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9. Genome-wide association analyses define pathogenic signaling pathways and prioritize drug targets for IgA nephropathy

Author

Kiryluk, Krzysztof, Sanchez-Rodriguez, Elena, Zhou, Xu-Jie, Zanoni, Francesca, Liu, Lili, Mladkova, Nikol, Khan, Atlas, Marasa, Maddalena, Zhang, Jun Y., Balderes, Olivia, Sanna-Cherchi, Simone, Bomback, Andrew S., Canetta, Pietro A., Appel, Gerald B., Radhakrishnan, Jai, Trimarchi, Hernan, Sprangers, Ben, Cattran, Daniel C., Reich, Heather, Pei, York, Ravani, Pietro, Galesic, Kresimir, Maixnerova, Dita, Tesar, Vladimir, Stengel, Benedicte, Metzger, Marie, Canaud, Guillaume, Maillard, Nicolas, Berthoux, Francois, Berthelot, Laureline, Pillebout, Evangeline, Monteiro, Renato, Nelson, Raoul, Wyatt, Robert J., Smoyer, William, Mahan, John, Samhar, Al-Akash, Hidalgo, Guillermo, Quiroga, Alejandro, Weng, Patricia, Sreedharan, Raji, Selewski, David, Davis, Keefe, Kallash, Mahmoud, Vasylyeva, Tetyana L., Rheault, Michelle, Chishti, Aftab, Ranch, Daniel, Wenderfer, Scott E., Samsonov, Dmitry, Claes, Donna J., Akchurin, Oleh, Goumenos, Dimitrios, Stangou, Maria, Nagy, Judit, Kovacs, Tibor, Fiaccadori, Enrico, Amoroso, Antonio, Barlassina, Cristina, Cusi, Daniele, Del Vecchio, Lucia, Battaglia, Giovanni Giorgio, Bodria, Monica, Boer, Emanuela, Bono, Luisa, Boscutti, Giuliano, Caridi, Gianluca, Lugani, Francesca, Ghiggeri, GianMarco, Coppo, Rosanna, Peruzzi, Licia, Esposito, Vittoria, Esposito, Ciro, Feriozzi, Sandro, Polci, Rosaria, Frasca, Giovanni, Galliani, Marco, Garozzo, Maurizio, Mitrotti, Adele, Gesualdo, Loreto, Granata, Simona, Zaza, Gianluigi, Londrino, Francesco, Magistroni, Riccardo, Pisani, Isabella, Magnano, Andrea, Marcantoni, Carmelita, Messa, Piergiorgio, Mignani, Renzo, Pani, Antonello, Ponticelli, Claudio, Roccatello, Dario, Salvadori, Maurizio, Salvi, Erica, Santoro, Domenico, Gembillo, Guido, Savoldi, Silvana, Spotti, Donatella, Zamboli, Pasquale, Izzi, Claudia, Alberici, Federico, Delbarba, Elisa, Florczak, Michał, Krata, Natalia, Mucha, Krzysztof, Pączek, Leszek, Niemczyk, Stanisław, Moszczuk, Barbara, Pańczyk-Tomaszewska, Malgorzata, Mizerska-Wasiak, Malgorzata, Perkowska-Ptasińska, Agnieszka, Bączkowska, Teresa, Durlik, Magdalena, Pawlaczyk, Krzysztof, Sikora, Przemyslaw, Zaniew, Marcin, Kaminska, Dorota, Krajewska, Magdalena, Kuzmiuk-Glembin, Izabella, Heleniak, Zbigniew, Bullo-Piontecka, Barbara, Liberek, Tomasz, Dębska-Slizien, Alicja, Hryszko, Tomasz, Materna-Kiryluk, Anna, Miklaszewska, Monika, Szczepańska, Maria, Dyga, Katarzyna, Machura, Edyta, Siniewicz-Luzeńczyk, Katarzyna, Pawlak-Bratkowska, Monika, Tkaczyk, Marcin, Runowski, Dariusz, Kwella, Norbert, Drożdż, Dorota, Habura, Ireneusz, Kronenberg, Florian, Prikhodina, Larisa, van Heel, David, Fontaine, Bertrand, Cotsapas, Chris, Wijmenga, Cisca, Franke, Andre, Annese, Vito, Gregersen, Peter K., Parameswaran, Sreeja, Weirauch, Matthew, Kottyan, Leah, Harley, John B., Suzuki, Hitoshi, Narita, Ichiei, Goto, Shin, Lee, Hajeong, Kim, Dong Ki, Kim, Yon Su, Park, Jin-Ho, Cho, BeLong, Choi, Murim, Van Wijk, Ans, Huerta, Ana, Ars, Elisabet, Ballarin, Jose, Lundberg, Sigrid, Vogt, Bruno, Mani, Laila-Yasmin, Caliskan, Yasar, Barratt, Jonathan, Abeygunaratne, Thilini, Kalra, Philip A., Gale, Daniel P., Panzer, Ulf, Rauen, Thomas, Floege, Jürgen, Schlosser, Pascal, Ekici, Arif B., Eckardt, Kai-Uwe, Chen, Nan, Xie, Jingyuan, Lifton, Richard P., Loos, Ruth J. F., Kenny, Eimear E., Ionita-Laza, Iuliana, Köttgen, Anna, Julian, Bruce A., Novak, Jan, Scolari, Francesco, Zhang, Hong, and Gharavi, Ali G.

