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[Alveolar damage of pneumocystis carinii pneumonia in renal transplantation recipients]. | LitMetric

AI Article Synopsis

  • The study aimed to investigate the changes in lung structure and the relationship between Pneumocystis carinii and the alveoli in patients with Pneumocystis carinii pneumonia after kidney transplants.
  • A total of 27 patients suspected of having Pneumocystis carinii pneumonia underwent bronchoscopy and testing, with 23 cases providing significant results indicating common symptoms, imaging patterns, and a diagnosis based on the presence of the organism.
  • Findings highlighted significant airflow impairment, inflammation, and structural damage in the alveoli, indicating that severe lung damage is a predominant issue in these post-transplant patients.

Article Abstract

Objective: To study the alveolar ultrastructural changes and the interaction between Pneumocystis carinii (PC) and alveoli in Pneumocystis carinii pneumonia (PCP) patients after renal transplantation.

Methods: Twenty-seven patients with suspected PCP after renal transplantation were examinated by bronchoscopy with bronchoalveolar lavage (BAL) and transbronchial lung biopsy (TBLB). The BAL fluid was centrifuged and the sediments were stained for PC. Cases for which electron microscope showed alveolar tissue in TBLB specimen were included. Then the clinical features, PC, alveolar epithelial damage, exudate in alveolar space, inflammatory cell infiltration, and fibrous tissue in the interstitial space were analyzed and evaluated.

Results: Twenty-three cases were studied. The mean time from renal transplantation to onset of illness was 5.6 months, and that from onset of illness to hospitalization was 5.5 days. Clinical features included fever, dyspnea, unproductive cough, and scanty chest signs, to hypoxemic respiratory failure. Chest CT showed diffuse lung interstitial changes in 22 of the 23 cases, 9 with consolidation. After treatment with SMZco, the fever resolved in 1 - 5 days, and the general state of the patients became better, and 19 patients were dischaged within 1 month. PC in BAL fluid was found by special staining in 18 patients, while PC was found by electron microscope in 14 patients. In most cases PC was few in the lung tissue, but in 3 cases abundant PC filled the alveolar space. PC was seen in two forms, the cyst and the trophozoite. Electron and light microscopes showed alveolar exudate, inflammation in interstitium and alveolar space, interstitial fibrosis, and alveolar epithelial damage in all patients.

Conclusion: In PCP patients after renal transplantation there was marked alveolar damage, which was the major pathological change in the lung.

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