In-Depth Topic Review

American Journal of

Nephrology Am J Nephrol 2004;24:511–521 Received: July 14, 2004

Accepted: August 31, 2004
DOI: 10.1159/000081041 Published online: September 23, 2004

Dialyzing a Patient with Human

Immunodeficiency Virus Infection: What
a Nephrologist Needs to Know
Sreedhar Mandayam Tejinder S. Ahuja
Department of Medicine, Division of Nephrology, University of Texas Medical Branch, Galveston, Tex., USA

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Key Words Introduction
Human immunodeficiency virus W Dialysis W Chronic
kidney disease W Anemia W Vaccination After the first recognition in 1984 of a distinct form
of focal segmental glomerulosclerosis termed human
immunodeficiency virus (HIV)-associated nephropathy
Abstract (HIVAN) that develops predominantly in HIV-infected
The percentage of dialysis centers that have reported blacks and progresses rapidly to end-stage renal disease
dialyzing human immunodeficiency virus (HIV)-infected (ESRD), the prevalence of HIV-infected patients receiv-
patients increased from 11% in 1985 to 37% in 2000. ing dialysis in the USA rose at an alarming rate until
Being primary care physicians for the dialysis patients, 1995, when over 900 new patients with HIVAN started
nephrologists are frequently confronted with the man- dialysis in the USA. Since then, the number of patients
agement of HIV-infected dialysis patients especially in with HIVAN starting dialysis has reached a plateau,
urban centers. The aims of the present review are to dis- although over 800 patients with HIVAN start dialysis
cuss issues that are unique to HIV infection and end- each year in the USA [1–4]. This is consistent with accu-
stage renal disease, and to provide dialysis caretakers mulating reports that use of highly active antiretroviral
with sufficient information to help them optimize care therapy (HAART) (available since 1996) slows down or
and improve outcomes of these patients. Issues related can cause remission of the rapidly progressive course of
to the choice of renal replacement therapy, vascular HIVAN [5–10]. Figure 1 shows the incident dialysis pa-
access, management of anemia, vaccination, and anti- tients with HIVAN starting dialysis in the USA from
retroviral therapies are discussed in detail. 1984 until October 2000. Although the epidemic of HIV
Copyright © 2004 S. Karger AG, Basel infection has reached a plateau in the USA, recent Centers
for Disease Control data suggests that the epidemic in the
population at risk for HIVAN (blacks) is still increasing.
Also with increasing prevalence of drug-resistant strains
of HIV, the incidence of HIVAN may not change even in
the HAART era [11]. In addition, the prevalence which

© 2004 S. Karger AG, Basel Tejinder S. Ahuja MBBS, Assoc. Prof.

ABC 0250–8095/04/0245–0511$21.00/0 4.200 John Sealy Annex
Fax + 41 61 306 12 34 301 University Boulevard
E-Mail [email protected] Accessible online at: Galveston, TX 77058 (USA)
www.karger.com www.karger.com/ajn Tel. +1 409 772 7407, Fax +1 409 772 5451, E-Mail [email protected]
Fig. 1. Number of new patients with HIV-
AN starting dialysis in the USA (derived

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from USRDS Database Standard Analysis
Files using PDIS codes 0429A).

