Human Immunodeficiency Virus (HIV) has been a major global health problem for longer than three decades now. With the advent of HAART or cART (combined anti retroviral therapy) and effective prophylaxis against opportunistic infections survival has increased markedly. Hence morbidity from other diseases like end stage liver disease, renal and heart disease is increasing rapidly. Presence of HIV infection used to be regarded as a contraindication for renal transplant for fear of exacerbating an already immunocompromised state further with immunosuppressants, use of limited supply of donor organs in individuals with unknown outcome and also the risk of spread of infection to health care staff. With HIV related kidney disease becoming a relatively common cause of ESRD requiring dialysis and its rapid progression to AIDS and mortality renal transplantation was attempted at various centers across the globe in HIV affected patients with good success rates allaying initial fears. Our experience in kidney transplantation of HIV patients are enthusiastic with very good patient and graft survival at par with nonHIV patients. HIV infection is now no longer a contraindication to renal transplantation and is being considered standard therapy. This review examines open questions in kidney transplantation in patients infected with HIV and clinical strategies that have resulted in good outcomes. It also discusses the clinical concerns associated with the treatment of renal transplant recipients with HIV.

1. RenaltransplantationinHIVpatients

2. Review Article
Renal transplantation in HIV patients
D.K. Agarwal a,
*, Aashish Sharma b
, Anupam Bahl c
, Nalin Nag d
, S.N. Mehta e
a
Senior Consultant, Department of Nephrology, Indraprastha Apollo Hospital, New Delhi, India
b
Associate Consultant, Department of Nephrology, Indraprastha Apollo Hospital, New Delhi, India
c
Registrar, Department of Nephrology, Indraprastha Apollo Hospital, New Delhi, India
d
Senior Consultant Internal Medicine, Indraprastha Apollo Hospital, New Delhi, India
e
Senior Consultant Transplant Surgery, Indraprastha Apollo Hospital, New Delhi, India
a r t i c l e i n f o
Article history:
Received 4 January 2013
Accepted 15 January 2013
Available online 24 January 2013
Keywords:
Human Immunodeficiency Virus
(HIV)
HAART
CART (Combined Anti Retroviral
Therapy)
HIV-related nephropathy (HIVAN)
a b s t r a c t
Human Immunodeficiency Virus (HIV) has been a major global health problem for longer
than three decades now. With the advent of HAART or cART (combined anti retroviral
therapy) and effective prophylaxis against opportunistic infections survival has increased
markedly. Hence morbidity from other diseases like end stage liver disease, renal and heart
disease is increasing rapidly. Presence of HIV infection used to be regarded as a contra-
indication for renal transplant for fear of exacerbating an already immunocompromised
state further with immunosuppressants, use of limited supply of donor organs in in-
dividuals with unknown outcome and also the risk of spread of infection to health care
staff. With HIV related kidney disease becoming a relatively common cause of ESRD
requiring dialysis and its rapid progression to AIDS and mortality renal transplantation
was attempted at various centers across the globe in HIV affected patients with good
success rates allaying initial fears.
Our experience in kidney transplantation of HIV patients are enthusiastic with very
good patient and graft survival at par with nonHIV patients. HIV infection is now no longer
a contraindication to renal transplantation and is being considered standard therapy. This
review examines open questions in kidney transplantation in patients infected with HIV
and clinical strategies that have resulted in good outcomes. It also discusses the clinical
concerns associated with the treatment of renal transplant recipients with HIV.
Copyright ª 2013, Indraprastha Medical Corporation Ltd. All rights reserved.
1. Introduction
With the introduction of anti retroviral therapy, prognosis of
HIV infection has been improved. While the frequency of AIDS
defining events has decreased as a cause of deathemortality
from nonAIDS related events including end stage renal dis-
ease has increased.
Renal diseases directly related to HIV infection include
HIV-related nephropathy (HIVAN), immune-complex dis-
eases and thrombotic microangiopathy. Most aggressive
HIV related renal disease is HIVAN. It is currently the third
most common etiology of ESRD among African Americans
after diabetes and hypertension in the 20e64 age group.1
Co-infection HBV or HCV is also common. Almost 1%
* Corresponding author. B-109, Alpha-1, Greater Noida, Gautam Budh Nagar, U.P. 201310, India. Tel.: þ91 120 2326068, þ91 9811200113
(mobile); fax: þ91 120 2320052.
