Corrigendum to �Tonelli M, Nkunu V, Varghese C, et al. Framework for establishing integrated kidney care programs in low- and middle-income countries� Kidney Int Suppl. 2020;10:e19�e23 (Kidney International Supplements (2020) 10(1) (e19�e23), (S2157171619300164), (10.1016/j.kisu.2019.11.002))

The authors regret that Bassam Bernieh was inadvertently left out as an author of the article. The authors and affiliations are as follows. The authors would like to apologize for any inconvenience caused. © 2020 International Society of Nephrolog

Biomarkers in Heart Failure: Clinical Insights

Heart failure (HF) is a clinical syndrome caused by structural and/or functional cardiac abnormalities and resulting from impaired cardiac output or an in-crease of intracardiac pressures at rest and/or during stress. Typical signs and symptoms of HF include ankle swelling, fatigue, dyspnea and peripheral edema, pulmonary crackles, or increased jugular venous pressure. Usually, patients with ejection fraction (EF) greater than or equal to 50% are defined as HF with preserved EF, where as those with EF less than 40% have HF with reduced EF. Patients with EF between 40% and 49% are now classified as HF with midrange EF

Kruppel-like factor 2+ CD4 T cells avert microbiota-induced intestinal inflammation

Summary: Intestinal colonization by antigenically foreign microbes necessitates expanded peripheral immune tolerance. Here we show commensal microbiota prime expansion of CD4 T cells unified by the Kruppel-like factor 2 (KLF2) transcriptional regulator and an essential role for KLF2+ CD4 cells in averting microbiota-driven intestinal inflammation. CD4 cells with commensal specificity in secondary lymphoid organs and intestinal tissues are enriched for KLF2 expression, and distinct from FOXP3+ regulatory T cells or other differentiation lineages. Mice with conditional KLF2 deficiency in T cells develop spontaneous rectal prolapse and intestinal inflammation, phenotypes overturned by eliminating microbiota or reconstituting with donor KLF2+ cells. Activated KLF2+ cells selectively produce IL-10, and eliminating IL-10 overrides their suppressive function in vitro and protection against intestinal inflammation in vivo. Together with reduced KLF2+ CD4 cell accumulation in Crohn’s disease, a necessity for the KLF2+ subpopulation of T regulatory type 1 (Tr1) cells in sustaining commensal tolerance is demonstrated