Chronic Kidney Disease in HIV Positive Patients

Perdana Liansyah Sihite

Internal Medicine Residence, Departement of Internal Medicine
University of Syiah Kuala, Banda Aceh

1. INTRODUCTION
Chronic kidney disease (CKD) encompasses a spectrum of different
pathophysiologic processes associated with abnormal kidney function and a
progressive decline in glomerular filtration rate (GFR). Recently updated
classification, in which stages of CKD are stratified by both estimated GFR and
the degree of albuminuria, in order to predict risk of progression of CKD.
Previously, CKD had been staged solely by the GFR. However, the risk of
worsening of kidney function is closely linked to the amount of albuminuria, and
so it has been included in the latest classification.1 The term End-Stage Kidney
Disease (ESRD), which is the stage of CKD where there is accumulation of
toxins, fluids, and electrolytes that cannot be excreted by the kidneys, causing
uremic syndrome. This syndrome causes death unless the toxin is released by
renal replacement therapy, using dialysis or kidney transplantation.2,3
The human immunodeficiency virus (HIV) pandemic has spread to every
country in the world and has infected 59 million people worldwide. It is estimated
that around 1.1 million people in the United States have been infected with HIV.
This disease is most often found in injection drug usersin hemophilia patients and
other recipients of blood transfusions, in sexual partners of patients with AIDS
and among babies born to mothers with AIDS. In 1983, human immunodeficiency
virus (HIV) was isolated from a patient with lymphadenopathy, and in 1984 it was
clearly demonstrated as the agent that causes AIDS. In 1985, an examination of an
enzyme-linked immunosorbent assay (ELISA) was developed which began a
further assessment of the scope and evolution of the HIV epidemic.4
Tremendous progress has been made in understanding and reducing risk of
human immunodeficiency virus (HIV) transmission from blood transfusion. The
major interventions that are used to minimize this risk include questioning of
donors concerning HIV risk behaviors and laboratory testing of each donated unit.

1
The rate of HIV seropositivity in the blood donor population has been shown to be
approximately 0.5 per 10,000 donations, a value much lower than the rate of 3.5
per 10,000 donations shortly after the introduction of routine HIV antibody
screening.5
This case report will describe CKD patients who undergo routine
hemodialysis with HIV positive.

2. CASE
A 42 years old Acehnese man come with anemic. The patient had been
diagnosed with chronic kidney disease since May 2013. The patient then started
hemodialysis in RS Sigli and in September 2013 patients cannot urinate. Patients
begin blood transfusions since 2017 every 2 months. On February 6, 2018 patients
were diagnosed with HIV. No weight loss, canker sores, lymph nodes or coughing
were found. There is no history of drug use or unsafe sex. Patients with a history
of smoking and have stopped in 2015. Patients have 2 children, the first child is
5.5 years old and the second child is 3 years old, the wife and children have been
carried out rapid tests with non-reactive results. Patients took Amlodipine 1x10
mg, valsartan 1x80 mg, 2x 400 mcg folic acid obtained from RSUDZA.
When a vital sign examination was performed, the patient is compos mentis
with blood pressure 160/90 mmHg, pulse 80 times per minute, breathing 20 times
per minute and temperature 36.9 oC. The nutritional status of patients is, body
weight 57 kg, height 160 cm, and body mass index of 22.2 Kg/m2. From the
results of physical examination found pale conjunctiva. No oral candidiasis and
enlarged lymph nodes were found, the breathing sounds normal without rhonki or
wheezing. No ascites or edema is found. Other physical examinations is in normal
limits. Laboratory results obtained Hb 7.2 g/dl, leukocytes 5.8 x 103/ul, platelets
74 x 103/ul, Hct 39%, urea 137 mg/dl, creatinine 14.39 mg/dl, sodium 137
mmol/L, potassium 6.1 mmol/L, chloride 113 mmol/L and GFR 5.39
ml/min/1.73m2. The patient has performed a renal ultrasound examination with
the results of chronic parenchymal right kidney disease. From the examination of
CD4 levels on November 2, 2018 the results were 292/μL.

