Manifestations of pulmonary alveolar paraproteinosis in MM patients were studied in the works of many authors . M.M. Ilkovich (2007) notes an important morphological difference between primary alveolar proteinosis (AP) and secondary proteinosis (found in hematological patients): during primary AP, there is a uniform staining of CHIC-positive substance in the alveoli, for secondary proteinosis it is characteristic granular staining; An additional diagnostic test is the reaction with immunoperoxidase. At present, the phenomenon described by OV Voeno-Yasenetsky as a tissue paraproteinosis is called NAMIDD syndrome (non-amyloid deposition in the tissues of monoclonal L and H chains or whole molecules of immunoglobulins) . Unlike amyloidosis, NAMIDD deposits have an amorphous non-fibrillar composition and are not detected by histological methods adopted for the diagnosis of amyloidosis .

Amyloidosis in MM is detected on average in 10–15% of patients. At the same time, according to GF. Grandma (1987), the deposition of amyloid masses in their lgk was detected in 26.3% of cases . In most patients, vessels and alveolar septa are involved in the process, which is clinically manifested by shortness of breath . X-ray examination of specific recognition can not be detected .

The susceptibility of patients with MM to bronchopulmonary infections is promoted by specific myeloma plasma cell filtration, as determined by G.A. Alekseev and N.E. Andreeva (1966) as a “myeloma light” [20]. Histological examination of the lungs shows a significant infiltration of lymphocytes and plasma cells of interstitial tissue, inter-alveolar septa, peribronchial spaces. Sometimes in bronchial cartilage and interstitial tissue there are multiple calcified foci of calcification .