depends not only on incidence but also on survival may antigen, antibody to hepatitis C virus and HIV infection.
not change or may increase with improving survival of The report of the last survey, for the calendar year 2000,
HIV-infected dialysis patients [3]. Therefore, we believe represented 3,683 dialysis facilities and 241,113 patients.
that in the coming decade, despite the impact of HAART Since 1999, the prevalence of HIV infection has been
on the incidence of HIVAN and ESRD, nephrologists in reported as the percentage of patients with HIV infection
the urban centers are going to be confronted with provid- who were present during a 1-week period in December
ing optimal care to HIV-infected ESRD patients. This divided by the total number of patients who were present
review is aimed at providing nephrologists with impor- during the same 1-week period in December. In 2000,
tant advancements in the treatment of HIV infection and 1.5% (range among networks 0.3–3.4%) of patients were
suggesting management strategies to optimize care of reported to have HIV infection and 0.4% (range among
these patients on dialysis. networks 0–1.0%) to have AIDS. During 1985–2000, the
percentage of centers that reported providing dialysis for
patients with HIV infection increased from 11 to 37% [4].
Epidemiology A similar incidence and prevalence of HIV-infected pa-
tients with ESRD has been reported by studies utilizing
The estimates of HIV-infected patients in the dialysis the USRDS database [3, 12, 13]. The number of incident
patients in the USA are available from surveillance of HIVAN patients starting dialysis each year increased
dialysis associated diseases conducted by the Centers for until 1995 when 939 patients with HIVAN started dialy-
Disease Control and Prevention (CDC) and from infor- sis. Since then, the number of HIVAN patients starting
mation available through the United States Renal System dialysis has reached a plateau around 800 per year. This
Database (USRDS). As dialysis patients are not routinely salutary effect on the incidence is probably from the
screened for HIV infection in the USA, the true incidence change in natural course of HIVAN due to the use of
and prevalence is probably higher than reported by either HAART. The incidence of HIV-associated renal diseases
the CDC or the USRDS. from 1995 to 1999 for black men aged 25–44 years fell
Since 1976, the CDC initiated a cooperative program from 8.5 to 6.8%. Despite this, the number of prevalent
with Health Care Finance Administration that provided a cases increased from 1,346 to 3,058 (0.4–0.8%) as 1-year
questionnaire from the CDC to be included in CFA’s survival rate improved from 52 to 69% [12]. ESRD Net-
annual facility survey. The questionnaire includes infor- work 2 (N.Y.) reported that 820 (5.5%) of 15,000 new
mation on incidence and prevalence of hepatitis B surface ESRD patients between 1992 and 1996 had renal failure

512 Am J Nephrol 2004;24:511–521 Mandayam/Ahuja

attributed to HIVAN. Another 354 ESRD patients had USRDS, we recently reported that dialysis modality was
AIDS but renal failure was attributed to other causes. not a factor in survival of patients with HIVAN after com-
Subsequently, the incidence of ESRD from HIVAN de- paring survival between 5,299 patients who received he-
clined to 2.5% (155 of 6,291) during 1999 and 2% (130 of modialysis and 716 patients who received peritoneal dial-
6,563) during 2000 [14, 15]. Although ESRD in HIV- ysis in the USA (hazard ratio: peritoneal dialysis vs. cen-
infected patients is largely attributed to HIVAN, the num- ter hemodialysis, 1.04, 95% CI, 0.96–1.13) [31]. How-
ber of patients that had the diagnosis confirmed by renal ever, the study was limited by the unavailability of infor-
biopsies is unavailable either from the CDC or the mation on plasma viral load and CD4 count. Until further
USRDS database. studies controlling for the stage of HIV infection and oth-
Several other countries have reported the prevalence of er co-morbidities are conducted, criteria for selecting dial-
HIV infection in dialysis patients. In a survey of 260 dial- ysis modality for HIV-infected patients should be similar
ysis facilities in France representing 22,707, a prevalence to other patients with ESRD.
of 0.36% was found [16]. In an Italian survey correspond- The arguments in favor of transplantation of HIV-
ing to 27,000 patients, the prevalence of HIV infection infected patients have gained a new impetus with im-
was 0.13% [17]. The prevalence reported from Japan and provement in survival of these patients with HAART.
Egypt in the pre-HAART era was low but Brazil reported The issue of transplantation in dialysis patients has been
a high prevalence (14%) of HIV infection in dialysis discussed in three recent reviews [32–34]. Long-term sur-

