First, we need to explain our selection of the BKV threshold. In 2004, a study showed that all active BKVAN showed BKV DNA load >E +07 copies/ml of urine samples. The guidelines published by the American Society of Transplantation in 2013 emphasize this result.
By monitoring the urine BKV DNA loads regularly after kidney transplant, we found that 13.4% of the patients (n=35) were diagnosed with high-level BK viruria at the median time of 181 days in our center. In 2020, several scholars summarized the incidence of BK virus infection in Asia and found that the incidence of BK viruria after kidney transplantation was between 5.9% and 86.9%. Although our data are also within this range, the wide range also affects the accuracy of these data. In fact, we must admit that the existing data were all reported by a single center, and there are too many uncontrollable factors leading to considerable differences in the results. Previously, some scholars also reported the prevalence of BKV infection among healthy people. Atonsson et al. reported that the serum positive rate of BK virus in Australians was as high as 99% in people between 25 and 60 years old. Gossai et al. investigated the prevalence of polyomavirus in the United States and found that the serum positive rate of BK virus was 87.6%. These reports reveal differences in the prevalence of BK virus infection in time and space. The highest incidence of BK viruria in renal transplant recipients was within 6 months of surgery, in accordance with other centers.
It is important to identify high-level BK viruria patients. Reischig et al. have demonstrated graft damage from BK viremia in studies. Many centers, in fact, have attempted to treat high-level BK viruria. There is also a concern that there is no specific treatment for BKV infection in kidney transplant patients. The primary goal is usually to reduce the intensity of immunosuppression. We began to carry out preemptive intervention in 2015 to intervene in high-level BK viruria to prevent the occurrence of BKVAN, and the results were satisfactory. Among the 38 patients, BK viruria was effectively controlled in 32 patients (84.2%) within 1 year of treatment, and the remaining 6 patients (15.8%) also showed no infection progression, and no rejection reaction occurred in all patients after the immunosuppression intensity was reduced [The article is under submission]. Some researchers have also found that BK viruria also causes serum creatinine elevation by analyzing the survival of renal transplant recipients infected with BK virus. Currently, the guidelines recommend high frequency BKV screening for all kidney transplant patients, which would undoubtedly result in significant medical costs. Early determination of a patient’s risk of infection can greatly save on medical costs and provide improved medical services to patients. Therefore, we conducted this study to explore the risk factors for high-level BK viruria.
As we know, no relevant studies have been reported internationally in this field, so we selected certain variables that may influence the occurrence of high-level BK viruria for analysis. The final results showed that DBCD, AR and DGF were independent risk factors for high-level BK viruria. AR and DGF were the expected results, and AR and DGF were also independent risk factors for BK viremia after renal transplantation. However, DBCD surprised us. As is known, donor sources in China have undergone considerable changes in the 21st century. Influenced by traditional culture and religion, the development of DBD donors has been greatly hindered, which also severely limits the quantity and quality of our transplant work. Therefore, the criteria for donation in China were developed to solve the problem of the extreme shortage of donors in China. DBCD is the third type of donor in China (C-III), which is similar to category 4 in the Maastricht criteria. Theoretically, we think that DCD might be one of the risk factors for the progression of BK virus infection. The incidence of DGF and primary nonfunction was significantly increased because DCD donors experienced hemodynamic disorders and the attack of underlying diseases. Generally, DBCD is similar to DBD, and the quality of the kidney is significantly higher than that of DCD. Therefore, DCD may be more closely associated with infection[5, 14]. These results are confusing. Whether the bias is caused by the small number of cases or the specificity of DBCD needs to be confirmed by more studies.
This study reports the risk factors for high-level BK viruria after renal transplantation, filling in the gaps in this field preliminarily, but there are also some limitations. In this single-center retrospective study, the insufficient sample size was still a limitation of its quality. Due to the limitation of objective factors, we could not compare all relevant factors. For example, there are limited types of immunosuppressive drugs that we use after transplant, induction therapy is not routine, donor-sourced BK virus surveillance has not been carried out, and so on.