1. Volume 94, Issue 5, Pages 843-845 (November 2018)
Journal Club 
Kidney International 
Volume 94, Issue 5, Pages (November 2018)
DOI: /j.kint
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2. Figure 1
Super-enhancers as chromatin sensors of potential stressors control the identity of renin cells and their molecular memory, and thus their ability to respond to stressors and maintain homeostasis. Chromatin is made accessible at the renin locus, with deposition of H3K27ac, and MED1 establishes the bridge between the renin enhancer and Pol II, and together activate transcription. AC, adenylate cyclase; β-AR, beta adrenergic receptor; CREBP, phosphorylated cAMP responsive element binding protein; Gsα, activating G-protein coupled subunit; PGE2, prostaglandin E2; PKA, protein kinase A. From Martinez MF, Medrano S, Brown EA, et al. Super-enhancers maintain renin-expressing cell identity and memory to preserve multisystem homeostasis [e-pub ahead of print]. J Clin Invest. Accessed September 14, Copyright © 2018 American Society for Clinical Investigation. Reprinted with permission.
Kidney International  , DOI: ( /j.kint )
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3. Figure 2
MIF has direct renoprotective effects on tubular cells in AKI and chronic kidney disease (CKD). In AKI, hypoxia-induced tubular cell death, in particular necroptosis, ferroptosis, and apoptosis, lead to necroinflammation. Treatment with recombinant MIF decreases tubular injury, cell death, and inflammation as well as oxidative stress, whereas interventions neutralizing MIF have the opposite effects (not shown). In CKD, treatment with MIF promotes cell cycle progression and regeneration of tubular cells leading to reduced inflammation and fibrosis.
Kidney International  , DOI: ( /j.kint )
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4. Figure 3
Subdistribution hazard ratios with 95% confidence intervals from fully adjusted proportional hazards models for the primary cardiovascular (CV) outcome (myocardial infarction [MI], stroke, or cardiovascular death) and each of the major components of the composite outcome, showing relative hazards with respect to IgA nephropathy (IgAN). The fully adjusted model was stratified by year of dialysis initiation and adjusted for cause of ESRD, demographic factors (age, sex, race, ethnicity), geographic region, socioeconomic factors, and baseline clinical factors at dialysis initiation (comorbidities, dialysis modality, BMI, laboratory values). ADPKD, autosomal dominant polycystic kidney disease; FSGS, focal segmental glomerulosclerosis; LN, lupus nephritis; MN, membranous nephropathy; MPGN, membranoproliferative GN. From O’Shaughnessy MM, Liu S, Montez-Rath ME, et al. Cause of kidney disease and cardiovascular events in a national cohort of US patients with end-stage renal disease on dialysis: a retrospective analysis [e-pub ahead of print]. Eur Heart J. Accessed August 2, Published on behalf of the European Society of Cardiology. All rights reserved. Copyright © The Author(s) Reprinted with permission.
Kidney International  , DOI: ( /j.kint )
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