Publisher: American Society of Nephrology   (Total: 2 journals)   [Sort by number of followers]

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Clinical J. of the American Society of Nephrology     Full-text available via subscription   (Followers: 24, SJR: 3.099, CiteScore: 5)
J. of the American Society of Nephrology     Full-text available via subscription   (Followers: 38, SJR: 4.819, CiteScore: 7)
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Journal of the American Society of Nephrology
Journal Prestige (SJR): 4.819
Citation Impact (citeScore): 7
Number of Followers: 38  
 
  Full-text available via subscription Subscription journal
ISSN (Print) 1046-6673 - ISSN (Online) 1533-3450
Published by American Society of Nephrology Homepage  [2 journals]
  • This Month's Highlights

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      PubDate: 2022-04-29T10:00:31-07:00
      DOI: 10.1681/ASN.2022030346
      Issue No: Vol. 33, No. 5 (2022)
       
  • Further Evidence for the Mucosal Origin of Pathogenic IgA in IgA
           Nephropathy

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      Authors: Cheung, C. K; Barratt, J.
      Pages: 873 - 875
      PubDate: 2022-04-29T10:00:31-07:00
      DOI: 10.1681/ASN.2022020201
      Issue No: Vol. 33, No. 5 (2022)
       
  • A View on Cathepsin C as a Target for Therapy in AAV

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      Authors: Kain, R; Nackenhorst, M. C.
      Pages: 875 - 878
      PubDate: 2022-04-29T10:00:31-07:00
      DOI: 10.1681/ASN.2022030309
      Issue No: Vol. 33, No. 5 (2022)
       
  • Clonal Hematopoiesis and CKD Progression

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      Authors: Niroula, A; Belizaire, R.
      Pages: 878 - 879
      PubDate: 2022-04-29T10:00:31-07:00
      DOI: 10.1681/ASN.2022030262
      Issue No: Vol. 33, No. 5 (2022)
       
  • Enabling Patient Choice: The "Deciding Not to Decide" Option for Older
           Adults Facing Dialysis Decisions

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      Authors: Saeed, F; Moss, A. H, Duberstein, P. R, Fiscella, K. A.
      Pages: 880 - 882
      PubDate: 2022-04-29T10:00:31-07:00
      DOI: 10.1681/ASN.2021081143
      Issue No: Vol. 33, No. 5 (2022)
       
  • SARS-CoV-2-Specific T Cell Responses Are Not Associated with Protection
           against Reinfection in Hemodialysis Patients

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      Authors: Shankar, S; Beckett, J, Tipton, T, Ogbe, A, Kasanyinga, M, Dold, C, Lumley, S, Dengu, F, Rompianesi, G, Elgilani, F, Longet, S, Deeks, A, Payne, R. P, Duncan, C. J. A, Richter, A, de Silva, T. I, Turtle, L, Bull, K, Barnardo, M, Friend, P. J, Dunachie, S. J, Hester, J, Issa, F, Barnes, E, Carroll, M. W, Klenerman, P.
      Pages: 883 - 887
      PubDate: 2022-04-29T10:00:31-07:00
      DOI: 10.1681/ASN.2021121587
      Issue No: Vol. 33, No. 5 (2022)
       
  • DGAT2 Inhibition Potentiates Lipid Droplet Formation To Reduce
           Cytotoxicity in APOL1 Kidney Risk Variants

