Hepatitis C positive donor to negative recipient kidney transplantation: A real world
experience
Running Head: Hepatitis C positive transplants
Authors:
Nicholas Jandovitz PharmD1,3, Vinay Nair DO2
, Elliot Grodstein MD3
, Ernesto Molmenti MD3,
Ahmed Fahmy MD3
, Mersema Abate MD2
, Madhu Bhaskaran MD2
, Lewis Teperman MD3
1. Department of Pharmacy, North Shore University Hospital – Northwell Health, Manhasset,
NY
2. Department of Medicine, Donald and Barbara Zucker School of Medicine at
Hofstra/Northwell, Manhasset, NY
3. Department of Surgery, Donald and Barbara Zucker School of Medicine at
Hofstra/Northwell, Manhasset, NY
Corresponding Author:
Nicholas Jandovitz
North Shore University Hospital
400 Community Drive
Manhasset, NY 11030
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[email protected]
Authorship:
Nicholas Jandovitz: participated in research design, writing of the paper, performance of the
research, and data analysis
Vinay Nair: participated in research design, writing of the paper, performance of the
research, and data analysis
Elliot Grodstein: participated in writing of the paper, performance of the research, and data
analysis
Ernesto Molmenti: participated in writing of the paper
Ahmed Fahmy: participated in writing of the paper
Mersema Abate: participated in writing of the paper
Madhu Bhaskaran: participated in writing of the paper
Lewis Teperman: participated in research design, writing of the paper, performance of the
research, and data analysis
Disclosure: The authors declare no conflicts of interest
Funding: No funding was received for this work
Abbreviations:
DAA, direct acting antiviral
GFR, glomerular filtration rate
HCV, hepatitis C virus
KDPI, Kidney Donor Profile Index
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NAT, nucleic acid testing
OPTN, Organ Procurement and Transplantation Network
SVR, sustained virologic response
SVR12, sustained virologic response at 12 weeks
Abstract
Background: Several studies have shown that transplanting a hepatitis C virus (HCV)
negative recipients with a HCV positive donor is feasible in a research setting. In February
2018 we began transplanting HCV negative recipients with HCV positive donors as standard
of care.
Methods: All patients, except those with previously cured HCV and those with cirrhosis,
were consented for HCV NAT positive donor kidneys. After transplantation, patients were
tested for HCV RNA until viremic. A direct acting antiviral (DAA) agent was prescribed based
on genotype and insurance approval. Sustained virologic response (SVR) at weeks 4 and 12
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were recorded. Renal function and death censored graft survival at one year were evaluated
and compared to recipients of HCV NAT negative kidneys.
Results: 25 HCV NAT positive donor kidney transplants from February to October 2018
were performed. All patients received basiliximab and maintenance with tacrolimus,
mycophenolate mofetil and prednisone. Median time from viremia to start of DAA was 13 (8-
22) days. The most common genotype was 1a (60%), followed by 3a (28%). The most
commonly prescribed DAA was ledipasvir/sofosbuvir (56%) followed by
velpatasvir/sofosbuvir (32%) then glecaprevir/pibrentasvir (12%). All patients achieved initial
SVR12, except one. One patient had a mixed genotype infection requiring retreatment to
achieve SVR12. Death censored graft survival was 96%. Recipients of HCV NAT positive
organs compared to HCV NAT negative organs received younger donors (mean 35±8.9 vs
45.1±15.7 years; p<0.01) and spent less time on the waitlist (median 479 (93–582) vs 1808
(567–2263) days; p=0.02).
Conclusion: HCV NAT negative recipients can be safely and successfully transplanted with
HCV NAT positive donor kidneys outside of a research protocol. Access to DAA and timely
administration of therapy is important and an insurance approval process within the
transplant center can be beneficial to patients. A case of mixed genotype infection was
presented, and though not as common, can be successfully treated. HCV organs can
expand the organ pool and should no longer be considered experimental. The use of these
organs in HCV negative recipient’s decreases waiting time, have excellent outcomes and
should be considered standard of care.
