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<p>Low birth weight (LBW) is a risk factor for development of hypertension and chronic kidney disease in adulthood. Here, we report the case of a forty-year-old man with a history of very low birth weight (VLBW) (1300 g) who had hypertensive emergency (233/142 mmHg), acute kidney injury (AKI) (serum creatinine, 8.47 mg/dL), elevated plasma renin activity (102 ng/mL/h), and posterior reversible encephalopathy syndrome. He received temporary hemodialysis but was eventually liberated following intensive antihypertensive therapy. A renal biopsy revealed focal segmental glomerulosclerosis (FSGS) with endothelial injury. In addition, the patient had pre-existing, undertreated hypertension. Taken together, the reduced nephron number and impaired vascular development due to LBW may be involved in the development of adult-onset, near fatal hypertensive emergency and subsequent AKI in our case. This case reinforces the long-term cardio-renal risks associated with LBW and illustrates the importance of evaluating perinatal history in the diagnostic workup and successful management of adult-onset nephropathy.</p>

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A case of hypertensive emergency in a patient who had a history of very low birth weight

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月18日

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  • Yoichi Kadoh,
  • Jun Yoshino,
  • Tomohiro Oka,
  • Fumika Kamei,
  • Ai Uchida,
  • Maki Hanada,
  • Mamiko Nagase,
  • Daisuke Niino,
  • Takeshi Kanda

摘要

Low birth weight (LBW) is a risk factor for development of hypertension and chronic kidney disease in adulthood. Here, we report the case of a forty-year-old man with a history of very low birth weight (VLBW) (1300 g) who had hypertensive emergency (233/142 mmHg), acute kidney injury (AKI) (serum creatinine, 8.47 mg/dL), elevated plasma renin activity (102 ng/mL/h), and posterior reversible encephalopathy syndrome. He received temporary hemodialysis but was eventually liberated following intensive antihypertensive therapy. A renal biopsy revealed focal segmental glomerulosclerosis (FSGS) with endothelial injury. In addition, the patient had pre-existing, undertreated hypertension. Taken together, the reduced nephron number and impaired vascular development due to LBW may be involved in the development of adult-onset, near fatal hypertensive emergency and subsequent AKI in our case. This case reinforces the long-term cardio-renal risks associated with LBW and illustrates the importance of evaluating perinatal history in the diagnostic workup and successful management of adult-onset nephropathy.