Introduction: IgA nephropathy (IgAN) is a heterogeneous disease with highly variable clinical and histopathological features. We investigated the effects of Oxford classification and clinical features on renal survival in patients with IgAN.Methods: This retrospective observational study conducted from 2013 to 2017. Ninety-seven patients who were followed up more than six months were examined.Results: A total of 97 patients (68% male and median age 40 years) were enrolled in this study. 13% of patients developed end stage renal disease (ESRD) within the median of 37 months of follow-up. Need for renal replacement therapy at the time of diagnosis, serum creatinine level of higher than 1.97 mg/dl, serum albumin level less than 3.5 gr/dl, 24-hour urine protein level of higher than>3.5 g/day, the percentage of glomerulosclerosis higher than 53%, T2 score and total MEST-C score higher than two were found to be significant predictors of development of ESRD. None of the clinical or histopathological features were found to be significant predictor of steroid treatment sensitivity except T1-2 scores.Conclusion: We think that IgA nephropathy is a heterogeneous disease that requires clinical and histopathological features to be evaluated together, but not individually, to determine renal survival.

No abstract

Background:Axial spondyloarthritis (axSpA) is a common chronic inflammatory disease of the axial skeleton. Some cytokines have important roles in initiation and progression of disease and are elevated in active disease. Additionally, Wnt signaling pathway inhibitors and noggin also appear to be involved in pathogenesis of ankylosing spondylitis. Anti-tumor necrosis factor-alpha (TNF) agents have dramatically improved the clinical outcome of axSpa; however, acceptable clinical improvement is not achieved in all patients and capacity of anti-TNF to slow or prevent structural damage still remains controversial.Objectives:To evaluate the effect of anti-TNF on inflammatory and noninflammatory milieu in patients with axSpA.Methods:In this prospective study we included 30 biologic treatment naive adult patients with axSpA and 30 healthy controls. All patients with high disease activity were treated with anti-TNF therapy for 6 months. Laboratory and clinical evaluation of all patients were performed at baseline and after 6 months of anti-TNF treatment. Following cytokines and wnt/BMP antagonists were measured; TNF-Alpha, COX-2, IL-6, IL-17, IL-22, IL-23, IL-33, dickkopf-1, sclerostin, noggin.Results:The mean age of patients with axSpA and healthy controls were 38.1±13.3 and 37.7±7.7 years, respectively (p>0.005). At baseline, the median (IQR) TNF-alpha was higher in axSpA patients when compared to healthy controls, 34.4 pg/ml (31.4-37.03) vs 18.1 pg/ml (12.1-28.4), (p<0.001), while the median (IQR) dickkopf-1 and sclerostin were lower in axSpA patients, 446.7 pg/ml (356.9-529.3) vs 1088.7 pg/ml (951.7-1244.4), (p<0.001) and 312.4 pg/ml (140.8-412.7) vs 412.3 pg/ml (295.4-512.8), (p<0.001), respectively. IL-17, IL-22, IL-33, dickkopf-1 and sclerostin increased with anti-TNF treatment (table 1).Conclusion:Elevation of some cytokines which are important in pathogenesis of axSpA and nonincrease in noggin with anti-TNF drugs may affect effectiveness of anti-TNF treatment.Table 1.Changes of cytokines, dickkopf-1, sclerostin and noggin with anti-TNF treatment.Pre-Anti-TNFPost-Anti-TNFP valueIL-645(39.1-68.8)47.6(27.3-61.1)0.750IL-1793.3 (85.1-104.8)102.1(86.6-114.6)0.026IL-22159,2 (151,9-178.4)183.5(156.3-304.6)0.033IL-2336.5 (26.1-52.9)41.3(28.4-55.5)0.658IL-33127.8 (106.6-186.1)147.06(128.5-213.4)0.016COX20.176 (0-0.374)0.202(0.051-1.151)0.469TNFalpha34.4(31.4-37.03)30.7(12.8-35.6)0.004Dickkopf-1446.7(356.9-529.3)881.3(663.1-972.2)<0.001Sclerostin312.4 (140.8-412.7)405.1(276.3-452.5)0.018Noggin48.3(17.04-153.9)31.2(11.3-103.7)0.264Disclosure of Interests:None declared