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patients [18–20]. vival was not an uncommon occurrence in HIV-infected
patients even in the pre-HAART era [35, 36]. It has been
well known that immunosuppressive agents such as cy-
Renal Replacement Therapy closporine and tacrolimus may retard replication of HIV
virus [37]. Starzl et al. [36] in the pre-HAART era re-
In the pre-HAART era several studies suggested that ported that HIV-infected transplant recipients who were
survival of HIV-infected patients was dismal to a point on cyclosporine-based immunosuppressive regimen had a
that it was an ethical dilemma whether chronic dialysis better survival. Recent reports have suggested that even
should be offered to these patients. However, with the use mycophenolate mofetil, another common drug used after
of HAART the survival of HIV-infected patients on dialy- transplantation, may potentiate the antiretroviral effect of
sis has improved considerably [3, 21]. The theoretical pos- commonly used HIV drugs [38, 39]. Although the concern
sibility that hemodialysis may actually increase the mor- about potential interactions between protease inhibitors
bidity of HIV-infected ESRD patients by enhancing viral and calcineurin inhibitor is real, this can be resolved by
replication through activation of white blood cells and monitoring drug levels and pharmacokinetic studies [40].
release of cytokines such as tumor necrosis factor-·, inter- Murphy et al. [41] have recently reported a short-term
leukin-1 and interleukin-6 that enhance HIV replication outcome of 23 HIV-infected patients who received kidney
remains unstudied [22–26]. Winston et al. [27] reported transplantation at different centers in the USA. The
faster early decay rate of HIV after starting antiretroviral patient and the graft survival was comparable to United
therapy in dialysis patients consistent with this hypothe- Network for Organ Sharing (UNOS) at 1 year. There was
sis. We in contrast did not find any day-to-day increase in no evidence of progression of HIV, as HIV RNA re-
plasma viral load with hemodialysis in our previous mained undetectable in 21 of the 23 patients [41, 42].
study. However we did not rule out the possibility of a Therefore, several centers have started offering solid or-
delayed increase in viral load [28]. Potent antiretroviral gan transplantation to HIV-infected patients. Conse-
activity of the newer HIV drugs has made the concern quently, we believe that asymptomatic HIV-infected pa-
regarding of activation of HIV virus due to hemodialysis tients with ESRD should be referred to these transplant
mute but with increasing prevalence of resistant strains of centers. The information regarding these centers and the
HIV this could become an important issue again. referral form is available at the following website http://
Although peritoneal dialysis may cause less immune spitfire.emmes.com/study/hiv-k/.
activation and cytokine alterations, these benefits may be
nulled by increased protein losses with peritoneal dialysis
[29]. Kimmel et al. [30] in the pre-HAART era in a small
number of patients did not find dialysis modality as a fac-
tor in survival of HIV-infected dialysis patients. Using the

HIV Infection and Dialysis Am J Nephrol 2004;24:511–521 513

 Vascular Access dard infection control practices are adequate to prevent
HIV transmission between patients and HIV-infected pa-
The complication rate of arteriovenous graft (AVG) in tients do not have to be isolated from other patients or
HIV-infected dialysis patients is reported to be higher dialyzed separately on separate machines. HIV is not
[43]. In one study, the 12- and 24-month patency rates of transmitted efficiently through occupational exposures
prosthetic grafts in HIV-infected ESRD patients was low- and reprocessing dialyzers from HIV-positive patients
er, as compared with HIV-negative patients (49 and 21% should not place staff members at increased risk of infec-
vs. 77 and 45%) and infection rate was higher, 30 vs. 7%, tion if necessary sterile precautions are undertaken. The
respectively. The patency and infection rate in patients CDC does not prohibit participation of HIV-infected
with autologous AVFs with or without HIV infection did patients in dialyzer reuse programs [50]. However, a
not differ [44]. Some other studies validated a higher break in proper infection control practices could lead to
infection rate of the AVG in asymptomatic HIV-infected transmission from patient to patient in a dialysis unit;
patients and patients with AIDS compared with control therefore it is extremely important to conform to the stan-
patients (36, 45 and 15%, respectively) [45]. The risk of dard infection-control practice guidelines in dialysis cen-
infection associated with dialysis catheters has also been ters [51–52].
reported in HIV-infected patients. Mokrzycki et al. [46] Although the risk is small, transmission of HIV infec-
compared tunnel-cuffed catheter-related bacteremia in 40 tion after a percutaneous (0.3%) and after a mucous mem-