E-mail address: dmas100@gmail.com (D.K. Agarwal).
Available online at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/apme
a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 5 0 e5 6
0976-0016/$ e see front matter Copyright ª 2013, Indraprastha Medical Corporation Ltd. All rights reserved.
http://dx.doi.org/10.1016/j.apme.2013.01.008

3. patients with ESRD in US and Europe are estimated to have
HIV.
Widespread use of cART has reduced the incidence of HIV
related renal disease though renal disease per se continues
to increase among this population.2
Potential explanations
include inadequate HAART, drug toxicity, increased survival
rates causing an increase in elderly population and chronic
viral co-infections. Nephrotoxic effects could be induced or
exacerbated by antiretroviral medications like indinavir,
atazanavir, ritonavir or infection prophylaxis drugs like tri-
methoprim sulfamethoxazole. Calcineurin inhibitors (CNIs)
like cyclosporine and tacrolimus used in immunosuppressive
therapy are nephrotoxic and their effects can be exacerbated
by cytochrome P450 inhibition by HAART agents like protease
inhibitors (PIs) and medications commonly used for fungal
prophylaxis like fluconazole. In addition some HAART
agents can induce diabetes mellitus, hypertension and
hyperlipidemia all of which are risk factors for ESRD. Man-
agement of coinfection with hepatitis C virus is another
challenge. Treatment by a team of specialists is critically
important in HIV infected renal transplant patients.
With HAART therapy now survival in CKD Stage V patients
on dialysis with high CD4þ T cell counts is similar to those
without HIV. Renal transplantation has also been found safe
and effective in patients with HIV.
In our study of HIV positive patients undergoing renal
transplant we found HIVAN to be the cause of renal failure in
33.3% of cases. Other causes were hypertensive nephro-
sclerosis (16.6%), analgesic nephropathy (16.6%) and CGN
(16.6%) and CIN (16.6%).
2. Early outcomes of transplantation
The first prospective study performed demonstrated a similar
1 year patient and graft survival rates in patients with and
without HIV.3
However more than half the patients suffered
acute rejection requiring aggressive treatment with anti lym-
phocyte globulin. Subsequent studies confirmed that patient
and graft survival rates are similar though rejection rates are
higher in HIV infected patients. Roland et al found patient and
graft survival rates 94% and 83% respectively at 3 years, with
high incidence of acute rejection.4
In study of 150 HIV infected
renal transplant patients by Stock PG et al, patient and graft
survival was found to be 88.2% and 73.7% respectively at 3
years.5
Rates of acute rejection of renal transplants in patients
with HIV range from 13% to 67%.6
A higher acute rejection rate
is seen in patients of sub Saharan African descent.7
In our case study of the six HIV infected patients who
underwent renal transplant one suffered acute rejection
[Table 1]. Of these four out of six had received induction with
IL-2 receptor blocker Basiliximab. Patient and graft survival
was 83.4% each at 30 months. We found no difference be-
tween use of cyclosporine Vs tacrolimus.
3. Patient selection criteria
These criteria keep evolving as our experience in managing
these patients increases. Traditional selection criteria were
predicted by the concern that immunosuppression would
accelerate progression of HIV to AIDS. This however did not
happen and the selection criteria gradually became more lib-
eral. These selection criteria are based on the North American
and European transplantation criteria.
3.1. Inclusion criteria
- Meets standard criteria for inclusion in renal transplant list
- CD4þ T cell count >200 at any time in the 4 weeks before
transplantation
- HIV RNA <40 log copies for 4 months prior to transplant
- No change in HAART regime for 3 months before
transplantation
- Ability and willingness to comply to the immunosup-
pressive regime and HAART therapy
- Primary medical care provider having expertise in HIV
treatment
- Ability and willingness to undergo prophylaxis for pneu-
mocystis pneumonia, herpes virus and fungal infection
- If hepatitis C co-infection is present ability and willingness
to undergo frequent post transplant monitoring as man-
dated by the medical care provider
- If h/o pulmonary coccidiodomycosis exists, patient must be
disease free for at least 5 years before transplantation
- If there is h/o neoplasms like cutaneous Kaposi sarcoma,
in situ anogenital carcinoma, adequately treated basal or
squamous cell carcinoma of he skin then patient should be
disease free for at least 5 years before transplantation
- If h/o renal cell carcinoma then patient should be disease
free for at least 2 years pretransplant
- Ability to provide informed consenteself or by guardian
- Female candidates should have negative HCG pregnancy
test 14 days pretranplant.
