SHI YIQIN, TSUBOI NAOTAKE, FURUHASHI KAZUHIRO, MARUYAMA SHOICHI, MATSUO SEIICHI Internal Medicine, Nephrology, Nagoya University Graduate School of Medicine Introduction: Mac-1 (CD11b/CD18), a leukocyte adhesion molecule, expressed on neutrophils, eosinophils and macrophages has been shown to mediate several adhesion-dependent processes. Recently, an association of genetic variations in Mac-1
with susceptibility to SLE has been reported in several studies. Methods: To determine the underlying mechanism of how Mac-1 participates in SLE, we introduced pristine (TMPD) to induce pulmonary hemorrhage and experimental lupus nephritis in Mac-1−/− mice on C57BL/6 background. Organ damage was histologically analyzed and flow cytometric analysis and ELISA were performed for the evaluation of leukocyte infiltration and cytokine concentration in inflamed sites including the peritoneal
cavity, lung and kidney. Results: Mac-1−/− AUY-922 purchase mice had reduced prevalence of pulmonary hemorrhage compared to wild-type (WT) mice within 1 month after TMPD injection, but after 4 months demonstrated severe proteinuria that was significantly higher than WT mice. In Mac-1−/− mice, lupus nephritis was evident with glomerular hypercellularity and leukocyte infiltration associated with glomerular IC deposition. The analysis of the peritoneal lavage on day 5 and 10 after pristine treatment revealed an Midostaurin datasheet increase in eosinophils and immune regulatory (M2) macrophages but lower numbers of neutrophils and classic (M1) macrophages in Mac-1−/− mice compared to WT. Higher expression of IL-4 and IL-13, both key mediators of macrophage polarization toward M2 macrophages, was observed in the peritoneal cavity of Mac-1−/− mice. Conclusion: Mac-1 promotes acute inflammatory immune responses that lead to pulmonary hemorrhage but downregulates chronic immune responses to protect mice from IC-mediated renal injury in a model of experimental lupus nephritis induced by TMPD. KUO LI-CHUEH1, HWANG JYH-CHANG2, CHENG BEN-CHUNG1, SU many YU-JEN1, CHEN JIN-BOR1 1Division of Nephrology, Kaohsiung Chang Gung Memorial Hospital and Chang
Gung University College of Medicine, Kaohsiung; 2Division of Nephrology, Chi-Mei Medical Center, Tainan, Taiwan Introduction: Hyperphosphatemia and residual renal function (RRF) had been demonstrated to linkage with prognosis in continuous ambulatory peritoneal dialysis (CAPD) patients. Present study was conducted to investigate whether hyperphosphatemia is a risk factor to accelerate decline in renal function. Methods: A total of 181 incident CAPD patients were enrolled, mean age 45 ± 15 year-old, male 40%, diabetes 13%. We defined rapid residual renal function downhill (RRFD) rate with a slope of trend equation based on the first three data of renal weekly creatinine clearance rate measured after initiation CAPD therapy. The data of hemogram, biochemistry were collected for comparison.