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HIV-infected patients with 41 control patients. Although, brane exposure (0.09%) can occur [53]. Dialysis care pro-
the tunnel-cuffed catheter-related bacteremia was not dif- viders who get exposed should start post-exposure pro-
ferent in HIV-infected patients compared with controls phylaxis (PEP) as soon as possible. PEP utilized remains
(2.23 vs. 2.53 per 100 tunnel-cuffed catheter days), HIV- largely empiric, however treatment for 4 weeks compris-
infected patients had a fivefold increased risk of gram- ing of two reverse transcriptase inhibitors (ZDV and lami-
negative rod bacteremia and sevenfold increased risk of vudine, stavudine and lamivudine, or stavudine and
fungal isolate. Therefore, arteriovenous fistula (AVF) didanosine) for minor exposures, and an expanded regi-
should be created early if progression of renal failure in men that includes addition of a third drug (usually a pro-
patients with HIVAN is rapid despite all therapies. Al- tease inhibitor) for more significant HIV exposures that
though HAART and use of angiotensin-converting en- pose an increased risk for transmission, is recommended
zyme inhibitors and steroids has decreased the rate of pro- [53]. As the prevalence of HIV drug resistance in un-
gression of renal failure, the majority would still progress treated patients appears to be increasing, the regimen cho-
over a period of time to ESRD [7–10, 47, 48]. If the renal sen should include drugs to which the virus is unlikely to
failure is progressing slowly or patients have renal disease be resistant [54, 55]. The regimens should be chosen after
other then HIVAN, the Dialysis Outcome Quality Initia- consultation with experts and antiretrovirals based on
tive (DOQI) guidelines should be used in timing place- local knowledge and experience in treating HIV infection
ment of vascular access, i.e. AVF should be placed when and disease and known drug resistance in the source
creatinine clearance is !25 ml/min and if the patient can- should be given consideration. Initiation of PEP should
not get AVF, dialysis AVG should be placed 3–6 weeks not be delayed in order to obtain drug resistance testing in
prior to the anticipated need for dialysis. the source, however changes in the PEP can be made after
it has been started and drug-resistant testing on the
source. Post-exposure testing should be performed at 6
Prevention of Transmission of HIV in Dialysis weeks, 12 weeks and 6 months, and persons exposed
Units should be monitored for drug toxicity.
In the pre-HAART era studies showed potentially via-
Routine testing of dialysis patients for HIV infection ble and infectious HIV-1 from the peritoneal dialysis
has not been recommended by the CDC [49, 50]. How- effluent and peritoneal dialysis exchange tubing in HIV-
ever, every patient starting dialysis should be evaluated infected patients [56, 57], therefore peritoneal dialysis
for risk factors for HIV infections and if present should be effluents should be discarded in a toilet and disinfected
tested. Practice guidelines do not exist for those patients and viricidal agents such as of Aukin or 10% household
who refuse to be tested for HIV. If infected, these patients bleach should be poured and should be left for at least
can receive appropriate medical care, including education 30 min after disposal. Every precaution should be taken
and counseling to prevent transmission of the virus. Stan- to avoid splashing, and gloves, aprons and face shields