3.2. Exclusion criteria
- Age < 1 year
- Detectable HIV RNA (or more than 40 log copies)
- h/o PML, lymphoma, chronic intestinal cryptosporidiosis
- h/o MDR fungal infection unlikely to respond to routinely
used antifungals
- h/o any neoplasm except those mentioned in the inclusion
criteria
- Substance abuse
- Any advanced cardiac or pulmonary disease
- Anatomic abnormality precluding transplantation surgery
- Use of IL2 or GMCSF in 2 months preceding transplantation
- Cirrhosis on liver biopsy unless patient is being taken up for
combined liver- kidney transplant
Table 1 e Post transplant complications n [ 6.
Complications n %
ATN 1 16.6
CNI toxicity 2 33.3
Sepsis 1 16.6
Acute rejection 0 16.6
Chronic rejection 1 16.6
Relapse HIV 0 0
a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 5 0 e5 6 51

4. Table 2 e Antiretroviral dosing recommendations in patients with renal impairment.
Antiretrovirals Renal insufficiency HD/CAPD
Nucleoside reverse transcriptase inhibitor’s (NRTI’S)
Abacavir No dosing adjustment is needed No dosing adjustment is needed
HD/CAPD minimally eliminated. Could be dosed
independently of HD session.
Didanosine
(enteric coated)
60 kg
CrCl 60:400 mg every 24 h
CrCl 30e59:200 mg every 24 h
CrCl 30:125 mg every 24 h
60 kg
CrCl 60:250 mg every 24 h
CrCl 10e59:125 mg every 24 h
CrCl 10:not suitable for use in patients
60 kg with CrCl10 ml/min an alternate
formulation of didanosine should be used
(videx pediatric powder for oral solution
75 mg every 24 h)
HD/CAPD; 125 mg every 24 h. It is not necessary to
administer a supplemental dose after HD
HD/CAPD; an alternate formulation of didanosine should be
used (videx pediatric powder for oral solution 75 mg every
24 h)
Emtricitabine Capsules
CrCl 50:200 mg every 24 h
CrCl 30e49:200 mg every 48 h
CrCl 15e29:200 mg every 72 h
CrCl 15 :200 mg every 96 h
Oral solution 10 mg/ml dueto a difference in
bioavailability of emtricitabine between the
hard capsule and oral solution presentations.
240 mg emtricitabine administered as the oral
solution (24 ml) should provide similar
plasma levels to those observed after
administration of one 200 mg emtricitabine
hard capsule.
CrCl 50:240 mg (24 ml) every 24 h
CrCl 30e49:120(12 ml)mg every 24 h
CrCl 15e29:80 mg (8 ml)every 24 h
CrCl 15:60 mg(6 ml) every 24 h
Capsules
HD: 200 mg every 96 h, after HD
CAPD:No data available
Oral solution (10 mg/ml)
HD:60 mg(6 ml) every 24 h after HD
CAPD- No data available
Lamivudine CrCl 50:150 mg every 12 h or 300 mg every
24 h
CrCl 30e49:150 mg every 24 h
CrCl 15e29:100 mg every 24 h(1st dose 150 mg)
CrCl 5e14:50 mg every 24 h(1st dose 150 mg)
CrCl 5:25 mg every 24 h(1st dose 50 mg)
HD:25 mg every 24 h(1st dose 50 mg),after HD
Stavudine 60 kg
CrCl 50:40 mg every 12 h
CrCl 26e49: 20 mg every 12 h
CrCl 10e25:20 mg every 24 h
CrCl 10:20 mg every 24 h
60 kg
CrCl 50:30 mg every 12 h
CrCl 26e49:15 mg every 12 h
CrCl 10e25:15 mg every 24 h
CrCl 10:15 mg every 24 h
HD:20 mg every 24 h,after HD
HD:15 mg every 24 h,after HD
Zidovudine Significantly elevated GZDV (the major
metabolite of zidovudine)plasma
concentrations
CrCl 10e50:250e300 mg every 12 h
CrCl 10:250e300 mg every 24 h
300 mg every 24 h after HD
HD and CAPD appeared to have a negligible effect on the
removal of zidovudine, whereas GZDV elimination was
enhanced
Nucleotide reverse transcriptase inhibitors (NtA’S)
Tenofovir
disoproxil
fumarate
CrCl 50: usual dose
CrCl 30e49: 300 mg every 48 h
CrCl 10e29: 300 mg every 72e96 h (dosing
twice a week)
No dosing recommendations can be given for
non-HD patients with creatinine
clearance10 ml/min
HD: 300 mg tenofovir disoproxil (as fumarate) may be
administered every 7 days following completion of an HD
session (assuming three HD sessions per week, each of 4 h
duration or after 12 h cumulative HD)
a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 5 0 e5 652

5. Table 2 e (continued)
Antiretrovirals Renal insufficiency HD/CAPD
Non nucleoside reverse transcriptase inhibitors (NNRTI’S)
Efavirenz Usual dose HD: limited data suggest that there is no reason to adjust the
dose
CAPD: pharmacokinetic data of only one patient suggest
that there is no reason to adjust the dose.
