International Journal of Science and Research (IJSR) ISSN (Online): 2319-7064 Index Copernicus Value (2016): 79.57 | Impact Factor (2015): 6.391 Volume 6 Issue 11, November 2017 www.ijsr.net Licensed Under Creative Commons Attribution CC BY Incidence of Polyoma Virus Allograft Nephropathy among Iraqi Kidney Transplant Patients Jawad Ibrahim Rasheed 1 , Ali Abdulmajid Dyab Allawi 2 , Safa Auldeen Jameel Alzuhairi 3 1 Department of Internal Medicine, Baghdad Teaching Hospital, Iraq 2 Department of Internal Medicine, Baghdad College of Medicine, University of Baghdad, Baghdad, Iraq 3 Alkarama Transplantation Centre, Alkarama Teaching Hospital, Baghdad, Iraq Abstract: Background : polyoma virus is a ubiquitous human virus with a peak incidence of primary infection in children 2 to 5 years of age and a seroprevalence rate of more than 60% to 90% among the adult population worldwide. Material and methods : All recruited patients were considered from nephrology and transplant outpatients' clinic medical city (162cases, 97 males& 65 females). The patients with graft dysfunction were recorded on an already prepared data sheet for the type of induction therapy antithymocyte globulin (ATG or baxiliximab ), type of immunosuppressant regimens , renal function test by estimation of Glomerular filtration rate(GFR by the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation, renal Doppler ultrasound , urine for decoy cell and renal graft biopsy for light microscopy and immunohistochmestry stain. Results : This cohort study enrolled Male patients were 97 while female patients were 65, the age ranges from 20 to 60 years 1 .There was high incidence of PVAN among patients receiving antithymocyte globulin (ATG) (28.6%) as compare to baxiliximab group (3%). There were increasing incidence of BK virus nephropathy among patients taking (Calcineurin inhibitors (CNIs), + Steroid + Mycophenolate mofetil (MMF)), group (1) patients, the difference was statistically significant (p=0.012). There was increasing incidence of decoy cells in the urine of patients with PVAN (100%). Conclusions : There was increasing incidence of PVAN among transplant recipient's patients. Histological feature of PVAN is reliable diagnostic tool and should be consider in every renal transplant patients. Keywords: Graft Rejection, Kidney Transplantation, Polyomavirus 1. Introduction Polyoma virus is a DNA virus that is a member of the polyomavirus family. It shares >70% homology to the other polyomaviruses such as JC virus [1]. BKVN is currently a major cause of allograft failure in RT recipients [2].After primary infection, polyoma virus preferentially establishes latency within the genitourinary tract and frequently is reactivated in the setting of immunosuppression [3]. In renal transplant recipients, polyoma virus is associated with a range of clinical syndromes including asymptomatic viruria with or without viremia, ureteral stenosis and obstruction, interstitial nephritis, and polyoma virus allograft nephropathy[4]. During the last decade, BK nephropathy has emerged as an important cause of allograft dysfunction after renal transplantation[5]. The highest prevalence of polyoma viruria and viremia occurs at 2 to 3 months and 3 to 6 months, respectively[6]. The risk for development of polyoma viremia increases when urine viral load is greater than 104 copies/ml, whereas polyoma virus allograft nephropathy is unusual in the absence of polyoma viremia [7]. PVAN commonly presents within asymptomatic rise in serum creatinine during the first post transplantation year. However, BK nephropathy may occur as early as the first week (where it is resemble delayed graft function DGF in first week) [8] to as late as 6 years after transplantation[7[. Diagnosis is made by allograft biopsy, which demonstrates BK viral inclusions in renal tubular cell nuclei and occasionally in glomerular parietal epithelium[9] .There are variable degrees of interstitial mononuclear inflammation, often with plasma cells, degenerative changes in tubules, and focal tubulitis, which may mimic acute rejection[10]. PVAN often is associated with very focal and sharply demarcated areas of tubulointerstitial inflammation, corresponding to foci of viral infection. Immunohistochemistry [11, 12, 13]. In late PVAN, few characteristic intranuclear inclusions are seen, and the histologic changes may be indistinguishable from chronic rejection[14]. A histological classification system for PVAN based on the degree of active inflammation, acute tubular injury, and tubulointerstitial scarring may have prognostic significance[15]. Urine cytology for decoy cells and quantitative determinations of surrogate markers for the diagnosis of PVAN[16,17,18]. The detected virus could originate anywhere along the urinary tract[19].Therefore, transplant kidney biopsy remains the gold standard for diagnosing PVAN[20] , However, in renal biopsy specimens it is often difficult to differentiate between the tissue effects of viral pathology and changes caused by acute cellular rejection[21]. Paper ID: ART20178297 DOI: 10.21275/ART20178297 1539