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INTRODUCTION: KEY POINTS

  • Infections are an important cause of morbidity and mortality in kidney transplant recipients.

Prior to Transplantation

  • Identify potential infectious issues in both donors and recipients.

  • Identify and evaluate both donors and recipients for past, present, and potential infections.

  • Confirm that recipients are properly vaccinated.

Posttransplantation

  • Some early recipient infections may be donor-derived.

  • Recognizing the time course of infections provides useful information and should be carefully considered.

  • Prophylaxis and treatment of acute rejection may alter or shift the timeline of infections.

  • The severity of immunocompromise should always be evaluated based on:

    • Time from transplant

    • Type/dose of immunosuppression

    • Presence of recent rejection

    • Use of T-cell–inhibiting agents

DIAGNOSTIC POINTS

  • Transplant recipients may present with altered inflammatory responses to infection.

  • Common infections may present in uncommon ways.

  • Clinicians must approach transplant patients with a high degree of suspicion for infection and consider that infection may be present until proven otherwise.

  • Concurrent infections (more than one single pathogen) are more likely in transplant patients than in the general population.

  • The differential diagnosis of potential pathogens is more extensive in transplant patients than in nonimmunocompromised individuals.

  • Have a low threshold for both enhanced imaging studies and biopsies. Imaging studies and biopsies should be obtained early in order to make a prompt definitive diagnosis and establish an adequate therapeutic approach—if in doubt, image and biopsy.

  • It may be difficult to distinguish between colonization and active infection.

IMMUNOLOGIC DEFICIT: T-CELL INHIBITION LEADS TO INCREASED RISK OF OPPORTUNISTIC INFECTIONS

  • Immunosuppression, although necessary to protect the transplanted kidney from rejection, increases the risk of infections.

  • Most immunosuppressive agents are associated with T-cell depletion, reduced T-cell activation, or inhibition of T-cell proliferation.

  • The net result of immunosuppression is reduced cell-mediated immunity.

  • Immunosuppression levels are the greatest from month 1 to 6 posttransplant, as well as during any subsequent episodes of rejection that require intensified immunosuppression.

  • Measurement of CD4+ T-helper cells is not as predictive of opportunistic infections in transplant recipients as it is in patients with HIV/AIDS.

CLINICAL PREDICTORS OF POSTTRANSPLANT INFECTIONS

  • Structural abnormalities

    • Ureteral strictures

    • Fluid collections

    • Foreign bodies

  • Environmental exposures

    • Heavy burden of exposure to opportunistic pathogens

    • Live vaccines

  • Degree of immunosuppression

DONOR/RECIPIENT SCREENING

  • Human immunodeficiency virus

  • Hepatitis A

  • Hepatitis B

  • Hepatitis C

    • Testing for bloodborne viruses (HIV, hepatitis B, hepatitis C) should be performed on the recipient and the donor no more than 2 weeks prior to transplant (and by nucleic acid testing (polymerase chain reaction [PCR]) to avoid potential transfer of infection from a donor recently exposed and in the “window period”

  • Herpes Simplex Virus (HSV)

  • Cytomegalovirus (CMV)

  • Epstein-Barr virus (EBV)

  • Toxoplasma

  • Human T-lymphotropic virus (HTLV-1) (controversial)

  • Strongyloides serology or stool assay (in recipients from endemic regions)

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