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Kidney transplantation in adults: Hepatitis C virus infection in kidney donors

Kidney transplantation in adults: Hepatitis C virus infection in kidney donors
Authors:
Marion Muche, MD
Seema Baid-Agrawal, MD
Section Editors:
Daniel C Brennan, MD, FACP
Adrian M Di Bisceglie, MD
Deputy Editors:
Albert Q Lam, MD
Allyson Bloom, MD
Literature review current through: Dec 2022. | This topic last updated: Sep 06, 2022.

INTRODUCTION — Transplantation of a kidney from a hepatitis C virus (HCV)-infected kidney donor may cause HCV infection in the recipient [1,2]. HCV infection has been associated with increased morbidity and possibly mortality in kidney transplant recipients [3-5].

These observations have led to the development of national and international policies concerning the allocation of organs from HCV-positive or negative donors into HCV-positive or negative recipients.

This topic reviews issues surrounding HCV-infected deceased or living kidney donors. HCV infection in kidney transplant recipients, transplant candidates, and nontransplant candidate dialysis patients is discussed elsewhere:

(See "Hepatitis C infection in kidney transplant candidates and recipients".)

(See "Hepatitis C virus infection in patients on maintenance dialysis".)

Methods of screening are discussed elsewhere. (See "Screening and diagnosis of chronic hepatitis C virus infection".)

EPIDEMIOLOGY — The seroprevalence of HCV infection in the general population is approximately 1 to 3 percent worldwide, although prevalence varies from region to region [6]. The best data regarding prevalence among deceased organ donors are from a study of 13,667 potential organ donors evaluated between 2004 and 2008 by 17 organ procurement organizations in the United States; HCV seroprevalence was 3.45 percent among normal-risk potential donors and 18.2 percent among high-risk potential donors [7]. In one study of 55 living, related potential donors, the seroprevalence of HCV was 3.6 percent [8]. The reported seroprevalence of HCV infection among kidney transplant recipients is approximately 1.8 to 8 percent [9-13]. (See "Hepatitis C infection in kidney transplant candidates and recipients", section on 'Epidemiology'.)

TRANSMISSION OF HCV INFECTION BY KIDNEY TRANSPLANTATION — The risk of transmission of HCV infection associated with organ transplantation from an HCV-seropositive donor is significant [1,14-18]. In two reports, among recipients of organs from HCV-seropositive donors, 14 to 100 percent tested positive for anti-HCV antibodies after transplantation, and 57 to 96 percent tested positive for HCV RNA by polymerase chain reaction (PCR) [1,14]. The differences in the rate of transmission of HCV infection by HCV-seropositive donors could be related to the prevalence of HCV RNA among these donors.

Transplant recipients who receive organs from HCV-seropositive donors have a high risk of acquiring HCV infection and liver disease. Some studies have shown nearly universal transmission; in one report, 75 percent of the 29 recipients of organs (19 kidneys, 6 hearts, 4 livers) from 13 HCV-seropositive donors became anti-HCV or HCV RNA positive [1]. Others have not found quite as strong an association; only 13 of 46 (29 percent) kidney recipients of recombinant immunoblot assay (RIBA)-positive donors developed posttransplant liver disease in a second series, although HCV RNA was not checked [19]. Despite the latter study, concern over the risk of HCV transmission is great.

There are occasional reports of infection of recipients who received kidneys from donors who were negative for anti-HCV antibodies at the time of organ donation [20-22]. Some cases have been presumed due to acute infection of the donor just prior to kidney donation [20]. However, in some cases, samples of blood archived at the time of organ donation subsequently tested positive for HCV RNA [21-24].

In 2012, a kidney recipient was infected with HCV from a donor who was negative for both anti-HCV antibody and HCV RNA [24]. HCV genotype 2b was isolated from donor splenocytes procured at organ recovery, which could also be detected in the kidney recipient. Active injection drug use and recent plasma transfusion were identified as HCV-related risks.

OUTCOMES OF TRANSPLANTATION OF HCV-SEROPOSITIVE KIDNEY — Recipients of kidneys from HCV-seropositive donors have decreased survival compared with those who receive kidneys from non-HCV-seropositive donors but better survival compared with individuals who remain on the waiting list. Further studies are needed to investigate whether safe and effective direct-acting antivirals (DAAs) improve long-term clinical outcomes in recipients (both HCV RNA positive and negative) of HCV RNA-positive kidneys.