2
 The patient diagnosed with chronic kidney disease in positive HIV.
Patients received Tenofovir 300 mg therapy every Wednesday post Hemodialysis,
Lamivudin 1x100 mg, Efaviren 1x600 mg and Cotrimoxazol 1x960 mg.

3. DISCUSSION
Chronic kidney disease (CKD) encompasses a spectrum of different
pathophysiologic processes associated with abnormal kidney function and a
progressive decline in glomerular filtration rate (GFR). Recently updated
classification, in which stages of CKD are stratified by both estimated GFR and
the degree of albuminuria, in order to predict risk of progression of CKD.
Previously, CKD had been staged solely by the GFR. However, the risk of
worsening of kidney function is closely linked to the amount of albuminuria, and
so it has been included in the latest classification.1,6 The CKD classification is
presented in figure 1.
The pathophysiology of CKD involves two mechanisms: (1) the occurrence of
specific mechanisms for the underlying etiology (for example, genetically
acquired abnormalities in development or integrity of kidney, immune complex
deposition and inflammation in certain types of glomerulonephritis) and (2) a
progressive mechanisms, which involve hyperfiltration and hypertrophy of the
nephron which are a common consequence after kidney mass reduction,
regardless of the underlying etiology. The response to the nephrons reduction is
mediated by vasoactive hormones, cytokines, and growth factors. The short-term
adaptation of hypertrophy and hyperfiltration becomes maladaptive because the
pressure and flow of the nephron increases which is a predisposing factor to the
distortion of glomerular architecture, abnormal podocyte function, and impaired
filtration barrier that leads to sclerosis and the breakdown of the remaining
nephrons. Increased intrarenal activity of the renin-angiotensin system (RAS)
contributes to early adaptive hyperfiltration as well as advanced maladaptive
hypertrophy and sclerosis.1,7
It is important to identify factors that increase the risk of CKD, even in
individuals with a normal GFR. Risk factors include low birth weight, history of
childhood obesity, hypertension, diabetes mellitus, autoimmune disease, elderly,

3
African, family history with kidney disease, previous acute kidney injury, and the
findings of proteinuria, abnormal urine sediments, or urinary tract structural
abnormalities. 1,8
Patients in this case report have hypertension as a risk factor. Other risk
factors such as diabetes mellitus, autoimmune diseases, a history of acute kidney
injury were not present.

Figure 1. Kidney Disease Improving Global Outcome (KDIGO) classification

for CKD.1,5

Based on this classification, patients in this case report, with GFR 5.39 ml /
min / 1.73m2 classified as kidney failure. Based on this classification, patients
with kidney failure have poor outcomes, so kidney replacement therapy is
recommended.
The main goal of management of hypertension in CKD patients is to prevent
extrarenal complications from high blood pressure, such as cardiovascular disease
and stroke. Although the benefits of such management in an effort to inhibit the
development of CKD have still not been proven, the benefits for heart and
neurological health are enormous. In CKD patients with diabetes or proteinuria> 1