514 Am J Nephrol 2004;24:511–521 Mandayam/Ahuja

should be used while disposing spent dialysate. Tubing required for anemia work in HIV-infected patients with
and peritoneal dialysis bags should be discarded carefully ESRD than recommended by NKF-DOQI guidelines. Re-
in bags marked as highly contagious. Caretakers of HIV- combinant human erythropoietin therapy or darbepoetin
infected peritoneal dialysis patients should also be edu- is an appropriate treatment option for patients with
cated regarding infection control practices to be followed symptomatic mild anemia or moderate anemia (hemoglo-
at home. bin level = 2 g/dl below the lower limit of normal range).
The target range for hemoglobin (hematocrit) recom-
mended for patients with CKD is hemoglobin 11–12 g/dl.
Anemia Unless more information becomes available, the same
target hemoglobin levels should be aimed for in HIV-
Prevalence of anemia is higher in HIV-infected pa- infected patients with CKD [67–69]. The response to
tients with renal disease as anemia is the commonest erythropoietin in HIV-infected patients appears to be
hematological abnormality in HIV-infected patients and similar to HIV-negative patients and in a small study of
occurs in 3.2% of patients without clinical or immuno- HIV-infected ESRD patients, Shrivastava et al. [61]
logic AIDS but in 36.9% of patients with AIDS defining found that after 8 weeks of 100 U/kg body weight erythro-
illness and 12.1% with immunologic AIDS [58–60]. Shri- poietin three times weekly the mean increase in hemato-
vastava et al. [61] found that the mean baseline hemato- crit in these patients was similar to HIV-negative patients

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crit of HIV-infected ESRD patients was 22% compared (5.8 vs. 6.7% in HIV-negative patients, respectively). Dar-
with 26% in HIV-negative, diabetic and non-diabetic bepoetin-· given once a week intravenously was found to
ESRD patients. Similarly, Abbott et al. [62] using data have a similar response to erythropoietin in 12 HIV-posi-
from Dialysis Morbidity and Mortality Wave 2 study tive hemodialysis patients. Ten of the 12 patients had
found that mean hematocrit levels in patients with hemoglobin 611g/dl at monthly assessment through to
HIVAN (n = 37) were significantly lower compared with the end of the study [70].
all other patients with ESRD starting dialysis (Hct 26.2 B Although rare, parvovirus B19 infection should be sus-
6.5 vs. 30.5 B 6.1, p ! 0.05), respectively. HIV infections pected if anemia in HIV-infected patients does not re-
could exacerbate the severity of anemia in patients with spond to erythropoietin and other causes are ruled out.
kidney disease by direct effects of HIV infection on eryth- The patients have intense reticulocytopenia; serum PCR
ropoiesis, opportunistic infections, antiretroviral drugs or for parvovirus viremia and parvovirus IgM antibodies
other drugs administered to treat infection or malignan- will establish the diagnosis in the majority of patients.
cies and from other rare mechanisms such as thrombotic Bone marrow is hypoplastic and giant pronormoblasts are
microangiopathies [63]. As the presence of anemia is commonly seen [71, 72].
independently of other factors associated with shorter sur- Iron is essential for hemoglobin formation as is eryth-
vival, it is imperative that it should be managed aggres- ropoietin. NKF-DOQI recommends that iron status be
sively in patients with HIV infection and chronic kidney monitored by the percent transferring saturation (TSA)
disease (CKD) [59, 64–65]. and serum ferritin levels and sufficient iron should be
The National Kidney Foundation-Dialysis Outcomes administered to maintain TSAT 620% and a serum ferri-
Quality Initiative (NKF-DOQI) recommends that ane- tin level of 6100 ng/ml, which requires administration of
mia work-up should be initiated in patients with CKD intravenous iron in the majority of dialysis patients [66].
when the hemoglobin level is !11 g/dl (Hct !33%) in pre- Not only are measurements of iron indices complicated in
menopausal females and pre-pubertal patients and hemo- HIV-infected patients, but ferritin, which is an acute
globin !12 g/dl (Hct !37%) in adult males [66]. Some phase protein, is often elevated in patients with HIV
studies have recommended that in HIV-infected patients infection, and high iron stores may also adversely in-
other etiologies of anemia should be ruled out once hemo- fluence the outcome of HIV-infected patients. Studies
globin !1 g/dl below the lower limit of normal range. The have shown that oxidative stress and iron may be impor-
same guidelines for starting work-up for anemia could be tant in activation of HIV-1. Induction of nuclear factor-
followed with HIV-infected patients with ESRD due to a ÎB expression, which regulates proviral transcription, can
higher chance of conditions (infections, drugs, etc.) other be influenced by iron through the production of reactive
than renal failure to be associated with anemia in HIV- oxygen species [73–75]. Therefore, the safety of intrave-
infected patients. In addition, more extensive work-up nous administration of iron needs to be studied in HIV-
with special attention to infections and drug toxicity is infected dialysis patients [76–80]. Until further studies

