What are the common clinical manifestations of multiple myeloma? Multiple myeloma can be asymptomatic in the early stage, only by chance to find the increase of blood sedimentation and abnormal immunoglobulin in the blood. (iii) pathological fracture; (iv) osteosclerosis, often limited, occurring around the osteolytic lesion. A variety of cytokines such as IL-1, IL-6, TNF-β, and osteoclast activating factor are currently thought to be involved in the formation of bone damage. New (2) Damage to the kidney: renal tubular damage due to excessive immunoglobulin light chains filtered by the glomerulus and then reabsorbed in the renal tubules. Hypercalcemia, hyperuricemia, hyperviscosity syndrome, amyloidosis, tumor infiltration, and cytokines (EPO reduction) can all aggravate the damage to renal function and result in renal anemia. Renal impairment is one of the important causes of death in patients. (3) Hypercalcemia: mainly non-ionized calcium is increased. The causes of increased blood calcium are ① abnormal immunoglobulin binding to calcium ions. (ii) Release of calcium ions after bone destruction. (3) Resorption of calcium ions by the distal renal tubules. (4) Hyperviscosity syndrome: Due to the large increase of abnormal immunoglobulins in the blood to increase blood viscosity, resulting in impaired blood circulation, mostly seen in IgG type, more easily caused by IgG3 subtype. (5) Amyloidosis: amyloidosis can occur in about 10-15% of myeloma patients. It may be due to antigen-antibody reactions resulting in deposition of protein light chains and polysaccharide complexes in tissues and organs. (6) Peripheral neuropathy and nerve root syndrome: amyloidosis, infiltration of tumor cells, hyperviscosity syndrome, and fracture compression are the main causes of neuropathy, but some patients fail to detect the cause of neuropathy.