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To the Editor: We read with interest the recently published article by Saha et al. [1]. The authors have described acute kidney injury in a neonate probably caused by exposure to olmesartan in the mother. We wish to add certain points.
The mother also had uncontrolled hypertension, and uncontrolled hypertension may sometimes lead to intrauterine growth restriction, chronic placental insufficiency, and oligohydramnios. Although exposure to ACE inhibitors and angiotensin receptor blockers (ARB) is one of the known causes of acute kidney injury in a neonate, definitive causality can only be established when other risk factors are absent. The mother received only a few doses of oral olmesartan in the third trimester for about seven days before delivery, and the fetal ultrasound at 34 wk showed severe oligohydramnios. It would have been more helpful for the readers to understand how the authors established a definite causal relationship between olmesartan exposure and acute kidney injury in this index case [2]. Most of the previous cases reported intake by the mother for weeks together starting from the first or second trimester.
Literature suggests that maternal exposure to ARBs can cause skull bone hypoplasia, pulmonary hypoplasia, Potter sequence, and polycythemia [3]. In the long term, many of these infants developed hypertension, developmental delay, and growth retardation, and together these manifestations were called “fetal RAS blockade syndrome” [4]. The authors didn’t mention the presence of any calvarial bone hypoplasia. This information would have been more informative for readers to determine whether the neonate had any other features of “fetal RAS blockade syndrome” or later developed growth retardation, which would have also proved the definitive causal association of olmesartan.
Lastly, the blood urea/creatinine ratio in the index case clearly suggests there was acute kidney injury and probably acute tubular necrosis, and in such cases, furosemide injection is usually counterproductive rather than beneficial.
References
Saha AK, Padhi P, Hota D, Rathore V. Neonatal acute kidney injury due to maternal olmesartan intake. Indian J Pediatr. 2024. https://doi.org/10.1007/s12098-024-05037-w.
García-Cortés M, Lucena MI, Pachkoria K, Borraz Y, Hidalgo R, Andrade RJ; Spanish Group for the Study of Drug-induced Liver Disease (grupo de Estudio para las Hepatopatías Asociadas a Medicamentos, Geham). Evaluation of Naranjo adverse drug reactions probability scale in causality assessment of drug-induced liver injury. Aliment Pharmacol Ther. 2008;27:780–9.
Bhat L, Bisht S, Khanijo K. Olmesartan intake during pregnancy leading to reversible renal failure and skull hypoplasia in a preterm newborn. Pediatr Oncall J. 2017;14:13–4.
Bullo M, Tschumi S, Bucher BS, Bianchetti MG, Simonetti GD. Pregnancy outcome following exposure to angiotensin-converting enzyme inhibitors or angiotensin receptor antagonists: a systematic review. Hypertension. 2012;60:444–50.
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Panda, P.K., Sharawat, I.K. Neonatal Acute Kidney Injury due to Maternal Olmesartan Intake: Correspondence. Indian J Pediatr (2024). https://doi.org/10.1007/s12098-024-05166-2
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DOI: https://doi.org/10.1007/s12098-024-05166-2