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Keywords: Kidney Transplant, Hepatitis C
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Introduction:
Kidney transplantation remains the preferred treatment for end stage renal disease1
However, there is a significant disparity between organ supply and demand. This has led to
increased waiting times for a kidney transplant, in many areas of the country exceeding 5
years. In the United States we have seen an increase in the incidence of hepatitis C virus
(HCV) infection2, 3. The increase in HCV has been associated with the nation’s opioid crisis3
According to the CDC from 2004 – 2014, HCV increased by more than 400% among people
aged 18-29 and 325% among people aged 30-392
Every year about 500 kidneys are discarded due to HCV infection4
. Many of these
organs are from young donors. The opioid epidemic in the United States has led to an
increase of deaths in young adults and increase of acute HCV incidence18. Maximizing the
use of these discarded organs would increase the donor pool4, 5. The emergence of the
direct acting antivirals (DAA) has significantly changed the way HCV is treated compared to
the days of interferon. PEGylated interferon has low sustained virologic response (SVR) and
unfavorable side effects, including kidney injury and graft loss amongst kidney transplant
recipients6, 7. The DAA’s have reported cure rates of greater than 95% in the literature8
Traditionally, HCV positive organs have been transplanted into HCV positive recipient’s, with
good outcomes9
Previous studies under research protocols, have seen success using the DAA’s in
HCV negative recipients of HCV positive donors. The original THINKER (Transplanting
Hepatitis C kidneys Into Negative KidnEy Recipients) trial evaluated 6 month outcomes for
10 HCV negative recipients of HCV positive kidneys who were all HCV genotype 1 donors.
All donors were tested for HCV through serologic and nucleic acid testing (NAT). They saw
100% HCV cure rates defined as an undetectable HCV RNA at 12 weeks post treatment
(SVR12) with a DAA and experienced good allograft function4
. The authors then explored 12
month outcomes of the original recipients plus an additional 10 HCV negative recipients of
HCV positive kidneys (genotype 1). The patients were treated with a DAA
(elbasvir/grazoprevir) for 12 weeks and resulted in 100% SVR12 for all recipients with
excellent kidney allograft function at 12 months and minimal side effects10. The EXPANDER
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(Exploring Renal Transplants Using Hepatitis C Infected Donors for HCV Negative
Recipients) trial transplanted 10 HCV negative recipients of HCV positive donors with
genotypes 1 or 3. All patients achieved SVR12 after 12 weeks of therapy with a DAA
(elbasvir/grazoprevir plus sofosbuvir for non-genotype 1)11
.
Outside of a research protocol, there are challenges patients face in terms of
affordability of the DAA’s if they were to receive a HCV positive kidney. Two recent studies
evaluated their experience of transplanting HCV NAT positive donors to HCV negative
recipients with positive outcomes 12,13. Kapila et al, described viral outcomes at SVR12 in
kidney, liver and heart transplant patients outside a research protocol. All patients were not
eligible for SVR12 viral clearance at the conclusion of the study but did prove that DAA
therapy was effective in clearing HCV in patients receiving HCV NAT positive organs.
Molnar et al, reported on safety and viral clearance at SVR12 in a real world experience in
kidney transplant recipients. All patients achieved 100% viral clearance. GFR was stable at
end of treatment and 12 weeks after therapy; majority of recipients did not experience and
rises in liver function tests. We report our real world experience of HCV positive transplants
as standard of care in our institution to better understand the feasibility and consequences of
accepting HCV NAT positive organs for HCV NAT negative recipients. Our study also
explores the unique insurance approval process to aid our patients in obtaining DAA therapy
and describes a challenging case of mixed genotype infection in a HCV viremic donor.
Materials and Methods:
This was a retrospective, single center study that evaluated outcomes of 25 HCV
NAT positive deceased donor kidneys transplanted into HCV NAT negative adult transplant
recipients from February to October 2018. This study was reviewed by Northwell IRB. All
patients received standard induction with basiliximab and maintenance immunosuppression
with tacrolimus, mycophenolate mofetil and prednisone. During evaluation or annual follow
up visit pre-transplant, patients were provided with an informed consent form to receive HCV
NAT positive organs. The transplant coordinator and physician review the risk and benefits,
success rates and medication regimen with the patient if they were an acceptable candidate
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for an HCV NAT positive kidney. Post-transplant, HCV RNA PCR and genotype were sent
on post-operative day 4. Once the HCV RNA PCR and genotype were detected a
prescription for a DAA was sent for insurance authorization and approval. In the unlikely
event that a DAA would not be available to the patient due to insurance rejection, our
institution agreed to supply the appropriate DAA without cost to the patient. Treatment was
initiated when the patients insurance approved the DAA therapy. All DAA therapy was
started after the patient was discharged from the hospital. A comparison of donor and
waitlist characteristics of the first 25 HCV NAT positive transplant recipients were compared
to the first 25 HCV NAT negative transplant recipients during the same study time period.