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      Authors: Chun, J; Riella, C. V, Chung, H, Shah, S. S, Wang, M, Magraner, J. M, Ribas, G. T, Ribas, H. T, Zhang, J.-Y, Alper, S. L, Friedman, D. J, Pollak, M. R.
      Pages: 889 - 907
      Abstract: BackgroundTwo variants in the gene encoding apolipoprotein L1 (APOL1) that are highly associated with African ancestry are major contributors to the large racial disparity in rates of human kidney disease. We previously demonstrated that recruitment of APOL1 risk variants G1 and G2 from the endoplasmic reticulum to lipid droplets leads to reduced APOL1-mediated cytotoxicity in human podocytes.MethodsWe used CRISPR-Cas9 gene editing of induced pluripotent stem cells to develop human-derived APOL1G0/G0 and APOL1G2/G2 kidney organoids on an isogenic background, and performed bulk RNA sequencing of organoids before and after treatment with IFN-. We examined the number and distribution of lipid droplets in response to treatment with inhibitors of diacylglycerol O-acyltransferases 1 and 2 (DGAT1 and DGAT2) in kidney cells and organoids.ResultsAPOL1 was highly upregulated in response to IFN- in human kidney organoids, with greater increases in organoids of high-risk G1 and G2 genotypes compared with wild-type (G0) organoids. RNA sequencing of organoids revealed that high-risk APOL1G2/G2 organoids exhibited downregulation of a number of genes involved in lipogenesis and lipid droplet biogenesis, as well as upregulation of genes involved in fatty acid oxidation. There were fewer lipid droplets in unstimulated high-risk APOL1G2/G2 kidney organoids than in wild-type APOL1G0/G0 organoids. Whereas DGAT1 inhibition reduced kidney organoid lipid droplet number, DGAT2 inhibition unexpectedly increased organoid lipid droplet number. DGAT2 inhibition promoted the recruitment of APOL1 to lipid droplets, with associated reduction in cytotoxicity.ConclusionsLipogenesis and lipid droplet formation are important modulators of APOL1-associated cytotoxicity. Inhibition of DGAT2 may offer a potential therapeutic strategy to attenuate cytotoxic effects of APOL1 risk variants.
      PubDate: 2022-04-29T10:00:31-07:00
      DOI: 10.1681/ASN.2021050723
      Issue No: Vol. 33, No. 5 (2022)
       
  • Galactose-Deficient IgA1 B cells in the Circulation of IgA Nephropathy
           Patients Carry Preferentially Lambda Light Chains and Mucosal Homing
           Receptors

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      Authors: Zachova, K; Jemelkova, J, Kosztyu, P, Ohyama, Y, Takahashi, K, Zadrazil, J, Orsag, J, Matousovic, K, Galuszkova, D, Petejova, N, Mestecky, J, Raska, M.
      Pages: 908 - 917
      Abstract: BackgroundIgA nephropathy (IgAN) primary glomerulonephritis is characterized by the deposition of circulating immune complexes composed of polymeric IgA1 molecules with altered O-glycans (Gd-IgA1) and anti-glycan antibodies in the kidney mesangium. The mesangial IgA deposits and serum IgA1 contain predominantly light (L) chains, but the nature and origin of such IgA remains enigmatic.MethodsWe analyzed L chain expression in peripheral blood B cells of 30 IgAN patients, 30 healthy controls (HCs), and 18 membranous nephropathy patients selected as disease controls (non-IgAN).ResultsIn comparison to HCs and non-IgAN patients, peripheral blood surface/membrane bound (mb)-Gd-IgA1+ cells from IgAN patients express predominantly L chains. In contrast, total mb-IgA+, mb-IgG+, and mb-IgM+ cells were preferentially positive for kappa () L chains, in all analyzed groups. Although minor in comparison to L chains, L chain subsets of mb-IgG+, mb-IgM+, and mb-IgA+ cells were significantly enriched in IgAN patients in comparison to non-IgAN patients and/or HCs. In contrast to HCs, the peripheral blood of IgAN patients was enriched with + mb-Gd-IgA1+, CCR10+, and CCR9+ cells, which preferentially home to the upper respiratory and digestive tracts. Furthermore, we observed that mb-Gd-IgA1+ cell populations comprise more CD138+ cells and plasmablasts (CD38+) in comparison to total mb-IgA+ cells.ConclusionsPeripheral blood of IgAN patients is enriched with migratory + mb-Gd-IgA1+ B cells, with the potential to home to mucosal sites where Gd-IgA1 could be produced during local respiratory or digestive tract infections.
      PubDate: 2022-04-29T10:00:31-07:00
      DOI: 10.1681/ASN.2021081086
      Issue No: Vol. 33, No. 5 (2022)
       
  • Chimeric Fusion between Clostridium Ramosum IgA Protease and IgG Fc
           Provides Long-Lasting Clearance of IgA Deposits in Mouse Models of IgA
           Nephropathy

