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Palabras clave – provistas por la editorial

inflammation; chronic kidney disease; anemia; anemia of inflammation; ESA hyporesponsiveness; renal tubular epithelial cells; macrophages; lipocalin-2; iron; cilastatin; hypoxia inducible factor-1-α; ischemia-reperfusion injury; acute kidney injury; cyclophilin A; fibrosis; renal fibrosis; tubular necrosis; preeclampsia; podocytes; VEGF; FSGS; proteinuria; endocan; ESM-1; renal replacement therapy; kidney transplantation; biomarker; diabetic nephropathy; focal segmental glomerulosclerosis; innate immunity; membranous nephropathy; minimal change diseases; TLR; NOX1; ML171; reactive oxygen species; ERK; T cells; glomerulonephritis; chemokines; renal disease; DJ-1; ND-13; renal inflammation; oxidative stress; UUO; autophagy; apoptosis; trehalose; simvastatin; endotoxin; tubular apoptosis; cytochrome C; Bcl-XL; survivin; hypercholesterolemia; xanthine oxidase; NF-κB pathway; tertiary lymphoid organs; B cells; BAFF; kidney fibrosis; myofibroblast activation; extracellular matrix; Hippo pathway; verteporfin; IgAN; CKD; progression; ACEI; corticosteroids; costimulation; coinhibition; kidney transplant; SPR; protein binding affinity; adaptive immunity; epithelial-to-mesenchymal transition; E. cava extracts; dieckol; spontaneously hypertensive rats; angiotensin II; n/a