Published
2023
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16. Genome-Wide Association Study in Acute Tubulointerstitial Nephritis

Author

Zhou, Xu-Jie, Su, Tao, Xie, Jingyuan, Xie, Qiong-Hong, Wang, Li-Zhong, Hu, Yong, Chen, Gang, Jia, Yan, Huang, Jun-Wen, Li, Gui, Liu, Yang, Yu, Xiao-Juan, Nath, Swapan K., Tsoi, Lam C., Patrick, Matthew T., Berthier, Celine C., Liu, Gang, Wang, Su-Xia, Xu, Huji, Chen, Nan, Hao, Chuan-Ming, Zhang, Hong, and Yang, Li

Published
2023
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20. Contributors

Author

Ahmad, Rizwan, primary, Ahsan, Haseeb, additional, Álvaro-Benito, Miguel, additional, Amezcua-Guerra, Luis M., additional, Awasthi, Amit, additional, Brunetta, Enrico, additional, Cook, Matthew C., additional, Costantini, Claudio, additional, Daadaa, Syrine, additional, Dalal, Rajdeep, additional, Elfishawi, Mohanad, additional, Elfishawi, Sally, additional, Folci, Marco, additional, Gan, Ting, additional, Hasan, Mohammad Yusuf, additional, Ito, Tatsuo, additional, James, Eddie A, additional, Jorgensen, Trine N., additional, Kechida, Melek, additional, Keller, Emma J., additional, Kumagai-Takei, Naoko, additional, Kumar, Vijay, additional, Kusaka, Masayasu, additional, Lee, Suni, additional, Lin, Aifen, additional, Mora-Ramírez, Mauricio, additional, Nishimura, Yasumitsu, additional, Otsuki, Takemi, additional, Patel, Neeva B., additional, Pucino, Valentina, additional, Ramponi, Giacomo, additional, Rezaei, Nima, additional, Sada, Nagisa, additional, Sadhu, Srikanth, additional, Shimizu, Yurika, additional, Srinivas, Bandaru, additional, Urakami, Kozo, additional, Valdes, Adrian Zelada, additional, Xu, Hui-Hui, additional, Yamamoto, Shoko, additional, Yan, Wei-Hua, additional, Yazdanpanah, Niloufar, additional, and Zhou, Xu-jie, additional

Published
2022
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23. Uromodulin and progression of IgA nephropathy.

Author

Chen, Zijin, Xu, Lin-lin, Du, Wen, Ouyang, Yan, Gu, Xiangchen, Fang, Zhengying, Yu, Xialian, Li, Junru, Xie, Lin, Jin, Yuanmeng, Ma, Jun, Wang, Zhaohui, Pan, Xiaoxia, Zhang, Wen, Ren, Hong, Wang, Weiming, Chen, Xiaonong, Zhou, Xu-jie, Zhang, Hong, and Chen, Nan

Subjects
GENOME-wide association studies, CHRONIC kidney failure, SINGLE nucleotide polymorphisms, UROMODULIN, GENETIC variation
Abstract

Background This study investigates the link between genetic variants associated with kidney function and immunoglobulin A (IgA) nephropathy (IgAN) progression. Methods We recruited 961 biopsy-proven IgAN patients and 651 non-IgAN end-stage renal disease (ESRD) patients from Ruijin Hospital. Clinical and renal pathological data were collected. The primary outcome was the time to ESRD. A healthy population was defined as estimated glomerular filtration rate >60 mL/min/1.73 m2 without albuminuria or hematuria. Fifteen single-nucleotide polymorphisms (SNPs) were selected from a genome-wide association study of kidney function and genotyped by the SNaPshot. Immunohistochemistry in renal tissue and ELISA in urine samples were performed to explore the potential functions of genetic variations. Results The rs77924615-G was independently associated with an increased risk for ESRD in IgAN patients after adjustments for clinical and pathologic indices, and treatment (adjusted hazard ratio 2.10; 95% confidence interval 1.14–3.88). No significant differences in ESRD-free survival time were found among different genotypes in non-IgAN ESRD patients (log-rank, P = .480). Moreover, rs77924615 exhibited allele-specific enhancer activity by dual-luciferase reporter assay. Accordingly, the urinary uromodulin–creatinine ratio (uUCR) was significantly higher in healthy individuals with rs77924615 AG or GG than in individuals with AA. Furthermore, uromodulin expression in tubular epithelial cells was higher in patients with rs77924615 AG or GG. Finally, we confirmed that an increased uUCR (P = .009) was associated with faster IgAN progression. Conclusion The SNP rs77924615, which modulates the enhancer activity of the UMOD gene, is associated with renal function deterioration in IgAN patients by increasing uromodulin levels in both the renal tubular epithelium and urine. [ABSTRACT FROM AUTHOR]