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      Authors: Xie, X; Li, J, Liu, P, Wang, M, Gao, L, Wan, F, Lv, J, Zhang, H, Jin, J.
      Pages: 918 - 935
      Abstract: BackgroundIgA nephropathy is a common primary glomerulonephritis caused by mesangial deposition of poly-IgA complexes. The disease follows a variable course of clinical progression, with a high risk of kidney failure. Although no specific therapy is available, enzymatic strategies to clear IgA deposits are being considered for the treatment of rapidly progressive IgA nephropathy.MethodsWe chose an IgA protease of commensal bacterium Clostridium ramosum, termed AK183, as the template for constructing a recombinant biologic. To extend the t1/2 in blood, we fused AK183 to the Fc segment of human IgG1. Activities of this Fc-AK183 fusion protein toward the cleavage and subsequent clearance of IgA were tested in mouse models.ResultsFirst, we discovered an autocleavage activity of AK183 that separates the N-terminal protease from its C-terminal autotransporter β domain. Therefore, we grafted Fc to the N terminus of AK183 and demonstrated its week-long enzymatic activity in mice. In addition, the proteolytic fragments of IgA generated in the reaction with Fc-AK183 were effectively removed from circulation via kidney filtration. The combined actions of Fc-AK183-mediated cleavage and subsequent renal clearance of IgA resulted in a lasting obliteration of blood IgA, as demonstrated in a human IgA-injection model and in a humanized α1KI transgenic model. Fc-AK183 was also able to remove chronic IgA and associated complement C3 deposits in the glomerulus.ConclusionWe constructed a chimeric fusion of IgA protease with Fc and demonstrated its long-lasting efficacy as a promising targeted therapy for IgA nephropathy in mouse models.
      PubDate: 2022-04-29T10:00:31-07:00
      DOI: 10.1681/ASN.2021030372
      Issue No: Vol. 33, No. 5 (2022)
       
  • Targeting Cathepsin C in PR3-ANCA Vasculitis

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      Authors: Jerke, U; Eulenberg-Gustavus, C, Rousselle, A, Nicklin, P, Kreideweiss, S, Grundl, M. A, Eickholz, P, Nickles, K, Schreiber, A, Korkmaz, B, Kettritz, R.
      Pages: 936 - 947
      Abstract: BackgroundThe ANCA autoantigens proteinase 3 (PR3) and myeloperoxidase (MPO) are exclusively expressed by neutrophils and monocytes. ANCA-mediated activation of these cells is the key driver of the vascular injury process in ANCA-associated vasculitis (AAV), and neutrophil serine proteases (NSPs) are disease mediators. Cathepsin C (CatC) from zymogens activates the proteolytic function of NSPs, including PR3. Lack of NSP zymogen activation results in neutrophils with strongly reduced NSP proteins.MethodsTo explore AAV-relevant consequences of blocking NSP zymogen activation by CatC, we used myeloid cells from patients with Papillon-Lefèvre syndrome, a genetic deficiency of CatC, to assess NSPs and NSP-mediated endothelial cell injury. We also examined pharmacologic CatC inhibition in neutrophil-differentiated human hematopoietic stem cells, primary human umbilical vein cells, and primary glomerular microvascular endothelial cells.ResultsPatients with Papillon-Lefèvre syndrome showed strongly reduced NSPs in neutrophils and monocytes. Neutrophils from these patients produced a negative PR3-ANCA test, presented less PR3 on the surface of viable and apoptotic cells, and caused significantly less damage in human umbilical vein cells. These findings were recapitulated in human stem cells, in which a highly specific CatC inhibitor, but not prednisolone, reduced NSPs without affecting neutrophil differentiation, reduced membrane PR3, and diminished neutrophil activation upon PR3-ANCA but not MPO-ANCA stimulation. Compared with healthy controls, neutrophils from patients with Papillon-Lefèvre syndrome transferred less proteolytically active NSPs to glomerular microvascular endothelial cells, the cell type targeted in ANCA-induced necrotizing crescentic glomerulonephritis. Finally, both genetic CatC deficiency and pharmacologic inhibition, but not prednisolone, reduced neutrophil-induced glomerular microvascular endothelial cell damage.ConclusionsThese findings may offer encouragement for clinical studies of adjunctive CatC inhibitor in patients with PR3-AAV.
      PubDate: 2022-04-29T10:00:31-07:00
      DOI: 10.1681/ASN.2021081112
      Issue No: Vol. 33, No. 5 (2022)
       
  • Serum Protein Exposure Activates a Core Regulatory Program Driving Human
           Proximal Tubule Injury

