Sustained activation of the renin–angiotensin–aldosteron system after fetal exposure to AT1 blockers: Effects on kidney and bone in a preterm newborn

The renin–angiotensin–aldosterone system (RAAS) plays a key role in development of fetal kidney. Angiotensin‐converting enzyme (ACE) inhibitors or angiotensin II receptor type 1 (AT1) antagonists alter RAAS‐signaling compromising metanephrogenesis, and vascular and tubular development. The result is a fetal “RAS blockage syndrome” that may occur not only following exposure during the second and third trimester, but also after the use of these drugs at the beginning of pregnancy. The in‐utero exposure to AT1 antagonists is not confined exclusively to the risk of neonatal renal failure, but also to skull ossification defect that worsens the neonatal prognosis. We report the case of early arterial hypertension development, marked increase of plasma renin and aldosterone, severe hypocalvaria, and low bone mineralization in a female preterm infant in‐utero exposed to AT1 antagonists.