Figure 1. The renal injury of preeclampsia is likely mediated by circulating anti-angiogenic factors sFlt-1 and soluble endoglin, inflammatory cytokines such as IL-6 and TNFα, reactive oxygen species, elevated circulating ET-1, and agonistic antibodies to the angiotensin II type 1 receptor (AT₁-AA).

This injury is characterized by significant damage and degradation of the vascular networks within the glomeruli leading to glomerular endotheliosis, podocyte injury or loss, and vasospasm of the renal microvasculature [increased RRI, PI, and RIVI, and shorter pulse transit time (PTT)], leading to the relative decreases in renal plasma flow and GFR and increased concentration and molecular weight of proteins in the urine compared with physiological pregnancy. Image of glomerular endotheliosis adapted from Stillman and Karumanchi [16] with permission.