It should be noted that HCV seropositivity does not necessarily mean HCV RNA positivity, which indicates an active replicating infection. The viremic rate of HCV seropositivity ranges from 64 to 81 percent [6,25]. The results of the studies cited below must be interpreted accordingly, with the appreciation that up to one-third of HCV-seropositive donors might have been HCV RNA negative, indicating a resolved infection and therefore not being contagious.

Compared with HCV-seronegative kidneys — HCV-seronegative recipients of HCV-seropositive kidneys may have decreased survival compared with recipients of HCV-seronegative kidneys [26,27]. This was suggested by a study of 20,111 kidney transplants performed between 1994 and 1998, of which 484 kidneys were seropositive for HCV, and 165 HCV-seropositive kidneys were transplanted into HCV-seronegative recipients [27]. Among all recipients, the three-year survival was lower with HCV-seropositive donor kidneys than with HCV-seronegative donor kidneys (85 versus 93 percent, respectively); among those who received HCV-seropositive donor kidneys, there was a trend toward higher mortality among HCV-seronegative recipients.

Several studies have found that transplant patients who received organs from HCV-seropositive donors suffer from higher rates of liver disease than transplant patients who received organs from negative donors [14,28,29].

However, before HCV RNA testing became mandatory, HCV positivity was defined only by HCV seropositivity, without consideration of the patient's viremic status. Recipients of HCV-seropositive/RNA-negative kidneys appear to have the same graft and patient survival as recipients of HCV-seronegative kidneys [30].

Compared with waitlisted patients — There appears to be a survival advantage associated with receiving a kidney from an HCV-seropositive donor compared with remaining on the deceased-donor waitlist [15,27,31]. Among nearly 40,000 United States Renal Data System (USRDS) patients awaiting transplantation, transplantation with such a kidney was associated with improved survival versus remaining on a transplant waitlist (adjusted hazard ratio [HR] 0.76) [15]. These results were supported by another retrospective analysis of data from the national Organ Procurement and Transplant Network (OPTN) registry from 1994 to 2014 [31]. In this study, although five-year graft and patient survival were worse among HCV-seronegative recipients receiving HCV-seropositive kidneys compared with those receiving HCV-seronegative kidneys, the five-year patient survival from the time of waitlisting was superior when compared with waitlisted controls.

Among HCV-seropositive recipients — The effect of transplanting a kidney from an HCV-seropositive donor into an HCV-seropositive recipient is not completely clear. Most studies suggest that morbidity and mortality of HCV-seropositive recipients are not increased by the transplantation of kidneys from HCV-seropositive donors, despite the possibility of superinfection with HCV [25,32-37]. In one report that included 468 HCV-seropositive recipients, 5- and 10-year survival were not different between recipients of kidneys from HCV-seropositive and HCV-seronegative donors [34]. By contrast, other single-center as well as large registry studies have shown increased mortality, graft loss, and adverse liver outcomes associated with the transplantation of HCV-seropositive kidneys in HCV-seropositive recipients [38-41]. Differences in immunosuppression or superinfection with another genotype may explain the observed differences in outcomes in different studies. Furthermore, the studies cited above mostly tested only for anti-HCV antibodies but not for HCV RNA, which could further contribute to the observed differences. A case-control study of 205 RNA-negative kidneys transplanted between 2014 and 2016 found that graft survival of the HCV-seropositive/RNA-negative kidneys transplanted in mostly HCV-seropositive recipients was similar to that of HCV-seronegative kidneys [42].

The practice of using kidneys from HCV-seropositive donors for transplantation in HCV RNA-positive patients, a policy recommended by Kidney Disease: Improving Global Outcomes (KDIGO) 2018 guidelines, may offer the advantage of shorter waiting times for HCV RNA-positive patients that may outweigh the risk of increased mortality in these patients [37-39,43]. Shorter times on the waiting list may even improve the graft survival in these patients [37]. Furthermore, the availability of highly effective and well-tolerated DAAs offers the possibility of curing HCV infection immediately after transplantation, unlike interferon-based regimens, which were contraindicated after kidney transplantation due to the risk of graft loss. In addition, the use of HCV-seropositive/RNA-positive or -negative kidneys in HCV RNA-positive recipients will limit the risk of HCV transmission from these donors without loss of organs from the donor pool [44].

