The lethal outcome was ascertained in 65 patients with MM. In the overwhelming majority of cases, death occurred due to the progression of the underlying disease — the presence of myeloma nephropathy, complicated by chronic renal failure (52 patients — 80%); hemorrhagic syndrome due to deep thrombocytopenia; anemic syndrome. Pneumonia and its complications were diagnosed in 28 patients (43% of all died), in all cases it was the direct cause of death. In 28 of 52 patients with MM (53.8%) who died with symptoms of myelomous nephropathy and chronic renal failure, inflammatory infiltrates were found in the lungs (in this situation, pneumonia was also the direct cause of death ).

A morphological study of the lungs, bronchi, and pleura of 65 patients who died from MM was performed . The following changes were diagnosed . In 26 people (40%), lymphoid and plasma cell infiltration took place in the form of cords or nodes in the inter-alveolar septa, along the vascular adventitia, in the bronchial mucosa and in the peri- bronchial spaces . The interalveolar septa were thickened due to their infiltration with plasma cells and / or lymphocytes.

Paraproteinosis of the lungs was diagnosed in 38 patients (58%). The protein masses filling the pulmonary alveoli created a pattern of protein pulmonary edema, impregnated thickened, hyalized interalveolar septa and filled small vessels (Fig. 36 – 37). Plasma cells and lymphocytes were often able to be detected along the periphery of protein masses . Manifestations of amyloidosis in this study were detected only in 9 patients (13.8% of all deaths). The masses of amyloid were stained red when using congo-mouth staining. In these patients, there was a deposition of protein masses in the alveolar spaces, perivascular, peribronchial, and also in the walls of blood vessels .

Plasma and lymphoid infiltration of the pleura occurred in 8 (12.3%) patients with MM and was accompanied by the development of exudative pleurisy, which is an extremely unfavorable preventive factor .

In 51 patients (78%), histological examination diagnosed pneumosclerosis. In 16 people (24.6%), foci of calcification were found in bronchial cartilage and interstitium. The occurrence of calcium deposits causes an inflammatory reaction with the next development of fibrosis . Many patients had one hundred uneven blood supply of pulmonary vessels, small perivascular hemorrhages. Foci of atelectasis alternated with areas of emphysematous expansion of the alveoli. In this case, we can speak of the compensatory nature of the localized emphysema. Since, due to the deposition of paraprotein and the development of atelectasis, some alveoli are excluded from ventilation, the ventilation capabilities of other alveoli are reduced as a result of edema, fibrosis, lymphoid and plasma infiltration of the interalveolar septa, the compensatory expansion of the preserved alveoli occurs.