Abstract.A hypothesis is presented according to which the pathogenesis of pregnancy‐induced hypertension can be attributed to disturbances in renal function caused by the upright posture of the human. In pregnancy, glomerular filtration rate (GFR) and tubular reabsorption, the latter stimulated by aldosterone, are working in high gear. A diminished GFR with continued stimulation of tubular re‐absorption would lead to sodium retention. That situation could result, particularly in the primigravida, from the enlarged uterus of late pregnancy exerting pressure on and interfering with venous return, arterial blood flow to kidneys, and/or ability of ureters to transport urine and maintain low pressure in the kidney pelvis. At an early stage, pre‐eclampsia can be controlled by bed rest, quite likely by removing dangerous uterine compression. Animal studies are required to test the hypot