Nevirapine CrCl 20 ml/min usual dose HD: an additional 200 mg dose of nevirapine following each
dialysis treatment is recommended.
Etravirine
(TMC-125)
Usual dose HD/CAPD: as etravirine is highly bound to plasma proteins,
it is unlikely that it will be significantly removed by HD or PD
Protease Inhibitors (PI’S)
Amprenavir Usual dose
Because of the potential risk of toxicity from
the large amount of the excipient propylene
glycol, agenerase oral solution is
contraindicated in patients with renal failure
HD/CAPD:as amprenavir is highly bound to plasma proteins,
it is unlikely that it will be significantly removed by HD or PD
Atazanavir Usual dose HD/CAPD:as atazanavir is highly bound to plasma proteins,
it is unlikely that it will be significantly removed by HD or PD
HD:consider using atazanavir boosted with ritonavir.
Although ATV was negligibly eliminated by HD (2%),
subjects on HD had substantially lower ATV levels than
controls(AUC 42% lower on HD days,28% lower on non HD
days). The mechanism of this effect is not known (limited
data). Therapeutic drug monitoring is advised.
Darunavir Usual dose HD/CAPD:as darunavir is highly bound to plasma proteins, it
is unlikely that it will be significantly removed by HD or PD
Fosamprenavir Usual dose HD/CAPD:as amprenavir is highly bound to plasma proteins,
it is unlikely that it will be significantly removed by HD or PD
Indinavir Usual dose HD: limited data, showed minimal elimination of indinavir
during a dialysis session
Lopinavir Usual dose HD: usual dose. In 13 patients 2 were on HD LPV AUC values
were similar to those obtained in patients with normal renal
function
CAPD: No data available as lopinavir and ritonavir are highly
bound to plasma proteins, it is unlikely that it will be
significantly removed by CAPD
Nelfinavir Usual dose HD:it is unlikely that it will be significantly removed by HD.
Data from one patient showed no removal of nalfinavir by
a 4 h HD session.
CAPD: it is unlikely that it wll be significantly removed by
PD.
Data from one patient showed dialysate nalfinavir
concentration below the limit of detection
Ritonavir Usual dose HD/CAPD:as ritonavir is highly bound to plasma proteins, it
is unlikely that it will be significantly removed by HD or PD
Saquinavir Usual dose HD/CAPD:as saquinavir is highly bound to plasma proteins,
it is unlikely that it will be significantly removed by HD or PD
Tipranavir Usual dose HD/CAPD:as tipranavir is highly bound to plasma proteins,
it is unlikely that it will be significantly removed by HD or PD
Fusion inhibitors
Enfuvirtide (T-20) No dose adjustment is needed HD: usual dose (limited data)
CCR5 Co receptor antagonist
Maraviroc (UK-427857) No dose adjustment is needed without potent
CYP-3A4 inhibitors or inducers. Postural
hypotension may increase the risk of
Cardiovascular adverse events in patients
receiving maraviroc who have severe renal
impairment or ESRD (CrCl 30 ml/min).
maraviroc should not be prescribed for
patients with severe renal impairment who
are receiving CYP-3A4 inhibitor or inducer.
