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REVIEW previously responded poorly to chemoimmunotherapy (7), but they have a more durable response when treated with the Bruton's tyrosine kinase (BTK) inhibitor ibrutinib (8), while patients with mutated IGHV have improvement in overall and progression-free survival when treated with chemoimmunotherapy (7). The first regimens for treatment of CLL focused on the use of alkylating agents, specifically chlorambucil and later cyclophosphamide, beginning in 1956 (9). Chlorambucil was later combined with corticosteroids in 1961 (10). The landscape of CLL therapy did not change for many years until the use of purine analogs, like fludarabine in the 1980s, which were used in patients who were refractory to chlorambucil. Subsequently, combination therapies were tested leading to the use of fludarabine/cyclophosphamide together as the backbone of standard CLL therapy (11). Rituximab, a human murine chimeric anti-CD20 monoclonal antibody, changed the approach to CLL treatment. Studies demonstrated efficacy of single agent rituximab in CLL (12, 13). Subsequently, rituximab was combined with cytotoxic agents, leading to the development of chemoimmunotherapy. For young fit patients, the combination of fludarabine/cyclophosphamide/rituximab has been shown to be superior to fludarabine/cyclophosphamide (14) in terms of progression and overall survival. Anti-CD20 antibodies have been successfully combined with other agents (11, 15-17). Recently, the treatment of CLL has transformed with the approval of two agents that interfere with B-cell receptor signaling. Ibrutinib, a BTK inhibitor that irreversibly inhibits BTK and CXCR4 signaling, has been shown to be an effective treatment in heavily pretreated patients, in those with 17p deletion, and in older patients in the front-line setting. Two recent studies have demonstrated an overall survival advantage over standard approaches (18). PI3K delta inhibition with idelalisib in combination with rituximab has also been shown to be effective as compared to single agent rituximab (19). Recently, advances have been made in targeting the antiapoptotic protein BCL2, which is overexpressed in many

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Patients with cancer are at risk for acute and chronic renal injury. The insult could be from the malignancy directly or a paraneoplastic process or due to treatment. In addition, cancer and its treatments can also lead to electrolyte and acid-base disorders, as well as hypertension. Monitoring kidney function in patients with cancer is important for early detection and management of these complications. This is also important for patients on newer cancer treatments whose renal effects may not be well known. In patients for whom nephrotoxicity is anticipated, specific precautions can be taken for its prevention. This chapter discusses direct tumor involvement of the kidney and treatment-associated kidney disease and closes by examining tumor lysis syndrome and kidney disease after hematopoietic cell transplantation.