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      Protein Restriction Ameliorates Renal Tubulointerstitial Nephritis and Reduces Renal Transforming Growth Factor-Beta Expression in Unilateral Ureteral Obstruction

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          In contrast to the substantial evidence for attenuation of the glomerular lesions by a low-protein (LP) diet, it remains to be determined whether and how such a diet lessens the progression of tubulointerstitial lesions, which show the strongest correlation with renal function. Chronic unilateral ureteral obstruction (UUO) results in interstitial fibrosis of the affected kidney. We investigated the therapeutic effects of an LP diet on the progression of interstitial fibrosis in UUO mice. Sixty ICR mice underwent UUO or sham operation; half of these mice were fed a normal-protein (NP) and the other half a LP diet. They were sacrificed at 3, 7 and 14 days postoperatively. The degree of tubular lesion, the distribution of transforming growth factor-β (TGF-β), α-smooth muscle actin and fibronectin and the activated TGF-β1 level were determined. The LP diet significantly reduced the progression of tubular injury, depositions of fibronectin, tubulointerstitial myofibroblast formation, the interstitial expression of TGF-β-positive cells (at 14 days; NP = 6.91 ± 3.35 vs. LP = 1.67 ± 0.41; p < 0.005), and renal active TGF-β1 concentration (at 14 days; NP = 5.72 ± 2.03 vs. LP = 2.96 ± 0.72; p < 0.01). We conclude that protein restriction may aid the attenuation of progression of tubulointerstitial fibrosis through the reduction in tubulointerstitial expression of TGF-β.

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          Transforming growth factor beta in tissue fibrosis.

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            Mode of hepatitis C infection not associated with blood transfusion among chronic hemodialysis patients.

            In a retrospective study carried out on about 730 patients with chronic renal failure who underwent ambulatory hemodialysis from January 1991 to June 1994, 49 patients were found to have developed acute hepatitis C, as confirmed by seroconversion for anti-HCV antibodies without blood transfusion in the preceding 6-month period. Epidemiological survey disclosed that two patients undergoing dialysis at consoles separated by one console developed acute hepatitis C in October 1992, and another three patients at adjacent consoles also developed acute hepatitis C within 2 weeks in April/May, 1993. It was found that some negligent nurses could have withdrawn needles from these patients one after another without changing gloves at the termination of the dialysis procedure. After reeducation of the staff members and introduction of a new type of adhesive pad to be placed on the needle wounds at the time of needle withdrawal, no new case of acute hepatitis C occurred for more than 1 year, suggesting nosocomial spread of HCV infection among hemodialysis patients in a mode that is preventable with very strict aseptic precautions.
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              Nephrotic Mice (ICGN Strain): A Model of Diffuse Mesangial Sclerosis in Infantile Nephrotic Syndrome

              The ICGN mouse strain is a unique model for naturally occurring nephrotic syndrome. In the present study, we examined the onset of the clinical manifestation of nephrotic syndrome and determined the sequence of intraglomerular events associated with progression of nephrotic conditions. Laboratory analysis revealed that homozygous (nep/nep) mice showed urinary albumin excretion during the suckling stage, rapidly leading to hypoalbuminemia accompanied by body growth failure. Renal pathology demonstrated that an initial intraglomerular event in the nephrotic mice was observed 3 weeks after birth in the form of mesangiolytic lesions, characterized by microaneurysm, platelet accumulation and capillary ballooning. In 6-week-old homozygous mice, mesangial sclerosis, characterized by mesangial expansion and glomerular hypertrophy, was observed in a diffuse fashion. Immunohistochemistry revealed that the glomerular cells in the 3-week-old homozygous suckling mice were positive for α-smooth muscle actin, suggesting a phenotypic change in the mesangial cells. Mesangial expansion, confirmed by the over-deposition of type I collagen, was evident until 6 weeks after weaning, while it was of interest that fibrogenic cytokines such as platelet-derived growth factor and transforming growth factor-β were not detected in the sclerotic glomeruli throughout the observations. Furthermore, the nephrotic features were shown to be resistant to steroid therapy with a high dose of prednisolone. Our results suggest that diffuse mesangial sclerosis, a hereditary glomerular disease, may be genetically generated through early myofibroblast formation, which occurs and develops probably independently of up-regulation of these fibrogenic cytokines. In conclusion, the homozygous nephrotic mouse (ICGN strain) is believed to be a good model for investigating not only nephrotic conditions but also cellular and molecular pathogenesis of diffuse mesangial sclerosis in steroid-resistant infantile nephrotic syndrome.

                Author and article information

                Nephron Exp Nephrol
                Cardiorenal Medicine
                S. Karger AG
                09 January 2002
                : 10
                : 1
                : 7-18
                aInstitute of Experimental Animal Sciences, Osaka University Medical School, Osaka; bDepartment of Veterinary Surgery, Faculty of Agriculture, Gifu University, Gifu; cSawashima Animal Hospital, Hyougo, Japan
                49893 Exp Nephrol 2002;10:7–18
                © 2002 S. Karger AG, Basel

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                Figures: 9, Tables: 1, References: 40, Pages: 12
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