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      Authors: Lidberg, K. A; Muthusamy, S, Adil, M, Mahadeo, A, Yang, J, Patel, R. S, Wang, L, Bammler, T. K, Reichel, J, Yeung, C. K, Himmelfarb, J, Kelly, E. J, Akilesh, S.
      Pages: 949 - 965
      Abstract: BackgroundThe kidneys efficiently filter waste products while retaining serum proteins in the circulation. However, numerous diseases compromise this barrier function, resulting in spillage of serum proteins into the urine (proteinuria). Some studies of glomerular filtration suggest that tubules may be physiologically exposed to nephrotic-range protein levels. Therefore, whether serum components can directly injure the downstream tubular portions of the kidney, which in turn can lead to inflammation and fibrosis, remains controversial.MethodsWe tested the effects of serum protein exposure in human kidney tubule microphysiologic systems and with orthogonal epigenomic approaches since animal models cannot directly assess the effect of serum components on tubules.ResultsSerum, but not its major protein component albumin, induced tubular injury and secretion of proinflammatory cytokines. Epigenomic comparison of serum-injured tubules and intact kidney tissue revealed canonical stress-inducible regulation of injury-induced genes. Concordant transcriptional changes in microdissected tubulointerstitium were also observed in an independent cohort of patients with proteinuric kidney disease.ConclusionsOur results demonstrate a causal role for serum proteins in tubular injury and identify regulatory mechanisms and novel pathways for intervention.
      PubDate: 2022-04-29T10:00:31-07:00
      DOI: 10.1681/ASN.2021060751
      Issue No: Vol. 33, No. 5 (2022)
       
  • Interleukin-33 Exacerbates IgA Glomerulonephritis in Transgenic Mice
           Overexpressing B Cell Activating Factor

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      Authors: Wang, Y. M; Shaw, K, Zhang, G. Y, Chung, E. Y. M, Hu, M, Cao, Q, Wang, Y, Zheng, G, Wu, H, Chadban, S. J, McCarthy, H. J, Harris, D. C. H, Mackay, F, Grey, S. T, Alexander, S. I.
      Pages: 966 - 984
      Abstract: BackgroundThe cytokine IL-33 is an activator of innate lymphoid cells 2 (ILC2s) in innate immunity and allergic inflammation. B cell activating factor (BAFF) plays a central role in B cell proliferation and differentiation, and high levels of this protein cause excess antibody production, including IgA. BAFF-transgenic mice overexpress BAFF and spontaneously develop glomerulonephritis that resembles human IgA nephropathy.MethodsWe administered IL-33 or PBS to wild-type and BAFF-transgenic mice. After treating Rag1-deficient mice with IL-33, with or without anti-CD90.2 to preferentially deplete ILC2s, we isolated splenocytes, which were adoptively transferred into BAFF-transgenic mice.ResultsBAFF-transgenic mice treated with IL-33 developed more severe kidney dysfunction and proteinuria, glomerular sclerosis, tubulointerstitial damage, and glomerular deposition of IgA and C3. Compared with wild-type mice, BAFF-transgenic mice exhibited increases of CD19+ B cells in spleen and kidney and ILC2s in kidney and intestine, which were further increased by administration of IL-33. Administering IL-33 to wild-type mice had no effect on kidney function or histology, nor did it alter the number of ILC2s in spleen, kidney, or intestine. To understand the role of ILC2s, splenocytes were transferred from IL-33–treated Rag1-deficient mice into BAFF-transgenic mice. Glomerulonephritis and IgA deposition were exacerbated by transfer of IL-33–stimulated Rag1-deficient splenocytes, but not by ILC2 (anti-CD90.2)–depleted splenocytes. Wild-type mice infused with IL-33–treated Rag1-deficient splenocytes showed no change in kidney function or ILC2 numbers or distribution.ConclusionsIL-33–expanded ILC2s exacerbated IgA glomerulonephritis in a mouse model. These findings indicate that IL-33 and ILC2s warrant evaluation as possible mediators of human IgA nephropathy.
      PubDate: 2022-04-29T10:00:31-07:00
      DOI: 10.1681/ASN.2021081145
      Issue No: Vol. 33, No. 5 (2022)
       
  • Association of Clonal Hematopoiesis of Indeterminate Potential with Worse
           Kidney Function and Anemia in Two Cohorts of Patients with Advanced
           Chronic Kidney Disease

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      Authors: Vlasschaert, C; McNaughton, A. J. M, Chong, M, Cook, E. K, Hopman, W, Kestenbaum, B, Robinson-Cohen, C, Garland, J, Moran, S. M, Pare, G, Clase, C. M, Tang, M, Levin, A, Holden, R, Rauh, M. J, Lanktree, M. B.
      Pages: 985 - 995
      Abstract: BackgroundClonal hematopoiesis of indeterminate potential (CHIP) is an inflammatory premalignant disorder resulting from acquired genetic mutations in hematopoietic stem cells. This condition is common in aging populations and associated with cardiovascular morbidity and overall mortality, but its role in CKD is unknown.MethodsWe performed targeted sequencing to detect CHIP mutations in two independent cohorts of 87 and 85 adults with an eGFR
      PubDate: 2022-04-29T10:00:31-07:00
      DOI: 10.1681/ASN.2021060774
      Issue No: Vol. 33, No. 5 (2022)
       
