BK Virus Nephropathy (BKVAN) is the clinical term for the condition in which the BK virus is actively harming the recipient's kidney graft. About 10% of renal transplant recipients will end up progressing from BK Viremia to BK Nephropathy. A plot of the data points of my collected data shows a slight upward increase in this number over the years 2000 to the 2014 ultimately leading to the most recent 10% statistic. A significant difference is found between the rates of incidence in first time and second transplant patients, with multi-transplant recipients being more at risk for nephropathy.
Though it is relatively easy to now detect whether or not the virus is in the bloodstream, it is much harder to see whether or not the viral infection has progressed to more severe stages. Renal biopsy (the sampling of some of the kidney tissue and then viewing it on a slide), remains the gold standard for recognizing BKVAN, however, many advancements in analyzing a hosts risk factors can lead to catching the disease in its earlier stages.
After a person has first come into contact with the virus (about 90% by the age of 23) it enters a state of non-replicative asymptomatic infection called “latency”. The very small virus particle embeds itself in the epithelial and urothelial cells in an immunocompetent host. Once an increased immunosuppressive load shifts the balance of immune system cells and virus particles towards the virus it begins to replicate and the graft goes through the three stages of BKVAN.
Stage A is where the virus starts to produce structural changes in the cells that make up the epithelial walls of the kidney. Unfortunately, it is hard for even a kidney biopsy conclusively determine that nephropathy is occurring at this early stage, often going undetected until it progresses to stage B. Stage B consists of tubulointerstitial inflammation; the swelling of the capillaries used throughout the kidney to carry and filter blood. Stage C is tubular atrophy and interstitial fibrosis which severely reduces the kidneys functionality and fills it with scar tissue.
Between 30 to 60% of BKVAN cases progress to Stage C.
Is it known what accounts for the slight upward increase of rates of incidence from 2000 to 2014? Is the increased frequency of multi-transplant recipients the only possible factor?
ReplyDeleteThough unable to definitively prove causation, my initial hypothesis (blogpost 1) is that this upswing is caused by a increase in the usage and strength of immunosuppressive agents during maintenance therapy for transplant patients. The increased frequency of BKVAN in multi-transplant patients is most likely due to the patients needing a larger amount of immunosuppression (still in accordance with my hypothesis). This difference in multi-transplant patients is much like the increased incidence of graft rejection in African American patients. Though it is known the trend exists, a direct reason explaining causation is not yet found.
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