**Table 1.**

**49**

*Viral Infections after Kidney Transplantation: CMV and BK*

**3. BK polyomavirus infection and disease in humans**

Polyomaviruses are non-enveloped, double-stranded ubiquitous DNA viruses living in birds and mammals as natural hosts. The name indicates their ability to produce tumors (Greek poly- many, multiple; -oma, tumors), particularly in

Seroprevalence in humans ranges from 20 to 90%, depending on the viral strain and patient age. It generally remains asymptomatic in the renourinary tract of healthy individuals, although may undergo periods of self-limiting transient asymptomatic activation with viruria and viremia, without causing disease [46]. However, in immunocompromised individuals, such as renal transplant recipients, it can be associated with various patterns of tissue injury, of which BK virus

Among approximately 18 polyomavirus strains, BK virus, JC virus, and simian virus (SV-40) have been considered to be pathogenic in humans. Infections with SV-40 were detected following the administration of contaminated polio vaccines

BK virus was isolated in 1971 from a patient with ureteral stenosis after kidney transplantation and was named after the initials of the infected patient. Similarly, JC virus was named after a patient with progressive multifocal leukoencephalopathy. Both strains are characterized by productive viral infection with tissue injury, showing specific tropism for the renourinary tract or central nervous system [46, 47]. Recent studies have indicated that BK virus may be involved in the tumorigenesis of bladder carcinoma in renal transplant recipients and salivary gland inflammation and sclerosis in HIV patients [48, 49]. Trichodysplasia spinulosa-associated polyomavirus and Merkel cell carcinoma polyomavirus, recently detected new strains, may be related to proliferative lesions and neoplasms without productive

PVN is a major causative agent in nephropathy after renal transplantation,

side effects, including PVN and hemorrhagic cystitis [47].

In the past, when immunosuppressive therapy was based mainly on cyclosporine, only sporadic PVN cases were reported. Although modern immunosuppressive drugs introduced after 1990 have enabled less rejection and improved allograft survival, they have been responsible for the occurrence of previously uncommon

Before screening protocols for PV reactivation in renal transplant recipients were routinely used, PVN was usually diagnosed late after transplantation, in an advanced histologic stage, with chronic renal changes leading to allograft loss within 1 year in 50–90% of cases [4, 50]. Potential misdiagnosis of concurrent rejection resulting in increased immunosuppression might contribute to accelerated

PVN is typically caused by the BK strain and only rarely by simultaneous activation of BK and JC viruses. The specific viral activation mechanisms remain unknown [47]. The transplant microenvironment may promote viral reactivation, because only sporadic detection of PV in native kidney of patients with other organ transplants or in immunodeficient patients has been reported [52, 53]. PVN also commonly occurs in patients with posttransplantation complications, including

in the late 1950s, without known clinical manifestation in humans [46].

*DOI: http://dx.doi.org/10.5772/intechopen.86043*

rodents and experimental models [46].

nephropathy is the most common.

viral replication [50].

**3.1 BK nephropathy**

allograft failure.

**3.2 Features of BKN**

affecting 1–10% of patients [51].

*Drugs used in therapy of CMV disease.*

*Perioperative Care for Organ Transplant Recipient*

**48**

**Drug** Cidofovir

**Dosage** 5 mg/kg i.v. once a week for 2

consecutive weeks. Following

induction dose, 5 mg/kg i.v. once

every 2 weeks administer with

probenecid to decrease side

effects to the kidney

Maribavir

To be determined

*i.v., intravenous; p.o., peroral; eGF, estimated glomerular filtration.*

**Table 1.**

*Drugs used in therapy of CMV disease.*

Inhibits UL97 kinase and stops

Taste disturbance; inferior at preventing

CMV disease

viral maturation and egress

**Action** After conversion to active

form, cidofovir diphosphate

competitively inhibits DNA

polymerase

**Formulation**

**Common side effects**

Nephrotoxicity, neutropenia, teratogenicity,

carcinogenicity, nausea, vomiting