  • Longitudinal TNFR1 and TNFR2 and Kidney Outcomes: Results from AASK and VA
           NEPHRON-D

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      Authors: Chen, T. K; Coca, S. G, Estrella, M. M, Appel, L. J, Coresh, J, Thiessen Philbrook, H, Obeid, W, Fried, L. F, Heerspink, H. J. L, Ix, J. H, Shlipak, M. G, Kimmel, P. L, Parikh, C. R, Grams, M. E, on behalf of the CKD Biomarkers Consortium (BioCon), CKD Biomarkers Consortium (BioCon), Ramachandran, Massaro, Clish, Schelling, Denburg, Furth, Warady, Bonventre, Waikar, McMahon, Sabbisetti, Coresh, Grams, Rebholz, Abraham, Tin, Parikh, Klein, Coca, Ferket, Nadkarni, Rhee, Kimmel, Gossett, Rovin, Shlipak, Sarnak, Levey, Inker, Foster, Gutierrez, Ix, Dubin, Seegmiller, Hostetter, Deo, Feldman, Anderson, Mifflin, Xie, Shou, Ballard, Whitehead, Collins, Greenberg, Ganz
      Pages: 996 - 1010
      Abstract: BackgroundHigher baseline levels of soluble TNF receptors (TNFR1 and TNFR2) have been associated with progressive CKD. Whether longitudinal changes in these biomarkers of inflammation are also associated with worse kidney outcomes has been less studied.MethodsWe evaluated associations of longitudinal changes in TNFR1 and TNFR2 with ESKD in the African American Study of Kidney Disease and Hypertension (AASK; 38% female; 0% diabetes) and kidney function decline (first occurrence of ≥30 ml/min per 1.73 m2 or ≥50% eGFR decline if randomization eGFR ≥60 or
      PubDate: 2022-04-29T10:00:31-07:00
      DOI: 10.1681/ASN.2021060735
      Issue No: Vol. 33, No. 5 (2022)
       
  • Interventions To Attenuate Vascular Calcification Progression in Chronic
           Kidney Disease: A Systematic Review of Clinical Trials

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      Authors: Xu, C; Smith, E. R, Tiong, M. K, Ruderman, I, Toussaint, N. D.
      Pages: 1011 - 1032
      Abstract: BackgroundVascular calcification is associated with cardiovascular morbidity and mortality in people with CKD. Evidence-based interventions that may attenuate its progression in CKD remain uncertain.MethodsWe conducted a systematic review of prospective clinical trials of interventions to attenuate vascular calcification in people with CKD, compared with placebo, another comparator, or standard of care. We included prospective clinical trials (randomized and nonrandomized) involving participants with stage 3–5D CKD or kidney transplant recipients; the outcome was vascular calcification measured using radiologic methods. Quality of evidence was determined by the Cochrane risk of bias assessment tool and the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) method.ResultsThere were 77 trials (63 randomized) involving 6898 participants eligible for inclusion (median sample size, 50; median duration, 12 months); 58 involved participants on dialysis, 15 involved individuals with nondialysis CKD, and 4 involved kidney transplant recipients. Risk of bias was moderate over all. Trials involving magnesium and sodium thiosulfate consistently showed attenuation of vascular calcification. Trials involving intestinal phosphate binders, alterations in dialysate calcium concentration, vitamin K therapy, calcimimetics, and antiresorptive agents had conflicting or inconclusive outcomes. Trials involving vitamin D therapy and HMG-CoA reductase inhibitors did not demonstrate attenuation of vascular calcification. Mixed results were reported for single studies of exercise, vitamin E–coated or high-flux hemodialysis membranes, interdialytic sodium bicarbonate, SNF472, spironolactone, sotatercept, nicotinamide, and oral activated charcoal.ConclusionsCurrently, there are insufficient or conflicting data regarding interventions evaluated in clinical trials for mitigation of vascular calcification in people with CKD. Therapy involving magnesium or sodium thiosulfate appears most promising, but evaluable studies were small and of short duration.
      PubDate: 2022-04-29T10:00:31-07:00
      DOI: 10.1681/ASN.2021101327
      Issue No: Vol. 33, No. 5 (2022)
       