HIV Infection and Dialysis Am J Nephrol 2004;24:511–521 515

addressing the safety and effect of intravenous iron on Vaccination
HIV become available, we would suggest closely monitor-
ing HIV disease progression in patients receiving intrave- Two important issues related to vaccination of HIV-
nous iron by measuring plasma viral loads and CD4 infected patients with CKD are its efficacy and effect on
counts. plasma viral load. The immunosuppression as a result of
Blood transfusions in HIV-infected patients with CKD HIV infection and uremia is likely to lead to suboptimal
should be avoided as some but not all studies have shown response to vaccination in these patients. The develop-
an increased activation of HIV-1 after transfusion, which ment of protective antibodies and the duration of the pro-
could potentially accelerate HIV disease [81, 82]. tection is likely to be short due to decline in the levels of
these protective antibodies as shown with anti-pneumo-
coccal antibodies, which decrease to non-protective levels
Bone Disease rapidly following pneumococcal vaccination in HIV-
infected patients [91–93]. Initial observations that in-
Osteopenia and osteoporosis are common in HIV- fluenza vaccination increases replication of HIV replica-
infected patients. Although an underlying mechanism tion has not been substantiated in more recent studies
triggering bone loss in HIV-infected patients is unknown, conducted in the era of HAART [94–101].
antiretroviral drugs, increased production of pro-inflam- Hepatitis B remains a significant risk to patients

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matory cytokines such as tumor necrosis factor and inter- receiving chronic hemodialysis. Compared to adults with
leukin-6 may have a role in osteoclast activation and normal immune status, the proportion of hemodialysis
resorption [83, 84]. Some studies have shown that HIV- patients who develop a protective antibody response after
infected patients have low basal and maximal secretion of vaccination (with higher dosages) is lower, for those who
parathyroid hormone (PTH) and 1,25-dihydroxyvitamin receive the three-dose schedule, the median is 64% (range
D3 levels [85, 86]. Parathyroid cells have been found to 34–88%) [102–104]. Immunization for hepatitis B in
express proteins recognized by antibodies directed against HIV-infected CKD patients is more important because
CD4, the HIV-1 receptor, suggesting that the parathyroid not only does HBV infection occur more frequently with
cells may be infected with HIV directly leading to im- HIV infection for behavioral reasons, but also because the
paired PTH release. Abbott et al. [62] found that the mean pre-HAART studies suggested that these patients are
PTH level was lower in patients with HIVAN and ESRD more likely to develop chronic infection [105]. However,
compared to patients with other causes of ESRD; the dif- several reports have suggested that antibody response to
ference however was not statistically significant (239 B hepatitis vaccination is impaired in HIV-infected patients
225 vs. 308 B 319 pg/l, respectively). Although informa- [106–108]. Although hepatitis vaccination may increase
tion on bone disease in patients with CKD and HIV infec- plasma viral load, the effect is minimal and transient and
tion is not available, HIV-infected patients with CKD is unlikely to be of clinical relevance [109, 110]. We have
develop complications of altered calcium and phosphate recently reviewed hepatitis vaccination information on
metabolism similar to HIV-negative patients [88]. Based 348 HIV-infected patients who received dialysis in Gam-
on these observations and with the previous knowledge bro Inc. dialysis units in the USA from 1994 to 2003.
that vitamin D3 enhances immune response, we suggest Complete information was available in 116 patients who
treating all HIV-infected ESRD patients with hyperpara- received three doses of 40 Ìg of subcutaneous Recombi-
thyroidism with 1,25-dihydroxyvitamin D3 or its ana- vax HBTM (Merck & Co. Inc.). Of these 116 patients, 63
logues (using the same laboratory parameters for calcium, (54.3%) developed protective antibody anti-HBs titers
phosphate and PTH levels as HIV-negative ESRD pa- 110 IU/l [unpubl. data]. Hepatitis vaccination should
tients) [89]. Recently, NKF-DOQI has published clinical therefore be offered to HIV-positive ESRD patients. Hep-
practice guidelines for bone metabolism and disease in atitis B surface antibody levels should be checked and a
CKD. However, whether vitamin D and phosphate booster should be attempted if antibody levels become
binders are equally effective in preventing bone disease in undetectable, although the response to a booster dose is
HIV-infected patients with CKD needs to be studied in not known. Table 1 lists the vaccinations that HIV-
controlled trials [90]. infected patients with CKD should be offered [111], how-
ever the protection that vaccines may offer in HIV-
infected ESRD patients is likely to be inadequate or tran-
sient and this underscores the importance that other