HD/CAPD:No data available
Integrase inhibitors
Raltegravir (MK-0518) No dose adjustment is needed No data available
a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 5 0 e5 6 53

6. - Substantial wasting or malnutrition
- Concomitant condition which inthejudgment ofmedicalcare
provide precludes transplantation or immunosuppression.
Approximately 30% patients with HIV have hepatitis C
co-infection and 10% hepatitis B co-infection. In patients
with either co-infection extent of liver damage needs to be
assessed before kidney transplantation. Data suggests that
treatment with HAART or MMF might help in slowing pro-
gression of liver disease and improve survival rates after
transplantation.
4. Donor selection criteria
United Network for Organ Sharing (UNOS) database has
demonstrated reduced death-censored graft survival at 1 year
in patients with HIV and renal transplants from deceased
donors older than 50 years of age and cold ischaemia time
longer than 16 h.8
Strategy to combat these problems is to use
living donors or infectious high risk donors i.e. individuals
who tested negative for HIV, HBV and HCV but based on social
history could have become infectious shortly before becoming
kidney donors. Use of extended criteria deceased donors is
appropriate for elderly HIV positive patients. Use of pediatric
en-bloc kidneys is not recommended because of high risk of
rejection and the possibility that these small kidneys might
not tolerate this rejection.
5. Strategies for immunosuppression
Agents used as immunosuppressives have antiretroviral
properties. MMF has virostatic action by depletion of guano-
side nucleosides required for virus replication. Cyclosporine
and tacrolimus interfere with HIV pathogenic protein. Siroli-
mus causes suppression of T cell activation and antigen pre-
senting cell function and disruption of virion replication and
entry into monocytes and lymphocytes by decreasing
expression of chemokine receptor.
Renal transplant recipients with HIV have a higher rejec-
tion rate hence induction therapy with IL2 receptor blocker
has been introduced.9
Most transplant centers are reluctant to
use lymphocyte depleting agents as they can severely deplete
CD4þ T cells for several months, though they have reversed
aggressive rejections successfully. In our patients four out of
six patients received IL2 receptor blocker Basiliximab without
any side effects (Table 1).
6. Drug interactions
Management of HIV patients post transplant is complicated by
multiple drug interactions between HAART agents and im-
munosuppressants. Most notable among these is induction or
inhibition of cytochrome P450 3A and P-glycoprotein 1 flux
transporters. These interactions can lead to unexpected in-
creases or decreases in drug levels leading to toxic side effects,
organ rejection and HIV disease breakthrough. PIs inhibit
P-glycoprotein and CYP 3A activity. This results in increased
level of circulating drugs. Non nucleoside reverse tran-
scriptase inhibitors (NNRTIs) like efavirenz reduce CYP 3A
activity increasing drug metabolism and reducing plasma
drug levels.
Patients on PIs and cyclosporine required only 20% of the
immunosuppressant dose administered to renal transplant
recipients without HIV as per a study describing the phar-
macokinetics and dosing modifications of cyclosporine, siro-
limus and tacrolimus in liver or kidney transplant recipients
on NNRTIs, PIs or both.10
Low dose ritonavir a potent inhibitor
of P glycoprotein 1 and CYP 3A4, is often used to boost plasma
levels of other PIs. Patients on a ritonavir boosted PI regimen
required even lower doses of immunosuppressants than pa-
tients on other HAART regimens. In patients on tacrolimus or
sirolimus immunosuppressant dose was markedly decreased
and the dosing interval too increased more than five fold. We
found that patients on one NRTI, one NNRTI and one PI
required a dose reduction of almost 97.5% instead of around
50% as has been routinely quoted. We needed a dose reduction
of around 92% in immunosuppressive dosage on a HAART
regime of 2NRTIs and 1PI instead of around 85% as routinely
quoted. On a 2NRTI and 1NNRTI combination an increase by
50% in CNI dose was seen in our patients instead of 25% as
routinely used.
Other drug interactions include azole antifungals and
macrolide antibiotics also inhibiting CYP3A 4 system. Proton
pump inhibitors routinely taken along with corticosteroids
reduce intestinal absorption of PI atazanavir. Therefore pa-
tients on proton pump inhibitors and atazanavir require PI
treatment to be boosted by use of ritonavir. Zidovudine and
MMF combination is not preferred as MMF antagonizes anti
retroviral effect of zidovudine and myelotoxic effect of MMF
gets enhanced with the additive myelosuppressive effect of
zidivudine11
[Tables 2 and 3].