Published
2024
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30. The genetics and epidemiology ofN-andO-IgA glycomics

Author

Visconti, Alessia, primary, Rossi, Niccolò, additional, Bondt, Albert, additional, Hipgrave Ederveen, Agnes, additional, Thareja, Gaurav, additional, Koeleman, Carolien A. M., additional, Stephan, Nisha, additional, Halama, Anna, additional, Lomax-Browne, Hannah J., additional, Pickering, Matthew C., additional, Zhou, Xu-jie, additional, Wuhrer, Manfred, additional, Suhre, Karsten, additional, and Falchi, Mario, additional

Published
2024
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33. An autoimmune disease variant of IgG1 modulates B cell activation and differentiation

Author

Chen, Xiangjun, Sun, Xiaolin, Yang, Wei, Yang, Bing, Zhao, Xiaozhen, Chen, Shuting, He, Lili, Chen, Hui, Yang, Changmei, Xiao, Le, Chang, Zai, Guo, Jianping, He, Jing, Zhang, Fuping, Zheng, Fang, Hu, Zhibin, Yang, Zhiyong, Lou, Jizhong, Zheng, Wenjie, Qi, Hai, Xu, Chenqi, Zhang, Hong, Shan, Hongying, Zhou, Xu-jie, Wang, Qingwen, Shi, Yi, Lai, Luhua, Li, Zhanguo, and Liu, Wanli

Published
2018

36. Interleukin 4-driven reversal of self-reactive B cell anergy contributes to the pathogenesis of systemic lupus erythematosus

Author

Liu, Yaoyang, primary, Zhang, Zhiguo, additional, Kang, Zijian, additional, Zhou, Xu-jie, additional, Liu, Shujun, additional, Guo, Shicheng, additional, Jin, Qianmei, additional, Li, Ting, additional, Zhou, Ling, additional, Wu, Xin, additional, Wang, Yan-na, additional, Lu, Liangjing, additional, He, Yanran, additional, Li, Fubin, additional, Zhang, Hong, additional, Liu, Yuncai, additional, and Xu, Huji, additional

Published
2023
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37. Machine learning in predicting T-score in the Oxford classification system of IgA nephropathy

Author

Xu, Lin-Lin, primary, Zhang, Di, additional, Weng, Hao-Yi, additional, Wang, Li-Zhong, additional, Chen, Ruo-Yan, additional, Chen, Gang, additional, Shi, Su-Fang, additional, Liu, Li-Jun, additional, Zhong, Xu-Hui, additional, Hong, Shen-Da, additional, Duan, Li-Xin, additional, Lv, Ji-Cheng, additional, Zhou, Xu-Jie, additional, and Zhang, Hong, additional

Published
2023
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45. Combined Genetic Association and Differed Expression Analysis of UBE2L3Uncovers a Genetic Regulatory Role of (Immuno)proteasome in IgA Nephropathy

Author

Xu, Lin-Lin, Gan, Ting, Li, Yang, Chen, Pei, Shi, Su-Fang, Liu, Li-Jun, Lv, Ji-Cheng, Zhang, Hong, and Zhou, Xu-Jie