516 Am J Nephrol 2004;24:511–521 Mandayam/Ahuja

Table 1. Immunizations recommended for adult HIV-infected dialysis patients (adapted from USPHS guidelines [111], dosages have been
changed to dosages appropriate for patients on dialysis)

Streptococcus pneumoniae Pneumovax®1 or PNU-IMUNE®2 23 0.5 ml, subcutaneously or i.m. ! 1 if CD4 count 1 200/Ìl repeat vaccination for patients
initially immunized at a CD4 count ! 200/Ìl whose CD4 count increases to 1 200/Ìl (vaccinate preferably prior to development
of ESRD). Revaccinate after 5 years
Influenza virus All patients annually
Hepatitis A Anti-HAV negative, patients at increased risk for HAV infection (e.g. illicit drug users, men who have sex with men) chronic
liver disease including chronic hepatitis B or hepatitis C
Hepatitis B virus Recombivax HBTM1 Engerix-B®3 Monitoring:
Check anti-HBs 1–2 months after the last primary
dose (i.m.) schedule dose (i.m.) schedule
vaccine dose (adequate response 610 mIU/ml)
Patients aged 620 years Revaccinate with three doses in patients who
Predialysis 10 Ìg 0, 1, 6 months 20 Ìg 0, 1, 6 months do not respond
Dialysis dependent 40 Ìg 0, 1, 6 months 40 Ìg 0, 1, 2, 6 months For responders, follow anti-HBs semiannually if
Patients aged ! 20 years 5 Ìg 0, 1, 6 months 10 Ìg 0, 1, 6 months levels ! 10 mIU/ml, administer a booster dose

