Pulmonary hypertension complicated with asbestos-related disease in a patient with severe renal impairment

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  • Yamamoto Yasutaka
    Division of Nephrology, Department of Medicine, Showa University School of Medicine
  • Wada Yukihiro
    Division of Nephrology, Department of Medicine, Showa University School of Medicine
  • Tomita Eiko
    Division of Nephrology, Department of Medicine, Showa University School of Medicine
  • Hayashi Junichi
    Division of Nephrology, Department of Medicine, Showa University School of Medicine
  • Saito Tomohiro
    Division of Nephrology, Department of Medicine, Showa University School of Medicine
  • Iseri Ken
    Division of Nephrology, Department of Medicine, Showa University School of Medicine
  • Inoue Takashi
    Division of Nephrology, Department of Medicine, Showa University School of Medicine
  • Shibata Takanori
    Division of Nephrology, Department of Medicine, Showa University School of Medicine

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Other Title
  • アスベスト関連疾患を合併し肺高血圧症を呈した腎不全患者の1例
  • 症例報告 アスベスト関連疾患を合併し肺高血圧症を呈した腎不全患者の1例
  • ショウレイ ホウコク アスベスト カンレン シッカン オ ガッペイ シ ハイ コウケツアツショウ オ テイシタ ジンフゼン カンジャ ノ 1レイ

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Abstract

<p>An 82-year-old female with severe renal impairment and therapy-resistant pulmonary hypertension (PH) was admitted on an emergency basis due to dyspnea. She had a history of occupational exposure to asbestos during her 20s and chronic kidney disease due to diabetic nephropathy and benign nephrosclerosis, an old myocardial infarction, and a pleural lesion that was compatible with asbestos-related disease (ARD). Laboratory tests performed upon admission revealed elevated levels of serum creatinine and brain natriuretic peptide. Hypoxia was also evident, but no pulmonary thromboembolisms were detected. Chest computed tomography demonstrated pleural thickening lesions with calcification. Ultrasound cardiography showed PH and congestion, but the patient’s left ventricular ejection fraction was within the normal range. Hemodialysis (HD) was started to reduce the burden of heart congestion and uremic toxins. However, the hypoxia persisted despite intensive care, including beraprost therapy and excess fluid removal by HD. The patient died as a result of complications (pneumonia, a myocardial infarction, and a stroke) on day 33 after admission. An autopsy revealed scattered pleural plaques (but no evidence of lung fibrosis or asbestos bodies) and marked medial thickening of the pulmonary artery. To the best of our knowledge, this is the first reported case of PH combined with ARD involving a patient with renal impairment. We consider that the patient’s asbestos exposure, renal failure, and left-sided heart disease all contributed to the development of therapy-resistant PH.</p>

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