<p>The kidney contains a heterogeneous endothelial cell population, with each subset serving distinct roles in the maintenance of tissue homeostasis and support of kidney function. This diverse cellular population comprises three broad subsets: vascular, glomerular and lymphatic endothelia. The vascular endothelium, which in this context refers to all vascular endothelial cells apart from those in the glomeruli and lymph vessels, supports parenchymal cells by delivering oxygen and nutrients, removing metabolic waste and facilitating tubular secretion and reabsorption processes. Although similar, the glomerular endothelium is a highly specialized capillary system designed to maintain the glomerular filtration barrier by selectively permitting the passage of water and electrolytes into the tubular filtrate while preventing the passage of cells and large solutes. The lymphatic endothelium aids the reabsorption of extracellular fluid and trafficking of immune cells out of the kidney to draining lymph nodes. These kidney endothelial populations undergo marked changes following kidney injury, involving the increased production of inflammatory cytokines, reduced expression of angiogenic and vasodilatory molecules and loss of the glycocalyx, which can result in endothelial dysfunction, capillary rarefaction and impaired barrier function, and can influence outcomes towards recovery or progressive damage. Improved understanding and an ability to therapeutically target the kidney endothelium after injury may lead to improved care and outcomes in kidney disease.</p>