  • Hematopoietic Stem Cell Transplant-Membranous Nephropathy Is Associated
           with Protocadherin FAT1

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      Authors: Sethi, S; Madden, B, Casal Moura, M, Nasr, S. H, Klomjit, N, Gross, L, Negron, V, Charlesworth, M. C, Alexander, M. P, Leung, N, Specks, U, Fervenza, F. C, Haas, M.
      Pages: 1033 - 1044
      Abstract: BackgroundMembranous nephropathy (MN) is a common cause of proteinuria in patients receiving a hematopoietic stem cell transplant (HSCT). The target antigen in HSCT-associated MN is unknown.MethodsWe performed laser microdissection and tandem mass spectrometry (MS/MS) of glomeruli from 250 patients with PLA2R-negative MN to detect novel antigens in MN. This was followed by immunohistochemical (IHC)/immunofluorescence (IF) microscopy studies to localize the novel antigen. Western blot analyses using serum and IgG eluted from frozen biopsy specimen to detect binding of IgG to new 'antigen'.ResultsMS/MS detected a novel protein, protocadherin FAT1 (FAT1), in nine patients with PLA2R-negative MN. In all nine patients, MN developed after allogeneic HSCT (Mayo Clinic discovery cohort). Next, we performed MS/MS in five patients known to have allogeneic HSCT-associated MN (Cedar Sinai validation cohort). FAT1 was detected in all five patients by MS/MS. The total spectral counts for FAT1 ranged from 8 to 39 (mean±SD, 20.9±10.1). All 14 patients were negative for known antigens of MN, including PLA2R, THSD7A, NELL1, PCDH7, NCAM1, SEMA3B, and HTRA1. Kidney biopsy specimens showed IgG (2 to 3+) with mild C3 (0 to 1+) along the GBM; IgG4 was the dominant IgG subclass. IHC after protease digestion and confocal IF confirmed granular FAT1 deposits along the GBM. Lastly, Western blot analyses detected anti-FAT1 IgG and IgG4 in the eluate obtained from pooled frozen kidney biopsy tissue and in the serum of those with FAT1-asssociated MN, but not from those with PLA2R-associated MN.ConclusionsFAT1-associated MN appears to be a unique type of MN associated with HSCT. FAT1-associated MN represents a majority of MN associated with HSCT.
      PubDate: 2022-04-29T10:00:31-07:00
      DOI: 10.1681/ASN.2021111488
      Issue No: Vol. 33, No. 5 (2022)
       
  • More Research is Still Needed To Support The Real-world Generalizability
           of The Benefits of Lifestyle Interventions for CKD

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      Authors: Huang, L; Zhang, F.
      Pages: 1045 - 1045
      PubDate: 2022-04-29T10:00:31-07:00
      DOI: 10.1681/ASN.2022020172
      Issue No: Vol. 33, No. 5 (2022)
       
  • Authors Reply: More Research is Still Needed to Support the Real-World
           Generalizability of the Benefits of Lifestyle Interventions for Chronic
           Kidney Disease

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      Authors: Beetham, K. S; Coombes, J. S, Howden, E. J.
      Pages: 1045 - 1046
      PubDate: 2022-04-29T10:00:31-07:00
      DOI: 10.1681/ASN.2022030244
      Issue No: Vol. 33, No. 5 (2022)
       
  • The Subcellular Localization of RRAGD

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      Authors: Ma, T; Zhang, L, Chen, L.
      Pages: 1046 - 1048
      PubDate: 2022-04-29T10:00:31-07:00
      DOI: 10.1681/ASN.2022010006
      Issue No: Vol. 33, No. 5 (2022)
       
  • Authors Reply: The Subcellular Localization of RRAGD

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      Authors: Schlingmann, K. P; Jouret, F, Knoers, N. V. A. M, de Baaij, J. H. F.
      Pages: 1048 - 1049
      PubDate: 2022-04-29T10:00:31-07:00
      DOI: 10.1681/ASN.2022030252
      Issue No: Vol. 33, No. 5 (2022)
       
  • Correction: Mycophenolate Mofetil after Rituximab for Childhood-Onset
           Complicated Frequently-Relapsing or Steroid-Dependent Nephrotic Syndrome

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      Pages: 1050 - 1050
      PubDate: 2022-04-29T10:00:31-07:00
      DOI: 10.1681/ASN.2022020134
      Issue No: Vol. 33, No. 5 (2022)
       
 
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