Inclusion criteria included kidney transplant patients greater than or equal to 18 years
old who consented to receiving HCV NAT positive kidneys. Patients had to be previously
HCV NAT negative and not treated for HCV in the past. Patients were excluded if they had
cirrhosis, abnormal liver function tests, or were hepatitis B surface antigen positive due to
the black box reactivation risks associated with DAA treatment.
The primary outcome was HCV cure at SVR 12, defined as an undetectable HCV
RNA PCR at 12 weeks post treatment completion. The quantity of HCV RNA in the serum
was determined at our hospital laboratory department using the Abbott M2000 machine. The
lower limit of quantification was 12 IU/mL. Secondary outcomes included death censored
graft survival, renal function at end of treatment and SVR12, incidence of rejection, adverse
effects to HCV treatment with DAA, and any clinical liver disease. Death censored graft
survival was assessed at 1 year. Adverse effects of DAA therapy was reported by patients.
Renal function was assessed as serum creatinine in mg/dL and incidence of rejection was
defined by the Banff criteria. Clinical liver disease was assessed through monitoring of liver
function tests for abnormalities.
Statistical analysis was performed for the comparison group analysis using Students
T-test for continuous variables and Fisher exact test for nonparametric categorical variables.
We identified donor characteristics using the Organ Procurement and Transplantation
Network (OPTN) registry. The OPTN provides data on all donors, waitlisted candidates and
transplant recipients in the United States. We compared between HCV positive donor group
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and the HCV negative donor group: donor age in years, terminal creatinine, body mass
index, Kidney Donor Profile Index (KDPI), PHS high risk, waitlist days, cardiac death, type of
donor (local vs import), and death censored graft survival.
Results:
A total of 25 HCV NAT positive to HCV NAT negative kidney transplants were
performed between February and October 2018. Patient demographics are described in
Table 1. The majority of the patients were male (n=19, 76%) and the average recipient age
was 57.7 ± 10.4 years. The average donor age was 36.5 ± 10.4 years. KDPI was 49 (38-66).
The two major HCV genotypes were 1a (n=15, 60%) and 3a (n=7, 28%). It took an average
of 7.1 ± 3.7 days for a patient to have a detectable HCV RNA PCR. After HCV was detected
and a genotype was determined, therapy was started at a median 13 (8-22) days, all
dependent on patients insurance and authorization process. Insurance approval for DAA
therapy was obtained in a median of 2 (1-5.5) days. All 25 patients received a DAA for
treatment (100%) and 24 patients were covered under insurance (96%). One patient was
covered by the hospital due to insurance refusal to cover a DAA. The majority of patients
were treated with ledipasvir/sofosbuvir (n=14, 56%) and velpatasvir/sofosbuvir (n=8, 32%).
All patients had a response at 4 weeks after therapy initiation. At the end of 12 weeks
of therapy all patients had an undetectable viral load, which continued to be undetectable at
SVR 4 and 12, defined as weeks after treatment completed, except for one patient. Median
tacrolimus concentration at SVR4 and SVR12 were 8.1 ng/mL (IQR 6.7-8.7) and 7.8 ng/mL
(IQR 6.4-8.9) respectively. Renal function, defined as serum creatinine was stable from end
of treatment to SVR12 at a median 1.25 mg/dL (1.05 – 1.71) and 1.25 mg/dL (0.95 – 1.57)
respectively. Death censored graft survival was 96% with no rejection episodes. One patient
lost their graft due to a renal artery aneurysm 55 days post-transplant. There were no
reported adverse effects from HCV treatments in any patient. Tacrolimus concentrations
were not adversely affected. Liver function tests at SVR12 remained normal, median AST 25
(15-33) U/L and median ALT 28 (12-36) U/L.
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One patient had a detectable viral load at SVR12 and was discovered to have a
mixed genotype infection. The patient was initially treated for a HCV genotype 1a infection
with ledipasvir/sofosbuvir for 12 weeks. The patient had a detectable viral load 4 weeks after
therapy initiation at 25 IU/mL and undetectable at end of treatment. SVR12 viral load was
detectable at 41,725,881 IU/mL. For this patient only, donor serum and HCV genotype were
checked and a 2b genotype was identified suggesting. a missed mixed genotype infection of
1a and 2b. The patient was treated with a pan genotypic agent
(sofosbuvir/velpatasvir/voxilaprevir) as per AASLD/IDSA 2019 guidelines14. The patient
completed 12 weeks of therapy and achieved HCV cure at SVR12 with no adverse effects,
abnormalities is in his liver function tests, or rejection.