Among HCV-seronegative recipients — Transplantation of kidneys from anti-HCV antibody-positive/RNA-positive or RNA-unknown donors into HCV-seronegative recipients has traditionally not been performed, due to the high risk of HCV transmission (see 'Transmission of HCV infection by kidney transplantation' above). As a result, a substantial number of high-quality kidneys from deceased donors with anti-HCV antibody positivity have been discarded each year. However, administration of DAAs around the time of transplantation minimizes the risk of chronic HCV infection in the recipient and could therefore potentially reduce waiting times and increase the organ supply by making HCV-infected kidneys available for transplantation. Some transplant centers have adopted this approach, which may be even more relevant in the United States, where the opioid crisis has been associated with increased availability of HCV-infected kidneys from deceased donors [45]. However, several issues still need to be clarified before it can be universally accepted into clinical practice [46]. These include the exact DAA regimen and timing of therapy in relation to transplantation, management of a possible relapse, and assurance of reimbursement of or access to DAA therapy. Long-term outcomes are also uncertain.

The efficacy and safety of transplanting kidneys from HCV RNA-positive donors into HCV-seronegative recipients have been demonstrated in several uncontrolled trials [47-55]. Early trials found that the administration of elbasvir-grazoprevir for 12 weeks, either prophylactically (first dose given pretransplant) or upon detection of HCV RNA after transplantation, prevented chronic HCV infection in all recipients, and patients maintained overall good kidney allograft function without experiencing acute rejection [47-50]. Subsequent studies have reported successful transplantation with the use of other DAA regimens (eg, glecaprevir-pibrentasvir, sofosbuvir-velpatasvir, and sofosbuvir-ledipasvir) and with shorter durations of treatment (eg, four or eight weeks) with DAA therapy [51-55]. Observational data also suggest that kidney function and rates of rejection at one year and graft survival at five years are similar for recipients of HCV RNA-positive and HCV RNA-negative donor kidneys [56,57]. The results of these studies suggest that transplantation of HCV RNA-positive kidneys into HCV RNA-negative recipients, in conjunction with DAA therapy, could provide well-functioning allografts and cure HCV infection.

A delay in initiation of HCV therapy may be associated with an increased incidence of cytomegalovirus and BK polyomavirus viremia, de novo donor-specific antibodies (DSA), and fibrosing cholestatic hepatitis, which have been reported in some of these studies [52,53]. These unexpected consequences may be seen in the real-world setting, where it often may not be possible to initiate preemptive/early therapy, as access to DAA therapy may be complicated by issues with insurance approval or lack of resources. Additional studies are required to assess the optimal timing of DAA treatment, long-term graft and patient outcomes, and potential risks of transplanting HCV RNA-positive kidneys into HCV RNA-negative recipients.

IDENTIFICATION OF HCV INFECTION AMONG DONORS — Prior to transplantation, the potential donor should be evaluated for evidence of HCV infection by blood tests (including assays for anti-HCV antibody and HCV RNA according to the United Network for Organ Sharing [UNOS]) and for the risk of HCV infection based on environmental or lifestyle factors. The assessment of risk is required because neither the blood test for anti-HCV antibodies nor HCV RNA is optimal for the identification of HCV infection. The evaluation of the donor for HCV infection and/or risk is necessary because the risk of HCV transmission to an HCV-negative recipient is high following transplantation of a kidney from an HCV-positive donor, and the recipient must be informed of the risk. While potential recipients may still choose to accept the kidney from an infected donor, the risk of infection must be discussed prior to transplantation. (See 'Transmission of HCV infection by kidney transplantation' above.)

The approach to detection of HCV infection or risk of infection varies slightly between deceased and living donors.

Deceased donors — Most organ procurement organizations have a policy for testing all deceased organ donors for evidence of HCV infection [2,58]. In the United States, the screening of deceased donors is regulated by the Public Health Service (PHS) through the Organ Procurement and Transplantation Network (OPTN). The PHS issued guidelines for screening deceased donors for HCV in 2014 [59]. The screening process includes the identification of criteria that placed the potential donor at increased risk for HCV infection and blood tests that indicate previous or current HCV infection. If risk factors cannot be determined, the deceased potential donor should be considered high risk. (See "Evaluation of the potential deceased organ donor (adult)", section on 'Evaluation of donor suitability'.)

The identification of increased-risk criteria – This is done though confidential interviews with next of kin, life partner, cohabitant, or primary treating clinician. High-risk criteria are listed in the table (table 1).

Blood tests – All deceased donors should be tested for the presence of anti-HCV antibodies and for HCV RNA prior to procurement of the kidney. One can determine the presence of HCV RNA using a variety of tests, which we collectively refer to here as nucleic acid testing (NAT); this terminology is consistent with that used by the Centers for Disease Control and Prevention (CDC) [60]. (See "Evaluation of the potential deceased organ donor (adult)", section on 'Infectious disease testing'.)

