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In 24 patients with a cadaveric renal allograft, serial measurements after transplantation were made of the diffusing capacity for carbon monoxide (DLCO) together with serial measurements of C3d, the stable conversion product of the complement factor C3, and determinations of the anaphylatoxin C3a. Twelve patients were studied during an active cytomegalovirus (CMV) infection, and 12 patients were studied during allograft rejection or during a stable phase after renal transplantation (control subjects). No patients had pulmonary symptoms nor abnormal chest radiographs or arterial blood gas determinations. During an active CMV infection, DLCO was significantly reduced compared with the measurements made during allograft rejection or during a stable phase after renal transplantation. This was true both with (p less than 0.01) and without (p less than 0.01) correction for the hemoglobin concentration. Serum C3d levels were increased in 8 of the 12 patients with a CMV infection, but not in any of the patients in the control group. In 8 patients with a CMV infection, measurements were made of the anaphylatoxin C3a, and were found to be significantly higher than the levels in the control population (p less than 0.01). We conclude that our data are consistent with pulmonary dysfunction in every patient with an active CMV infection. The concomitant findings of complement activation and formation of anaphylatoxins suggest a causal relationship of the complement activation and a decreased DLCO, although further studies are warranted to determine the exact role of complement in the pulmonary events during an active CMV infection after renal transplantation.(ABSTRACT TRUNCATED AT 250 WORDS)

Pulmonary function tests, including spirometry, transfer factor of the lungs for carbon monoxide (TlCO), and the two components of TlCO, the diffusing capacity of the alveolocapillary membrane (Dm) and pulmonary capillary blood volume (Vc), were carried out in a group of patients with testicular carcinoma during and after treatment with the Einhorn regimen. The lung function parameters of patients who developed bleomycin-induced pneumonitis were compared with those recorded in a group of patients who did not develop this syndrome. We suggest that bleomycin-induced damage to the pulmonary capillary vasculature can be monitored by measuring Vc and that ensuing fibrosis can be measured by recording Dm. The decrease in Dm is probably compensated for by an increase in Vc, leading to a smaller change in TlCO.