Abstract

Introduction:IgA nephropathy (IgAN) is a leading cause of end-stage renal disease. The exact pathogenesis of IgAN is not well defined, but some genetic studies have led to a novel discovery that the (immuno)proteasome probably plays an important role in IgAN. Methods:We firstly analyzed the association of variants in the UBE2L3region with susceptibility to IgAN in 3,495 patients and 9,101 controls, and then analyzed the association between lead variant and clinical phenotypes in 1,803 patients with regular follow-up data. The blood mRNA levels of members of the ubiquitin-proteasome system including UBE2L3were analyzed in peripheral blood mononuclear cells from 53 patients and 28 healthy controls. The associations between UBE2L3and the expression levels of genes involved in Gd-IgA1 production were also explored. Results:The rs131654 showed the most significant association signal in UBE2L3region (OR: 1.10, 95% CI: 1.04–1.16, p= 2.29 × 10−3), whose genotypes were also associated with the levels of Gd-IgA1 (p= 0.04). The rs131654 was observed to exert cis-eQTL effects on UBE2L3in various tissues and cell types, particularly in immune cell types in multiple databases. The UBE2L3, LUBAC, and proteasome subunits were highly expressed in patients compared with healthy controls. High expression levels of UBE2L3were not only associated with higher proteinuria (r= 0.34, p= 0.01) and lower eGFR (r= −0.28, p= 0.04), but also positively correlated with the gene expression of LUBACand other proteasome subunits. Additionally, mRNA expression levels of UBE2L3were also positively correlated with IL-6 and RELA, but negatively correlated with the expression levels of the key enzyme in the process of glycosylation including C1GALT1and C1GALT1C1. Conclusion:In conclusion, by combined genetic association and differed expression analysis of UBE2L3, our data support a role of genetically conferred dysregulation of the (immuno)proteasome in regulating galactose-deficient IgA1 in the development of IgAN.

Published
2024
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48. An Update on the Genetics of IgA Nephropathy.

Author

Xu, Lin-Lin, Zhou, Xu-Jie, and Zhang, Hong

Subjects
*IGA glomerulonephritis, *GENETICS, *GENOME-wide association studies, *CHRONIC kidney failure, *NUCLEOTIDE sequencing, *PHENOTYPIC plasticity
Abstract

Immunoglobulin A (IgA) nephropathy (IgAN), the most common form of glomerulonephritis, is one of the leading causes of end-stage kidney disease (ESKD). It is widely believed that genetic factors play a significant role in the development of IgAN. Previous studies of IgAN have provided important insights to unravel the genetic architecture of IgAN and its potential pathogenic mechanisms. The genome-wide association studies (GWASs) together have identified over 30 risk loci for IgAN, which emphasizes the importance of IgA production and regulation in the pathogenesis of IgAN. Follow-up fine-mapping studies help to elucidate the candidate causal variant and the potential pathogenic molecular pathway and provide new potential therapeutic targets. With the rapid development of next-generation sequencing technologies, linkage studies based on whole-genome sequencing (WGS)/whole-exome sequencing (WES) also identify rare variants associated with IgAN, accounting for some of the missing heritability. The complexity of pathogenesis and phenotypic variability may be better understood by integrating genetics, epigenetics, and environment. We have compiled a review summarizing the latest advancements in genetic studies on IgAN. We similarly summarized relevant studies examining the involvement of epigenetics in the pathogenesis of IgAN. Future directions and challenges in this field are also proposed. [ABSTRACT FROM AUTHOR]

Published
2024
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49. Intensive blood pressure control and the progression of IgA nephropathy: a cohort study using marginal structural models.

Author

Tang, Chen, Chen, Pei, Si, Feng-Lei, Yao, Yu-Xuan, Lv, Ji-Cheng, Shi, Su-Fang, Zhou, Xu-Jie, Liu, Li-Jun, and Zhang, Hong

Subjects
STATISTICAL models, IGA glomerulonephritis, BLOOD pressure, SYSTOLIC blood pressure, CHRONIC kidney failure
Abstract

Background In chronic kidney disease, current guidelines recommend systolic blood pressure (SBP) below 120 mmHg. However, the renoprotective effect of intensive blood-pressure (BP) lowering on immunoglobulin A nephropathy (IgAN) remains undetermined. We aimed to determine the effect of intensive BP control on the progression of IgAN. Methods At Peking University First Hospital, 1530 patients with IgAN were enrolled. An examination of the relationship between baseline and time-updated BP and composite kidney outcomes, defined as development of end-stage kidney disease (ESKD) or a 30% decline in estimated glomerular filtration rate (eGFR), was conducted. Baseline and time-updated BPs were modeled using multivariate causal hazards models and marginal structural models (MSMs). Results In a median follow-up of 43.5 (interquartile range 27.2, 72.7) months, 367 (24.0%) patients experienced the composite kidney outcomes. No significant associations were found between baseline BP and the composite outcomes. Using MSMs with time-updated SBP for analysis, a U-shaped association was found. In reference to SBP 110–119 mmHg, hazard ratios (95% confidence intervals) for the SBP categories <110, 120–129, 130–139 and ≥140 mmHg were 1.48 (1.02–2.17), 1.13 (0.80–1.60), 2.21 (1.54–3.16) and 2.91 (1.94–4.35), respectively. The trend was more prominent in patients with proteinuria ≥1 g/day and eGFR ≥60 mL/min/1.73 m2. After analyzing time-updated diastolic BP, no similar trend was observed. Conclusions In patients with IgAN, intensive BP control during the treatment period may retard the kidney disease progression, but the potential risk of hypotension still needs to be considered. [ABSTRACT FROM AUTHOR]

Published
2024
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