Multiple myeloma (MM) is a neoplastic clone of plasma cells in the bone marrow that causes more than one-tenth of all hematologic malignancies with an annual incidence of sixty cases/million. The clinical features of MM are heterogeneous, including bone pain, bone fracture, anemia, impaired humoral immunity, and renal malfunction. MM affects the kidneys in varied ways, injuring glomeruli, tubules, and interstitium. The effect of multiple myeloma on the glomerulus is due to light chain (LC), heavy chain (HC) deposition, and amyloidosis. Damage to the kidney tubules by cast formation in MM is called myeloma kidney or cast nephropathy. Kidney involvement in MM significantly affects long-term outcomes. Monoclonal gammopathies, amyloidosis, dehydration, hypercalcemia, cryoglobulinemia, and others are precipitating factors for kidney dysfunction in MM. Although the pathogenesis of MM-associated nephropathy is not well understood, MM causes high serum levels of immunoglobulins (Igs), leading to a high ratio of lambda- and kappa-free chains in serum and filtrate, leading to direct or indirect nephron damage. Serum Igs and free light chain levels reduction by chemotherapy, plasmapheresis, or cutoff hemodialysis significantly affect the outcome. Furthermore, increasing the rate of FLC excretion by good hydration and urine alkalization are the cornerstones for MM-induced nephropathy prevention. In this clinically oriented review, updates and prospects are discussed. The databases PubMed, Google Scholar, EMBASE, Google, and Scopus, were searched for literature on MM-induced nephropathies. We utilized keywords, sentences, and phrases, including CKD and myeloma, amyloidosis in multiple myeloma, light and heavy chain kidney diseases in myeloma, myeloma kidney, free light chain disease, renal failure, amyloidosis, kidney and myeloproliferative diseases, CKD pathogenesis in MM, update in MM pathogenesis, and treatment.