The antibody test should be made available prior to transplantation. Although the HCV RNA result may not be known prior to transplantation, data may be subsequently used to guide treatment of the recipient. If donor blood is hemodiluted (as among deceased donors who received blood products or crystalloid prior to death), the donor should be considered high risk since the assays are not reliable.

The organ procurement organization is advised to archive blood samples for at least 10 years. The organ procurement organization should notify both the OPTN and transplant center regarding the identification of increased-risk criteria or evidence of infection.

Both antibody and HCV RNA testing are important for evaluation. The antibody or enzyme-linked immunosorbent assay (ELISA) test for HCV only detects evidence of prior infection. This test does not indicate whether active transmissible infection is present, which is indicated by a positive HCV RNA test. False-positive ELISA tests are also possible, but the third-generation anti-HCV tests in donor screening are more sensitive and specific than earlier tests and minimize the rate of false-positive results [61].

However, the ELISA may not identify donors who were recently infected (ie, within eight weeks prior to death), since it takes at least eight weeks for detectable antibodies to develop [12]. HCV RNA testing closes the window of a false-negative anti-HCV result in the early phase of HCV infection. HCV RNA testing is mandatory in the United States but generally does not yield a result quickly enough to be useful for the evaluation of deceased donors with an unknown status of HCV infection [62]. Furthermore, a single negative RNA test may not exclude the possibility of transmitting HCV [63,64]. HCV RNA testing can be falsely negative in infected, deceased individuals who received blood products or crystalloid just prior to death, or who became infected just before death, since HCV first replicates in target cells (ie, hepatocytes) before it appears in blood [59].

If a deceased donor is identified as being at increased risk for or known to have HCV infection, the transplant center team should include this information in discussion of risk with the transplant candidate or medical decision maker. However, HCV-infected donors are not excluded from donation. (See 'Approach to the use of kidneys from donors with HCV infection' below.)

Living donors — The screening of living potential donors is closely regulated by PHS/OPTN in the United States. (See "Kidney transplantation in adults: Evaluation of the living kidney donor candidate", section on 'Medical evaluation'.)

As per the 2014 PHS guidelines, all living-donor candidates should be interviewed regarding high-risk criteria. (See 'Deceased donors' above.)

All living-donor candidates should be tested for anti-HCV antibodies and for HCV RNA. The tests should be performed at least within 28 days prior to surgery and as close to the time of surgery as possible. If an HCV RNA-positive donor is identified, the transplant center should be notified and risk discussed with the potential recipient. If a kidney from an HCV RNA-positive donor is used, OPTN should be notified.

APPROACH TO THE USE OF KIDNEYS FROM DONORS WITH HCV INFECTION

Deceased donors with HCV seropositivity — The decision to accept a kidney from a donor that is at high risk for or has evidence of HCV infection depends on many recipient-related variables. These variables include recipient HCV status, the anticipated time on the waiting list, and morbidity conferred by dialysis.

Transplantation of an HCV-seropositive/RNA–negative organ might be considered a safe approach since the risk of transmission of HCV is very low [63,65,66]. With the availability of direct-acting antiviral (DAA) therapy that can be used to treat a new infection, the use of such organs has been shown to increase the donor pool by 48 kidneys annually in the United States [67], and recipient willingness to accept such an organ is higher [68].

The 2018 Kidney Disease: Improving Global Outcomes (KDIGO) guidelines recommend that kidneys from HCV-seropositive and RNA-positive donors should only be given to HCV RNA-positive recipients [69]. However, emerging data demonstrating the safety of transplanting kidneys from HCV RNA-positive donors into HCV RNA-negative recipients with early or pre-emptive DAA therapy [47-53,70-72] support the use of kidneys from high-risk deceased donors in uninfected patients when medical need is urgent and the benefits appear to outweigh the risks. In all such cases, the recipient should receive specific counseling, be well informed, and participate in decision making. (See 'Among HCV-seronegative recipients' above.)

The presence of HCV-related kidney disease among HCV RNA-positive donors is generally excluded by an evaluation of kidney function, urinalysis for detection of hematuria, and assessment of proteinuria. Although clinically silent immune-complex glomerulonephritis has been detected in patients undergoing liver transplantation for HCV-induced cirrhosis [73], we are not aware of any report suggesting clinically silent glomerular disease in HCV RNA-positive subjects in the absence of any liver or known kidney disease (ie, in autopsies), nor in any biopsy studies of HCV-positive donor kidneys at the time of transplantation. Among deceased potential donors, pretransplant (preimplantation) biopsy of deceased-donor kidneys can be used to evaluate the quality of the HCV RNA-positive donor kidney and to exclude pre-existing kidney disease. However, it should be kept in mind that frozen sections are not reliable for assessment of mesangial cellularity, glomerular capillary wall thickening, and microthrombi. Fixation of the biopsy specimen in formalin followed by paraffin sectioning overcomes the limitations of frozen sections but typically takes four to five hours. The benefits of biopsy-guided decision making must therefore be balanced against the risks emanating from increased cold ischemic time.

