[Arterial hypertension and the kidney in pregnancy]

Hypertension complicates approximately 10 per cent of all pregnancies and accounts for 20% of all maternal deaths. Blood pressure normally decreases in the first trimester of pregnancy, secondary to a decrease in peripheral vascular resistance, reaches its lowest point in the second trimester and then gradually increases to or near pregravid levels at term. Normal pregnant women develop vascular resistance to the pressor effect of angiotensin II, which is precociously lost in women who develop gestational hypertension. Prostaglandins seem to be involved in the development of this vascular refractoriness. An acute and reversible lesion--defined "Glomerular endotheliosis"--has been described as the basic pathologic pattern of pre-eclamptic nephropathy, although gestational hypertension can be superimposed on undiagnosed essential hypertension or any of a variety of renal diseases. The primary goal when treating gestational hypertension is successful termination of the pregnancy with the least trauma to mother and fetus. Antihypertensive drugs could be administered to prolong pregnancy when this is considered desirable, although pharmacological therapy of gestational hypertension remains a subject for dispute, because of the lack of closely controlled studies. Hydralazine and methyldopa are drugs with a long history of use in gestational hypertension. Beta-blockers have been shown to be as effective as methyldopa. Clinical experience with nifedipine is limited, but controlled clinical trials, currently in progress, suggest its suitability.