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Chronic kidney disease (CKD) after AHSCT is defined as eGFR<60 ml/min/1.73m² body surface area beyond 100 days posttransplant [48]. Drugs used in conditioning regimens or for disease control prior to AHSCT, which can commonly lead to renal toxicity, are carboplatin and ifosfamide. A single‐institution retrospective cohort study demonstrated a cumulative CKD incidence of 3.8% in 5‐year AHSCT survivors [49]. Notably, the incidence of CKD in AHSCT recipients was comparable to that with matched sibling donor allogeneic‐transplant but lower than matched unrelated donor allogeneic‐transplant. Analysis of the entire cohort showed older age at transplant and prophylaxis or treatment of GVHD with cyclosporine +/‐ tacrolimus as independent risk‐factors for subsequent CKD [49]. Another cohort study showed the cumulative incidence of dialysis to be 2.3% posttransplant compared to a pretransplant prevalence of 1.4% in auto‐transplant recipients [3]. Posttransplant dialysis was also a risk‐factor for subsequent cardiovascular disease. In pediatric populations, AHSCT for neuroblastoma is an independent risk‐factor for development of subsequent hypertension, which can further predispose to kidney complications [50]. Monitoring for renal complications after transplant should include measurement of serum creatinine, blood urea nitrogen, urine protein, and blood pressure management [17]. Further investigations, including imaging or kidney biopsy, should be performed as clinically indicated. A small randomized clinical trial demonstrated renal‐protective benefit to initiation of captopril in patients receiving TBI‐based conditioning prior to transplant [51]. Patients in the captopril arm had a lower serum creatinine and higher eGFR at 1 year compared to placebo.