Living donors with HCV infection — If an individual with chronic HCV infection is planning on donating a kidney, we suggest they undergo antiviral treatment prior to transplantation. The vast majority of HCV infections can be successfully treated with short (8 to 12 week) DAA regimens. Successful antiviral treatment results in sustained virologic response (SVR), at 12 weeks, which is considered a marker for cure of HCV infection [74]. Thus, this approach minimizes the risk of HCV transmission to HCV RNA-negative recipients or superinfection with another genotype in HCV RNA-positive recipients.

The safety of transplanting a kidney from an HCV-seropositive living donor who has undergone successful antiviral treatment into an HCV-negative recipient or into an HCV RNA-positive recipient with a different HCV genotype is unknown, as data are limited [75]. However, extrapolating from data on transplantation of anti-HCV antibody-positive/RNA-negative, deceased-donor organs into HCV-negative recipients, the risk seems to be low [47-50,53,65,66]. (See 'Among HCV-seronegative recipients' above.)

There remains a small chance for transmission of HCV to an HCV-negative recipient with transplantation of a kidney from a treated HCV-seropositive donor. Although rare, late relapses (ie, SVR at week 12 but detectable HCV RNA at week 24) have been reported [76]. Additionally, there could be false-negative HCV RNA testing of the donor, especially after a short follow-up (ie, 12 weeks). "Occult hepatitis C infection" is a theoretical possibility, but it may have no clinical relevance, and data on the possibility of transmission are lacking [13].

If HCV is transmitted through a living donor kidney transplantation, the recipient should undergo antiviral therapy posttransplant. (See "Hepatitis C infection in kidney transplant candidates and recipients", section on 'Antiviral treatment'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Hepatitis C infection in solid organ transplant candidates and recipients".)

SUMMARY AND RECOMMENDATIONS

Transplantation of a kidney from a hepatitis C virus (HCV) RNA-positive kidney donor causes HCV infection in the recipient. HCV infection has been associated with increased morbidity and possibly mortality in kidney transplant recipients. (See 'Introduction' above and 'Outcomes of transplantation of HCV-seropositive kidney' above.)

Although recipients of kidneys from HCV-seropositive/RNA-positive donors have worse outcomes compared with those who receive kidneys from HCV-seronegative donors, they have better outcomes compared with individuals who remain on the kidney transplant waiting list. (See 'Outcomes of transplantation of HCV-seropositive kidney' above.)

Using kidneys from HCV-seropositive donors for transplantation in HCV-seropositive/RNA-positive patients may be a safe approach in the long-term as the risk of increased mortality is likely overweighed by the survival benefit conferred by shorter waiting times. In addition, the availability of highly effective direct-acting antivirals (DAAs) may cure HCV infection after transplantation. (See 'Among HCV-seropositive recipients' above.)

Prior to transplantation, the potential donor should be evaluated for evidence of HCV infection and for the risk of HCV infection based on environmental or lifestyle factors. The assessment of risk is required because the blood tests may be falsely negative in some donors. The potential recipient must be informed of the donor HCV status and the potential risk of infection prior to transplantation. (See 'Identification of HCV infection among donors' above.)

Most organ procurement organizations have a policy for testing all deceased and living potential organ donors for evidence of HCV infection. In the United States, there are mandated guidelines for screening deceased donors for HCV risk. If risk factors cannot be determined, the deceased potential donor should be considered high risk. (See 'Identification of HCV infection among donors' above.)

The 2018 Kidney Disease: Improving Global Outcomes (KDIGO) guidelines recommend that kidneys from HCV-seropositive/RNA-positive deceased donors should only be given to HCV RNA-positive recipients. However, the use of HCV RNA-positive kidneys in HCV RNA-negative recipients followed by early DAA therapy has been increasingly described in promising pilot trials and reports of single-center experiences. Until larger trials clearly define potential risks and long-term outcomes, this practice should be considered investigational with thorough informed consent processes in place.

In cases of HCV RNA-positive living donors for HCV RNA-positive recipients, the risks of delaying transplantation for the antiviral treatment should be weighed against the benefits. (See 'Approach to the use of kidneys from donors with HCV infection' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Svetlozar Natov, MD, and Brian JG Pereira, MD, who contributed to earlier versions of this topic review.

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