AKI is a common complication after HSCT. The increased severity of AKI was associated with an increased risk of death. The pathogenesis of AKI after HSCT was complicated and affected by many factors. Prerenal azotemia was a common cause of AKI in HSCT patients. Common adverse reactions to chemotherapy include nausea, vomiting, diarrhea, and mucositis, which often caused excessive fluid loss through the gastrointestinal tract or insufficient oral intake to cause circulation blood volume to be reduced, which eventually resulted in prerenal kidney injury[13, 14]. In addition, acute tubular necrosis was also a common cause of AKI after HSCT. Hypovolemic shock, septic shock, or nephrotoxic drugs, such as amphotericin B, vancomycin and the drugs used to prevent and treat aGVHD and CSA could cause acute renal tubular necrosis and cause renal AKI, which could cause AKI alone or in synergy with prerenal etiology[13–15]. Urinary obstruction might be the cause of AKI in patients with HSCT. Intravenous infusion of ganciclovir and other antiviral drugs could precipitate in the urine and form crystals in the renal tubules, causing obstruction, and blood clots formed by HC could lead to urinary tract obstruction, resulting in obstructive postrenal AKI. Although these complications might not be independent risk factors for AKI, their combination might lead to the occurrence of AKI. In addition, nephrotoxic drugs used to treat these complications could also cause AKI.In addition, hypertension and diabetes also lead to the occurrence of AKI after HSCT[3, 15]. Several risk factors for AKI in patients undergoing HSCT had been reported. The descriptions of trans-plant characteristics, such as donor, race, TBI, nephrotoxic agents, and post-transplant adverse events, such as aGVHD and infection, were inconsistently described as risk factors for the development of AKI[18–20]. Studies had shown that unrelated donors were closely associated with AKI(HR,6.26;P = 0.042).It had been reported that transplantation of hematopoietic stem cells from unrelated donors was associated with a significant increase in the risk of infection, severe aGVHD, and organ toxicity[22–27]. Calmodulin neurophospholipase inhibitors (CNIs) caused AKI by arteriolar vasoconstriction, reducing kidney perfusion, tubular toxicity, and endothelial injury [28, 29]. CNIs nephrotoxicity after hematopoietic transplantation was reported in up to 31% of patients. The infection could lead to hemodynamic changes and inflammatory damage, leading to AKI. The infection resulted in systemic arteriole constriction and endothelial damage, causing capillary leakage and renal insufficiency. Damage to the tubules themselves led to the release of local cytokines and chemokines, resulting in local inflammation and further intrarerenal damage. In addition, antimicrobials commonly used to treat infection were often nephrotoxic. However, the mechanism of AKI induced by triazole antifungals remained unclear. Liu et al. found that HLA mismatched was closely related to AKI after HSCT (OR = 3.6;95%CI = 1.1–13.0). And ABO mismatched was found to be associated with a significantly increased risk of grade II-IV aGVHD. This might be the reason why ABO mismatched were associated with AKI.
AKI after HSCT could seriously affect the survival and prognosis of patients, so it was important to identify the risk of AKI in advance. At present, studies were using the hematopoietic cell transplantation-specific comorbidity index (HCT-CI) to study the incidence of AKI after allogeneic HSCT. HCT-CI factors included high disease risk, related donor, myeloablative conditioning regimen, stem cell source, prior stem cell transplant. At present, this study was the first time to use the nomogram model to predict the risk of AKI within 100 days after HSCT.
In this paper, we introduced perioperative parameters to develop the nomogram of predicting AKI risk. The C-index was 0.842 and 0.809 in the training and validation set respectively, which revealed that the prediction ability of the nomogram was characterized by high accuracy. The study showed that the higher the C-index of internal validation, the better the efficiency of identification and comparison. In addition, we performed the decision curve analysis to estimate the actual clinical benefit of the nomogram. The results of DCA also showed high validity and predictive effect. The risk of AKI after HSCT could be predicted in advance by using the nomograph model, which could guide the management of HSCT patients, improve the survival of patients and improve the quality of life of patients. The results of this study showed that the factors included in predicting the risk of AKI after, HSCT were donor, HLA, blood type matching, FK506, aGVHD, infection and triazole antifungal drugs.
However, this paper had some limitations. (1) This study was a retrospective analysis without a prospective study. (2) More cases need to be added to verify the nomogram.