HCV NAT positive donor kidney recipients were compared to the first 25 HCV NAT
negative kidney recipients during the same time period. This is described in Table 2.
Recipients who received a HCV NAT positive kidney had statistically significant younger
donors, average age 35 ± 8.9 vs 45.1 ± 15.7 years (p < 0.01). Days on the wait list were
significantly reduced in the HCV NAT positive group, median days 479 (93 – 1582) vs 1808
(567 – 2263), p = 0.02. There were also less local kidneys and more PHS increased risk
kidneys accepted for the HCV NAT positive vs HCV NAT negative group (local 4 (13%) vs
20 (80%), p < 0.01 and PHS high risk 20 (80%) vs 3 (12%), p < 0.01). No differences were
found between the groups in terms of terminal creatinine, diabetes, body mass index and
KDPI. There was no difference in death censored graft survival in the two groups (96% vs
92%; p=0.56).
Discussion:
In this report of a single center, real world experience we evaluated transplantation
from HCV NAT positive donors to 25 HCV NAT negative kidney transplant recipients. DAA’s
were utilized post-transplant after insurance approval. All patients were treated for 12 weeks
with their respective DAA and HCV cure was achieved in 96% of patients. Tacrolimus
concentrations in our population were appropriate not adversely affected by the DAA’s.
Certain DAA’s may have an interaction with tacrolimus, a calcineurin inhibitor, resulting in
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increased tacrolimus concentrations, such as elbasvir/grazoprevir and
glecaprevir/pibrentasvir14. All recipients had excellent graft function. There were no reported
adverse effects from DAA’s used by the patients and no rejections occurred to date. What
was interesting about our population was more than a quarter of our patients had HCV
genotype 3 infections. This genotype is the most difficult to treat out of all the 6 major
clinical HCV genotypes and leads to higher rates of steatosis, cirrhosis and hepatocellular
carcinoma15. Historically, HCV genotype 3 agents such as teleprevir and boceprevir have
not shown significant benefit at achieving SVR12. The newer DAA’s including
sofosbuvir/velpatasvir and glecaprevir/pibrentasvir have shown excellent cure rates
comparable to the other genotypes16-18. We utilized these newer DAA’s and observed 100%
HCV clearance and cure in our genotype 3 recipients. Mixed genotype expression can be
seen in 5% - 25.3% of patients from previous studies19-22. Our mixed genotype infection was
initially treated with ledipasvir/sofosbuvir for genotype 1a. Repeat testing of the donor and
recipient revealed genotype 2b and required treatment with
sofosbuvir/velpatasvir/voxilaprevir because as ledipasvir/sofosbuvir is not active against
genotype 2b.
Previous studies by Reese, et al and Durand, et al were under a research protocol
and showed excellent outcomes where all patients achieved HCV cure. All of these patients
had access to DAA, regardless of insurance approval, and were started immediately post￾transplant or a day before transplant10, 11. In practice it is not feasible to obtain the DAA’s
pre-transplant or even immediately post-transplant because most institutions do not have
them on formulary due to the high costs associated with these agents12, 13. Previous studies
by Molnar, et al and Kapila, et al also showed favorable outcomes in transplanting HCV
positive organs into HCV negative recipients. We explored a real world use of treating HCV
NAT negative kidney transplant recipients of a HCV NAT positive donors with a DAA utilizing
a unique, multidisciplinary insurance approval process. We utilized a transplant pharmacist
and our outpatient pharmacy with pharmacy practice coordinators to assist the transplant
physicians and surgeons with obtaining these vital medications. The institution covered one
patient for treatment because insurance approval was unable to be obtained.
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Medication access to DAA therapy can be difficult for patients and transplant
programs to obtain. We have a unique process to obtain insurance approval for DAA therapy
for transplant patients receiving HCV NAT positive organs. All patients who consent to an
HCV NAT positive kidney transplant have their prescription insurance reviewed by a
pharmacy practice coordinator who specialize in medication access and approval. The
pharmacy practice coordinator has a goal turnaround time to achieve approval of 48 hours.
