreversible sclerosis of the peritoneal membrane. Inflammation, fibrosis, and neoangiogenesis are the main features of the pathophysiology. No evidence-based therapy is currently available for EPS. In recent years, anti-inflammatory and immunosuppressive (IS) treatment modalities have become more popular. The aim of the present study was to investigate the effects of various IS treatment strategies—glucocorticosteroid (GC), azathiopurine (AZT), and cyclosporin (CsA)—on regression of EPS. We divided 52 nonuremic Wistar albino rats into six groups: Control group—2 mL isotonic saline injected intraperitoneally (IP) daily for 3 weeks; CG group—2 mL/200 g 0.1% chlorhexidine gluconate (CG) and 15% ethanol dissolved in saline injected IP daily for 3 weeks; Resting group—CG (weeks 1 – 3), plus peritoneal rest (weeks 4 – 6); Corticosteroid (GC) group—CG (weeks 1 – 3), plus 10 mg/L prednisolone in drinking water (weeks 4 – 6); AZT group—CG (weeks 1 – 3), plus 100 mg/L azathioprine in drinking water (weeks 4 – 6); and CsA group—CG (weeks 1 – 3), plus cyclosporin 7.5 mg/kg by subcutaneous injection daily (weeks 4 – 6). At the end of the study, under ketamine HCl anesthesia, the rats were humanely killed by bleeding. Parietal peritoneal samples were then taken from same location (away from the injection site) and changes of parietal peritoneum morphology were examined by a single pathologist. The CG severely disturbed parameters of peritoneal morphology, increasing peritoneal thickness, inflammatory activity, vascularity, and fibrosis score as compared with the Control group ( p < 0.05). No benefit was observed for any parameter in the Resting group as compared withthose parameters in the CG group ( p < 0.05). We observed a lower fibrosis score and less peritoneal thickness in the GC group as compared with the Resting group ( p < 0.05). No beneficial effects of AZT on peritoneal morphology were observed as compared with the effects of peritoneal rest or corticosteroid therapy. Treatment with cyclosporin resulted in more fibrosis, vascularity, and inflammation than was seen with corticosteroid therapy ( p < 0.05). Immunosuppressive therapies, especially those that are corticosteroid-based, may have therapeutic value in the management of EPS. Patients treated with cyclosporin may have a risk for developing EPS.