7. Management of comorbidities
HBV- Lamivudine resistance is common in kidney transplant
patients with lamivudine containing HAART regimens.
Tenofovir is an acceptable alternative.
HCV- Management of HIVeHCV co-infection is problem-
atic. Post transplant immunosuppression exacerbates hepa-
titis C infection. Clearance of HCV should be attempted pre-
transplant as interferon therapy post-transplant leads to
increased graft rejection in a population that is already at
a greater threat of rejection. Early data on kidney trans-
plantation has shown favourable results of transplantation in
patients with HIV HCV co-infection. Long term studies are
however required and are currently underway.9
7.1. Bone metabolism disorders
Renal transplant patients with HIV are particularly at risk
because of renal failure associated hyperparathyroidism, low
vitamin D levels leading to low bone turnover, metabolic
acidosis and reduced patient physical activity leading to
osteoporosis, steroid intake, HIV associated low androgen
levels in males and females and administration of anti-
retrovirals like tenofovir and didanosine which have been
a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 5 0 e5 654

7. associate with low bone mass. Bisphosphonates can be tried
to restore bone mass levels.
7.2. Prophylaxis to prevent comorbidities
Renal transplant recipient patients with HIV should receive
the standard postetransplantation prophylaxis [Table 4]. If
patients receive lymphocyte depleting agents as anti-rejection
therapy then prophylaxis should be given for 3e6 months
after discontinuation of antirejection therapy. For PCP lifelong
prophylaxis with TMP-SMX is recommended by most centers.
Vaccinations according to HIV guidelines should be given to
these patients.12
7.3. Cardiovascular diseases
Presence of hypertension, dyslipidemia caused by PIs, CNIs
causing vasoconstriction and abnormal vascular remodeling,
steroids and CNIs causing diabetes all aggravate car-
diovascular risk. Atorvastatin or pravastatin are preferred
agents as they have lower propensity to inhibit CYP3A or
P-glcoprotein 1. Combination with fibrates increases myotoxic
effects.
7.4. Cancer
Since advent of HAART incidence of Kaposi sarcoma and non-
Hodgkin’s lymphoma rates have declined. Hepatocellular
carcinoma rates have increased probably in part related to
the increased longevity of HIV patients with HBV, HCV
co-infection. Regular surveillance for HCC is required. Patients
should be offered all conventional therapies including liver
transplantation in case of its occurrence. There is increased
risk of development of human papilloma virus associated
cervical and anal cancers for which routine Pap smears and
colonoscopies should be performed.
8. Conclusions
Renal transplantation is both safe and effective in patients
with HIV associated renal failure.
In these patients HIV load remains suppressed, CD4þ T cell
counts stable and opportunistic infections do not seem to
increase considerably.
Rates of acute rejection are higher. However graft survival
is at par with nonHIV transplant patients now a days.
HIVeHCV coinfection is a major concern in terms of
treatment options and long term effects.
It is important to have a team of doctors to oversee
treatment comprising HIV and infectious disease specialist,
nephrologist, transplant surgeon and primary care
physician.
Table 3 e Antiretroviral drug regimens for HIV infected
transplant patient.
1. NRTIs
A combination of two NRTIs (for example tenofovir plus
emtricitabine or abacavir plus lamivudine) can be used safety
in renal transplant recipients with dose adjusted to renal
function.
Tenofovir should be used with caution and close monitoring of
renal function.
Abacavir should not be used in recipients receiving a kidney
from an HLA-B57*01-positve donor to avoid the potential risk
of hypersensitivity reaction to abacavir.
2. NNRTIs and protease inhibitors
Can be used safely in combination with two NRTIs.
Important interactions with immunosuppressive drugs may
appear, mainly with protease inhibitors.
3. Novel classes of antiretrovirals
Must be considered in combination with NRTIs.
Integrase inhibitors (raltegravir): have no interactions with
immunosuppressive agents at the CYP450 level.
Entry inhibitors (enfuvirtide (T20): could be an alternative in
combination with NRTIs, although subcutaneous admin-
istration is a limitation.
