A 7-year-old boy was born at a gestational age (GA) of 39 weeks, with a birth weight of 3,360 g (50th–75th percentile). His mother had a history of pregnancy-induced hypertension and valsartan was administered from the second trimester of pregnancy until delivery. Oligohydramnios was observed at 30 weeks of gestation. On the 4th day after birth, the patient was transferred to our center because of persistent anuria and azotemia. At the time of admission, his vital signs were as follows: blood pressure 64/38 mmHg, heart rate 142 beats/min, respiratory rate 52 breaths/min, and body temperature 36.6 °C. A physical examination revealed no remarkable findings. Initial laboratory results showed blood urea nitrogen (BUN) and creatinine (Cr) of 20.5 mg/dL and 4.85 mg/dL, but neither electrolyte imbalance nor acidosis was detected. Urinalysis showed no abnormal findings, while renal parenchymal echogenicity was increased on sonography. However, the patient’s body weight increased over time, azotemia became aggravated (Cr, 5.01 mg/dL), and hyponatremia developed (Na, 129 mmol/L). Peritoneal dialysis was initiated on the 2nd day of admission, and urination was observed on the 4th hospital day (HD). The modality of renal replacement therapy (RRT) was changed to continuous RRT (CRRT) on HD 5 for volume control but returned to peritoneal dialysis after 2 days due to platelet consumption. The RRT was maintained for a total of 24 days. The patient exhibited no other complications, and the last laboratory finding before discharge of HD 38 showed a BUN and Cr of 13.8 mg/dL and 1.71 mg/dL (Fig. 1A). He has been undergoing regular checkups for 7 years.

An 8-year-old boy was born at a GA 36 weeks with a birth weight of 2,560 g (25th–50th percentile). His mother had a history of hypertension, diabetes mellitus, and transient ischemic attack. She was treated with olmesartan until an incidental diagnosis of pregnancy at an estimated GA 30 weeks. A history of oligohydramnios was not available as appropriate antenatal care was not provided. The patient’s Apgar scores were 4 and 8 at 1 and 5 minutes, respectively. Mechanical ventilation and inotropics were applied for meconium aspiration and neonatal hypotension (mean blood pressure 20–30 mmHg). On the 2nd day after birth, pneumothorax was detected. The anuria persisted for 4 days. The patient was transferred to this center 4 days after birth because of anuric acute kidney injury (AKI). The patient’s vital signs and initial laboratory findings upon transfer were as follows: blood pressure 60/52 mmHg, heart rate 145 beats/min, respiratory rate 44 breaths/min, body temperature 36.5 ℃, BUN/Cr 45.2/6.18 mg/dL, Na-K-Cl 126-5.90-81.0 mmol/L, and Ca-P-Uric acid 9.40-7.10-19.3 mg/dL. Blood gas analysis revealed a pH of 7.37, partial pressure of carbon dioxide (pCO₂) of 38.7 mmHg, and HCO₃ of 22.2 mmol/L. Urinalysis showed no abnormal findings, while renal parenchymal echogenicity was increased on sonography. CRRT was initiated immediately after the admission and was maintained for 4 days. Urination was observed on the 2nd day after admission (Fig. 1B). During hospitalization, the patient was diagnosed with hemorrhagic periventricular leukomalacia and cerebellar hemorrhage. He was discharged on HD 31 and after 8 years of regular follow-up, the patient was transferred to another hospital near his residence.

Table 1 briefly describes the long-term outcomes of the two cases. Both patients maintained favorable growth. For renal functions, their glomerular filtration rate did not recover to normal range which is over 90 mL/min/1.73 m² even after discharge. Also, ultrasonographic findings were persistently compatible with those of chronic kidney disease (CKD), exhibiting abnormal renal parenchymal echogenicity and poor corticomedullary differentiation. Glycosuria and proteinuria, implying proximal tubular dysfunction, were not detected in either of the patients. However, case 1 was sustained impaired urinary concentration (urine osmolality 101 mOsm/kg) since birth, suggesting distal tubular dysfunction although his growth was within the normal range. Confirmatory tests such as water restriction test for nephrogenic diabetes insipidus (NDI) were not conducted considering the normal aldosterone/renin level. He had started amlodipine use 2 years prior to this report for hypertension without secondary causes. Case 2, on the other hand, exhibited preserved tubular function but neurological sequelae, including delayed development and intellectual disability, associated with perinatal cerebral insult.