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Abstract: TH-PO633

Transient Hypertension in a Preterm Infant after the Administration of Indomethacin for Patent Ductus Arteriosus

Session Information

Category: Nephrology Education

  • 1302 Fellows and Residents Case Reports


  • Tominaga, Takahiro, Saitama Municipal Hospital, Saitama, Japan
  • Omori, Sayu, Saitama Municipal Hospital, Saitama, Japan
  • Awazu, Midori, Keio University School of Medicine, Tokyo, Japan

While hypertension is a known complication of non-steroidal anti-inflammatory drugs (NSAIDs) in adults, it has not been reported in children. We report a preterm infant who developed hypertension after the administration of indomethacin for patent ductus arteriosus (PDA).


A preterm boy was delivered at 31 weeks’ gestation via caesarean section for placenta previa. Birth weight was 1676 g. PDA was detected on day 2. Indomethacin 0.2 mg/g/dose was given intravenously from day 2 to day 4. On day 5, the ductus arteriosus was still patent. Although serum creatinine increased from 0.62 mg/dL to 1.05 mg/dL, urine output was normal (2.4 ml/kg/hr) and indomethacin was readministered on day 5 and 6. On day 7, the ductus arteriosus was closed. On day 8, urine output decreased to 0.8 ml/kg/hr, and fluid was restricted to 60 ml/kg/day. FENa was 2.2% which could be normal for preterm infants. Urine output gradually increased. Blood pressure (BP) had been normal until day 12. On day 13, BP increased to 82/41 mmHg and became 90/58 mmHg (99th percentile for postconceptional age 34 weeks) on day 14. Body weight did not change from day 7 to day 14. Physical examination was unremarkable with heart rate of 140 beates/min with no edema. Blood urea nitrogen was 2.5 mg/dL, serum creatinine 0.41 mg/dL, calcium 9.2 mg/dL, phosphorus 3.8 mg/dL, sodium 130 mmol/L, potassium 4.3 mmol/L, chloride 101 mmol/L, bicarbonate 16.3 mmol/l, uric acid 1.0 mg/dL, TP 4.7 mg/dL, albumin 3.0 mg/dL, NT-pro BNP 18210 pg/dL, plasma renin activity 1.1 ng/mL/hr, and aldosterone 382 pg/mL. Cardiac ultrasonography showed mean velocity of circumferential fiber shortening (mVcfc) of 0.6 circ/s and end-systolic wall stress (ESWS) of 119.3 g/cm2 suggesting afterload mismatch, which occurs in response to an acute increase in vascular resistance. Nitroglycerin infusion was started. On day 15, BP decreased to 78/44 mmHg. Cardiac ultrasonography showed improvement of after load mismatch.


NSAID-induced hypertension has been ascribed to sodium retention due to COX-2 inhibition in the kidney. The major mechanism of the increased blood pressure of this patient, however, is thought to be high afterload due to increased peripheral vascular resistance presumably by indomethacin.