Progressive renal diseases are characterized by tubulointerstitial inflammatory cell recruitment, tubular atrophy and fibrosis. Various aspects of the recruitment of leukocytes have been extensively studied, but the exit routes (i.e. the lymphatic vessels and their biology) have only recently found attention. Similar to the recruitment of inflammatory cells, the exit is coordinated by an orchestrated interaction of chemotactic cytokines and adhesion molecules. During inflammatory injury, new routes are created by the de novo formation of lymphatic vessels, i.e. neolymphangiogenesis. These newly formed lymphatic vessels help to cope with the increase in interstitial fluid related to inflammation. Here, we review some aspects of lymphatic biology and the current knowledge about lymphatic vessels in renal inflammation.