Before the patient receives the medication the transplant pharmacist reviews the medication
with the patient and educates on timing of dosing, duration of therapy, blood draw for
monitoring HCV viral load, and adverse effects to be aware of when starting DAA therapy.
This has been a successful process for our transplant center and as noted before, 96%
(24/25 patients) received approval for DAA therapy through the pharmacy process and the
institution covered one patient who could not obtain DAA approval through insurance. All 25
patients were able to receive appropriate DAA therapy with an average therapy initiation of
15.8 ± 10.4 days and all patients achieved viral clearance.
The opioid epidemic in the United States has led to an increase in HCV across the
population23, 24. In 1999, there was a rise in prescription opioid overdose deaths and in 2010
we saw a second rise in heroin overdose deaths. A third rise in opioid related deaths
occurred in 2013 to present and this coincided with the increase in incidence of acute HCV
infection. The CDC reported an increase of HCV by 400% in people aged 18-29 and an
increase in HCV by 325% in people aged 30-3923. This increase in HCV has led to a
potential increase in access to younger a younger donor population in the United States. In
our comparison between the HCV NAT positive and HCV NAT negative donor groups we
found encouraging results with patients needing to wait on the list a shorter time when
accepting a HCV NAT positive kidney. Based on data from the United Network of Organ
Sharing an average of about 7,000 candidates die on the waitlist every year25. A candidate
consenting to receive a HCV NAT positive organ will reduce the risk of a patient dying on the
waitlist. The patients also received younger donor grafts which have been correlated with
better outcomes post-transplant26-28
.
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This study had some limitations. This was a single center, real world experience. We
utilized a non-lymphocyte depleting induction agent, while other centers may use a
lymphocyte depleting agent. Further studies are needed to confirm these results with other
immunosuppressive regimens.
In conclusion, this study adds to previous literature that HCV NAT positive donor
kidney transplant into HCV NAT negative recipients is safe and successful. The unique
insurance approval process is something that other centers could adopt. The DAA have
changed the landscape of hepatology and now solid organ transplant by expanding the
donor pool, decreasing wait times and having younger organs available to our patients.
Transplanting HCV NAT positive donors into HCV NAT negative recipients should be
standard of care in kidney transplantation.
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Table 1: Recipient Baseline Demographics
N = 25
Age, years (mean, SD)
Recipient 57.7 ± 10.4
Donor 35 ± 8.9
Male (%) 19 (76)
Blood Type
A 7 (28)
B 3 (12)
AB 6 (24)
O 9 (36)
KDPI, median (IQR) 49 (38 – 66)
Dialysis before 24 (96)
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transplant
PHS High Risk 20 (80)
CMV serostatus
D+/R- 4 (16)
D+/R+ or D-/R+ 18 (72)
D-/R- 3 (12)
DGF 16 (64)
Comorbidity
Diabetes 15 (60)
Hypertension 18 (72)
IgA nephropathy 2 (8)
Lupus 1 (4)
*All data presented as n (%) unless otherwise noted
CMV – cytomegalovirus; DGF – delayed graft function; KDPI – kidney
donor profile index;
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Table 2: Comparison HCV NAT positive to HCV NAT negative cohort
HCV (+) Donor
(n=25)
HCV (-) Donor
(n=25)
P-value
Donor Age, Years (mean, SD) 35 ± 8.9 45.1 ± 15.7 < 0.01
Donor Male Gender 18 (72) 13 (52) 0.14
Terminal Cr (mg/dL) [median,
IQR]
1 (0.8 – 1.2) 0.69 (0.5 – 1.1) 0.58
Donor Diabetes 0 (0) 2 (8) 0.49
Donor BMI (median, IQR) 25.3 (22 – 30) 28.7 (23 – 31) 0.59
KDPI (median, IQR) 49 (38 – 66) 59 (35 – 74) 0.57
PHS High Risk 20 (80) 3 (12) < 0.01
Days wait list (median, IQR) 479 (93 – 1582) 1808 (567 – 2263) 0.02
Local 4 (13) 20 (80) < 0.01
DCD 1 (3) 6 (24) 0.1
Death Censored Graft
Survival
24 (96) 23 (92) 0.56
*All data presented as n (%) unless otherwise noted
Cr – creatinine; DCD – donor after cardiac death; KDPI – kidney donor profile index; PHS – public health service
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