While CMV serostatus play an important role in CMV infection development in kidney Transplant recipients, it is yet not clear whether there are other risk factors could act as well. The present study aimed to investigate the risk factors which increase CMV infection occurrence in this group.
In the present study, we compare the results of serum laboratory tests in CMV positive patients to the negative patients to find the tests which significantly differ between two groups. Besides, we investigate the incidence of early or late CMV infection, risk factors and consequences of CMV viremia among kidney transplant recipients compare to the control patients.
The presented results indicate that RT patients who received the allograft from deceased donor faced with higher risk of CMV viremia after transplantation mostly among the first four months. Recent analysis among RT patients suggests grafting from a cadaveric would rise the risk of CMV viremia.
CMV viremia in our study emerged mostly after 4 months after transplantation, likewise, in a cohort study in the Europe, among 19.2% of CMV + patients, viremia emerged within the first three months after transplantation(12). given acute rejection episodes occurred within the first month post transplantation, the association with CMV infection in this period may be attributed to excessive immunosuppression associated with acute rejection treatment. Infection recuurence probably promotes by the initial immunosuppression and cessation of anti-viral prophylaxis. Notably, it is suggested that during this time, patients be monitored and treated by antiviral prophylaxis in accordance with the higher risk of CMV infection. Even though, there was no significant different between the time of CMV detection among both CMV+/- groups, our results presenting that early CMV infection emerges in 4 months after transplantation that may consider an alarming time to examine the presence of CMV viremia in the RT patients.
The results show that late onset CMV infection has not occurred frequently since the late months among the investigated patients recorded on month 7 of receiving the kidney. In other studies, late-onset CMV disease still develops in approximately 18% of patients even in the presence of either prophylactic strategies (15, 16).
In the present study, CMV viremia did not significantly affect the allograft and patient’s survival contrary to other studies (17). Given we investigated seropositive RT patients and in patients who are CMV seropositive, viral replication occurs in the context of pre-existing immunity, hence the observed replication rate is slower in such individuals. As a result of the widespread use of antiviral prophylaxis and preemptive therapy, the incidence and severity of CMV disease and its indirect effects are significantly reduced. The incidence of CMV in the renal transplant population is estimated to be between 8 and 32 percent (7).
Patients in the case group displayed worse serum creatinine values post transplantation, albeit without significant differences in graft and patient survivals (5). Serum Creatinine raised and platelets diminished. This result confirms the precedent facts which CMV infection should be considered in any renal transplant recipient who has a rise in creatinine even if symptom-free (18).
Our results did not investigate the local detection of CMV in the allograft, it is important to consider that the mere detection of CMV does not essentially exclude the presence of CMV in the blood. Indeed, lack of serum CMV positive test does not completely rule out CMV infection in these patients. Since transient periods of CMV viremia had been found in some cases due to the compartmentalized or localized CMV diseases (19, 20). In the present study, all subjects had received CMV antivirals including ganciclovir (1.25 mg/kg IV daily as induction for 1 month, which then was switched to oral valgancyclovir) or valcyte (450 mg, according to their plasma creatinine levels) for the first 3 months post transplantation. In the cases of CMV DNAemia, some patients did not show any typical syndromes of CMV infection.
In our investigation, we selected CMV viremia detection by finding the virus DNA in the patients’ blood. Given new diagnostic method based on the amplification of CMV RNA in blood samples has been commercialized, we recommend that future studies categories the case-control patients by these novel techniques (21, 22)