1 Merck & Co. Inc., West Point, Pa.

2 Lederle.
3 SmithKline Beecham Biologicals, Philadelphia, Pa.

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infection control strategies should be simultaneously im- adjustment in patients with ESRD. Since the liver mainly
plemented in addition to vaccination. Further studies are metabolizes it, the fraction removed during dialysis is not
required in the HAART era to determine safety and effi- clinically significant; hence it can be administered at any
cacy of vaccinations in HIV-infected patients. time on dialysis days [117]. Tenofovir, the first nucleotide
RTI, is administered as a 300-mg tablet once daily, has
rare and mild side effects, and is active against NRTI-
Highly Active Antiretroviral Therapy resistant strains. As tenofovir is primarily eliminated by
the kidneys, it can be given once a week after dialysis
In the recent years, use of HAART, improved prophy- [118]. NNRTI and PI are mainly metabolized by the liver
laxis, and treatment of opportunistic infections have led by cytochrome P450 isoenzymes, and do not need dose
to dramatic improvement in survival of HIV-infected adjustments in patients with ESRD. NNRTI should be
patients [112, 113]. Despite the benefits of HAART in administered after hemodialysis to minimize loss during
patients with HIV infection and ESRD, two recent re- dialysis. In contrast, PI could be administered regardless
ports have showed underutilization of HAART in HIV- of the dialysis schedule. The dosages of antiretroviral
infected dialysis patients [114, 115]. In addition, the dose drugs in dialysis patients and their side effects have been
of antiretroviral drugs administered was inconsistent with summarized in table 2.
current treatment guidelines [115]. Several antiretroviral drugs (PI and NNRTI) are po-
A recent review by Izzedine et al. [116] has summa- tent inhibitors of cytochrome P450 isoenzymes (CYP3A4).
rized the pharmacokinetics of antiretroviral drugs in Therefore, concomitant administration of other drugs
HIV-infected patients on hemodialysis. There are three metabolized by these isoenzymes may lead to an increase
main groups of antiretroviral drugs, nucleoside and non- in their blood levels and side effects. An HIV specialist
nucleoside reverse transcriptase inhibitors (NRTI and should be consulted if other drugs metabolized by these
NNRTI) and protease inhibitors (PI). In most patients, a isoenzymes need to be prescribed to them. The nephrolo-
combination of either two NRTI with a PI or two NRTI gist taking care of HIV-infected dialysis patients should
plus one NNRTI are used. NRTI used in HIV therapy are work closely with the HIV specialist and should monitor
primarily excreted by the kidneys, therefore the dose response to therapy by following plasma viral load and
administered is 30–50% of the normal dose for various CD4+ lymphocyte counts at least every 3 months. We sug-
drugs. In addition, on dialysis days the NRTIs should be gest following the same guidelines for the treatment of
dosed after dialysis. Abacavir is the only NRTI whose HIV-infected HD patients as with other HIV-infected
absorption, elimination and distribution phases are not patients [119]; the guidelines with recent updates are
altered by renal insufficiency and does not need dose available on the World Wide Web at http://www.

HIV Infection and Dialysis Am J Nephrol 2004;24:511–521 517

Table 2. Dosage of antiretroviral drugs for
patients with ESRD Drug Dose for dialysis patients Normal dose

NRTI
Zidovudine 100 mg three times/day 200 mg three times/day or
Didanosine 300 mg/twice/day
BW 1 60 kg 100 mg once/day 200 mg twice/day
BW ^60 kg 50 mg once/day 125 mg twice/day
Zalcitabine 0.75 mg once/day 0.75 mg three times/day
Stavudine
BWB 6360 kg 20 mg once/day 40 mg once/day
BW ^60 kg 15 mg once/day 30 mg once/day
Lamivudine 150 one dose followed by 150 mg twice/day
25–50 mg once/day
Abacavir 300 mg twice/day Same dose
NNRTI
Nevirapine Normal dosage 200 mg once/day for 14 days
thereafter 200 mg twice
Delavirdine Data not available 400 mg three times/day
Efavirenz Normal dose 600 mg once/day

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Protease Inhibitors
Indinavir Normal dosage 800 three times/day
Ritonavir 600 mg twice/day
Nelfinavir 750 mg three times/day
Saquinavir/invirase 400 mg twice/day
Amprenavir 1,200 mg twice/day
Tenofovir 300 mg once a week 300 mg once/day

NRTI = Nucleoside reverse transcriptase inhibitors; NNRTI = non-nucleoside reverse

transcriptase inhibitors.

cdcnac.org and http://www.hivatis.org. Nephrologists HAART leads to an increase in CD4 lymphocyte counts
should also ensure that HIV-infected dialysis patients above specified levels [119].
with low CD4 count should be receiving prophylaxis We conclude that nephrologists taking care of HIV-
against opportunistic infections. In 1995, the USPHS/ infected ESRD patients need to take care of the special
IDSA suggested guidelines for prophylaxis against oppor- issues relevant to HIV-infected patients with ESRD and
tunistic infections in HIV-infected patients. These guide- should participate actively with HIV specialists to im-
lines have recently been revised and updated. These prove the outcome and quality of life of this group of
guidelines have suggested that it may be safe to stop pri- patients.
mary or secondary prophylaxis for some pathogens if

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