CCRS co-receptor antagonists (Maraviroc): a substrate of
CYP450. Its levels can be modified by inducers or inhibitors.
Experimental studies have suggested that maraviroc could
have an important role as an antirejection drug.
Table 4 e Recommended prophylaxis regimens for renal transplantation candidates with HIV.
Condition Primary prophylaxis Secondary prophylaxis
Pneumocystis carinii Indicated for life; TMP-SMX Same as primary
Pneumonia Alternative- dapsone or atovaquone
Toxoplasmosis when þ ve Toxoplasma IgG or CD4þ T cell200/ml, T/t
of Choice- TMP-SMX Discontinue when
CD4þTcell200/ml for 3e6months
CD4þTcell200
sulphadiazine þ pyrimethamine þ leucovorin Discontinue
when CD4þTcell 200/ml for 3e6months
Mycobacterium
avium complex
when CD4þTcell50/ml drug- azithromycin/
clarithromycin discontinue when CD4þTcell100/ml
for 3e6months
when CD4Tcell50/ml drug clarithromycin þ ethambutol
CMV no HIV specific indication when CD4þTcell75e100/ml Drug- valganciclovir Or
foscarnet or cidofovir Discontinue when CD4þTcell 200/ml
for 3e6months
Extrapulmonary
Cryptococcus
no specific HIV indication when CD4þTcell200/ml drug- fluconazole Discontinue
when CD4þTcell 200/ml for 3e6 months
Histoplasmosis no specific HIV indication Indicated for life regardless of CD4þTcell count Drug-
itraconazole
a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 5 0 e5 6 55

8. Conflicts of interest
All authors have none to declare.
Acknowledgement
We acknowledge the contribution of our transplant team
including doctors, nurses and health workers.
r e f e r e n c e s
1. Trullas JC, Barril G, Cofan F, et al. Prevalence and clinical
characteristics of HIV type-1 infected patients receiving
dialysis in Spain: results of a Spanish survey in 2006: GESIDA
48/05 study. AIDS Res Hum Retroviruses. 2008;24:1229e1235.
2. Ahuja TS, Borucki M, Funtanilla M, et al. Is the prevalence of
HIV-associated nephropathy deceasing? Am J Nephrol.
1999;19:655e659.
3. Stock PG, Roland ME, Carlson L, et al. Kidney and Liver
transplantation in human immunodeficiency virus einfected
patients: a pilot safety and efficacy study. Transplantation.
2003;76:370e375.
4. Roland ME, Barin B, Carlson L, et al. HIV-Infected liver and
kidney transplant recipients: 1- and 3 year outcomes. Am J
Transplant. 2008;8:355e365.
5. Stock PG, Barin B, Murphy B, et al. Outcomes of kidney
transplantation in HIV-infected recipients. N Engl J Med.
2010;363:2004e2201.
6. Gruber SA, Doshi MD, Cincotta E, et al. Preliminary experience
with renal transplantation in HIVþ recipients: low acute
rejection and infection rates. Transplantation.
2008;86:269e274.
7. Kumar MS, Sierka DR, Damask AM, et al. Safety and success of
kidney transplantation and concomitant immunosuppression
in HIV-positive patients. Kidney Int. 2005;67:1622e1629.
8. Locke JE, Montgomery RA, Warren DS, et al. Renal Transplant
in HIV positive patients: long term outcomes and risk factors
for graft loss. Arch Surg. 2009;144:83e86.
9. Tan PT, Kaczorowski DJ, Basu A, et al. Living-related donor
renal transplantation in HIVþ recipients using alemtuzumab
preconditioning and steroid free tacrolimus monotherapy:
a single center preliminary experience. Transplantation.
2004;78:1683e1688.
10. Frassetto LA, Browne M, Cheng A, et al. Immunosuppressant
pharmacokinetics and dosing modifications in HIV-1 infected
liver and kidney transplant recipients. Am J Transplant.
2007;7:2816e2820.
11. Joan C trullas, Federico Cofan, Montse tuset, et al e renal
transplant in HIV infected patients: 2010 update.
12. Pollet C, Paul SM, Morgan R. Immunisations in the HIV-
infected patient. N J Med. 2002;99:23e31.
a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 5 0 e5 656

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