1. What type of infections do kidney transplant recipients develop?

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  Donor-derived infections

  
  
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  Recipient-derived infections

  
  
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  Nosocomial-acquired infections

  
  
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  Community-acquired infections

2. Is there any pattern to infections that occur post transplantation?

Yes. Karuthu et al. reviewed this recently, including the timing of infections post transplant. Infections occur in a generally predictable pattern after kidney transplantation. See Fig. 60.1

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  First month post transplant:

  
  
  
  
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    Nosocomial and surgery-related infections are the predominant infections

    
    
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    Aspiration pneumonia

    
    
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    Catheter infections

    
    
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    Wound infections

    
    
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    Anastomotic leaks

    
    
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    Clostridium difficile colitis

    
    
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    Resistant organisms such as methicillin-resistant Staphylococcus aureus

  
  
  
  
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  Months post transplantation 1 through 6:

  
  
  
  
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    Activation of latent infections is most common

    
    
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    Pneumocystis jiroveci (previously Pneumocystis carinii ) pneumonia

    
    
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    Fungal infections

    
    
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    Herpes-related disease

    
    
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    BK virus

    
    
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    Clostridium difficile colitis

    
    
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    Hepatitis C virus

    
    
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    Adenovirus

    
    
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    Influenza

    
    
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    C ryptococcus

    
    
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    Mycobacterium tuberculosis .

  
  
  
  
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  Posttransplant month 6 and beyond:

  
  
  
  
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    Community-acquired infections are predominant (urinary tract infections [UTIs], pneumonia)

    
    
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    Fungal infections, including Nocardia, Aspergillus, and Mucor

    
    
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    Late viral infections (cytomegalovirus [CMV], hepatitis B and C, herpes simplex virus, John Cunningham (JC) virus)

  
  

Timeline of common infections in transplant recipients. CMV , Cytomegalovirus; EBV , Epstein-Barr virus; HBV , hepatitis B virus; HCV , hepatitis C virus; HSV , herpes simplex virus; LCMV , lymphocytic choriomeningitis; MRSA , methicillin-resistant Staphylococcus aureus ; PCP , Pneumocystis jiroveci pneumonia; PML , progressive multifocal leukoencephalopathy; PTLD , posttransplant lymphoproliferative disorder; SARS, severe acute respiratory syndrome; VRE , vancomycin-resistant enterococci; VZV , varicella-zoster virus. (From New England Journal of Medicine, Fishman, J. A., Infection in solid-organ transplant recipients, Volume 357, page 2606, Copyright 2007 Massachusetts Medical Society. Reprinted with permission from Massachusetts Medical Society.)

3. What is the most common bacterial infection that leads to hospitalizations in kidney transplant patients?

UTIs. The most common bacterial cause is Escherichia coli .

4. What infectious prophylaxis do patients receive post transplant?

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  Valganciclovir to prevent CMV for 3 to 6 months

  
  
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  Trimethoprim-sulfamethoxazole to prevent Pneumocystis jirovici and UTIs for 6 months

  
  
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  Nystatin or clotrimazole to prevent esophageal candidiasis for 3 months

5. What is BK virus?

BK virus is a ubiquitous, double-stranded DNA polyomavirus with a 5300–base pair genome that replicates in the host nucleus. The polyoma family includes JC virus (infectious cause of progressive multifocal leukoencephalopathy [PML]), SV40, and monkey polyomavirus. Although the human polyomaviruses are highly seroprevalent in humans, they appear to cause clinical disease only in immunocompromised hosts.

6. What is BK-associated nephropathy?

BK virus damages the transplant kidney. The prevalence of BK nephropathy ranges from 1% to 10%. BK nephropathy is characterized by a tubulointerstitial disease pattern that closely resembles acute rejection.

7. Besides nephropathy, can BK virus cause any other kidney problems?

Yes. BK virus is associated with ureteral stenosis/strictures, which may lead to obstructive uropathy. Obstructions associated with BK virus usually occurs 2 to 4 months post transplant, whereas ischemia-induced stenosis usually occurs 1 to 2 weeks postoperatively.

8. What are the risk factors for the development of BK-associated nephropathy?

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  Human leukocyte antigen mismatch

  
  
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  Previous acute rejection

  
  
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  Use of lymphocyte depleting therapy

  
  
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  Use of steroid pulses

  
  
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  Age >55

  
  
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  Male gender

  
  
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  White race

  
  
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  Diabetes

9. Discuss BK screening.

BK virus is detectable both in the blood and the urine. The virus first appears in the urine (viruria) and then is detectable in the blood (viremia) several weeks later. The preferred screening test at most transplant centers is the blood BK quantitative viral DNA polymerase chain reaction (PCR). The sensitivity between the serum and urine BK viral testing is the same at 100%, but the specificity of serum testing is 90% versus 80% for urine testing. BK viremia is also a better predictor of BK nephropathy. There is an alternative strategy that does use BK viruria for screening because it appears earlier that BK viremia. Once BK viruria is present, the clinician considers lowering immunosuppression and now switching to BK viremia for screening.

Recommended screening times are monthly for the first 6 months and then every 3 months up to 24 months post transplant.

A BK viral load greater than 10,000 copies is strongly associated with BK nephropathy. BK viruria greater than 1,000,000 copies is associated with BK nephropathy. The next step is a kidney transplant biopsy, which is the gold standard to confirm the diagnosis and see the degree of nephropathy.