Background: Opportunistic viral infections make an important threat to renal transplantation recipients (RTRs), and with the use of more intense newly-developed immunosuppressive drugs; the risk of renal allograft loss due to reactivation of these viruses has increased considerably. At the top priority of these viruses lie BK polyomavirus (BKV) and human cytomegalovirus (CMV). Reactivation of these viruses in these chronically immunosuppressed RTRs can lead to renal impairment and subsequently allograft loss, unless early detected and properly treated. Objectives: The study aimed to detect and quantify plasma viral load of BKV and CMV in RTRs using quantitative real time PCR (qRT-PCR), in order to study the prevalence of these two viruses in the sole renal transplantation center in Baghdad, and correlate viral load with the diseases severity. Furthermore, the prevalence of BKV-CMV coexistence in RTRs, to find out whether infection by one of them is a risk factor for infection by the other was investigated. Patients and Methods:A total of 99 RTR were enrolled in the study, and 15 non-transplanted patients with chronic kidney diseases (CKD) together with 15 health living donors (LD) were taken as controls. Plasma samples were taken from all participants. From which viral DNA was extracted, and then real time PCR technique was used to measure the viral load. Results:Out of 99, 12 (12.12%) of RTR patients were positive for BK viremia with a viral load (VL) ranging from (1x102 to 1x109 copies/ml), while none of the control groups was BK positive, and 5 patients out of these 12 had BKV nephropathy. For CMV, 13.13% of RTR patients had positive CMV viremia with a VL ranging from (1.25x102 to 7.94x107 copies/ml), and only one of the CKD controls was CMV positive. Only 3 patients had BK-CMV coexistence, which was statistically not a significant risk factor for one another. Conclusion: Our study suggests that both BK polyomavirus and CMV should be considered important causes for nephropathy and allograft loss in RTRs in Iraq.