4
g per 24 hours, blood pressure should be reduced to 130/80 mmHg, if no adverse
side effects. Salt restriction must be first-line therapy. When volume management
alone is not enough to reduce blood pressure, the choice of antihypertensive
agents given is similar to the general population. ACE inhibitors and ARBs can
slow the rate of decline in kidney function through a mechanism of systemic
arterial pressure reduction and correction of intraglomerular hyperfiltration. 1,9
Patients in this case report received amlodipine 1x10mg and valsartan 1x80
mg as a therapy for hypertension
Normocytic, normochromic anemia can be observed in CKD stage 3 patients
and can be found in almost all stage 4 patients. The main cause of anemia in CKD
patients is a lack of erythropoietin (EPO) production. Anemia in CKD patients is
associated with a number of adverse pathophysiological consequences, including
a decrease in the delivery and utilization of tissue oxygen, increased cardiac
output, ventricular dilation, and ventricular hypertrophy. Clinical manifestations
include fatigue and reduced exercise tolerance, angina, heart failure, decreased
cognition and mental acuity, and impaired host defense against infection. In
addition, anemia can play a role in growth restriction in children with CKD. 1
Based on theory, patients in this case report had anemia with hemoglobin 7.2
mg/dl. Patients do not get ESA therapy but patients get blood transfusions every 2
months.
The prevalence of HIV infection in dialysis patients varies based on the
demographics of the ESRD population. HIV seropositivity has been reported in
nearly 20 percent of dialysis patients in cities with high HIV seroprevalence.
Based on data from the United States Renal Data System (USRDS), there is 800
to 900 cases of HIV acquired nephropathy (HIVAN) every year in the US,
especially in black people. The prevalence of HIV infection among dialysis
patients based on serological examination and/or polymerase chain reaction (PCR)
also does not show definite numbers. Like previous data, HIV seroprevalence
varies according to community and local demographic features, ranging from 0 to
20 percent. In addition, there is no consensus regarding HIV testing in dialysis
populations, making it difficult to obtain representative data nationally.4,10

5
 HIV is transmitted primarily through sexual contact, blood or blood products
and by infected mothers to infants, intrapartum, perinatal, or through breast milk.
There is no evidence that HIV is transmitted through direct contact or that viruses
can be spread by insects, such as mosquito bites.4 Table 1 explains the risk of HIV
transmission.

Table 1. Estimated Risk of HIV Transmission4

Type of exposure Risk per 100,000 Exposures
Parenteral
Blood transfusion 9250
Needle-sharing during injection drug use 63
Percutaneous (needle-stick) 23
Sexual
Receptive anal intercourse 138
Insertive anal intercourse 11
Receptive penile-vaginal intercourse 8
Insertive penile-vaginal intercourse 4
Receptive oral intercourse Low
Insertive oral intercourse Low
Other
Biting Negligible
Spitting Negligible
Throwing body fluids (including semen or saliva) Negligible
Sharing sex toys Negligible

Based on the table it can be seen that the highest risk of HIV transmission
is through blood transfusion. HIV can be transmitted to individuals who get
transfusions of HIV-contaminated blood, blood products, or transplanted tissue.
Although blood screening for HIV has been universally carried out even in
developing countries, unfortunately in some resource-poor countries HIV
continues to be transmitted by blood, blood products, and tissues due to
inadequate screening. Whole blood transfusions, packet red blood cells, platelets,
leukocytes, and plasma can transmit HIV. In other hand, hyperimmune gamma
globulin, hepatitis B immune globulin, plasma-derived hepatitis B vaccine, and
Rho immune globulin are not associated with transmission of HIV infection.4
At present, the application of the following steps has made the risk of
transmitting HIV infection through transfused blood or very small blood products

6
such as HIV-1 and HIV-2 antibody screening and HIV nucleic acid, careful
selection of potential blood donors with medical history questionnaires to exclude
Individuals with risky behavior, screening HIV-negative individuals through
serological testing of patients with infections who have a risk of HIV, such as
hepatitis B and C and syphilis. It is currently estimated that the risk of HIV
infection in the United States through blood transfusions is around 1 in 2 million
units of blood. Because there are 16 million blood collected in the United States
each year, one cannot completely eliminate the risk of HIV-related transmission
through transfusion. HIV transmission (both HIV-1 and HIV-2) by blood or blood
products is still a threat in developing countries, especially in countries where
routine blood screening is not done universally. 4,11
According to the theory, the high risk of HIV transmission through blood
transfusion is a major cause of HIV transmission to these patients. This allegation
is also strengthened by the absence of unsafe sexual contact by patients.
The hallmark of HIV is an immune deficiency caused mainly by
progressive deficiency of a subset of T lymphocytes called T helper cells. The
phenotypic helper T cells are found on the surface of the CD4 molecule, which
functions as the main cellular receptor for HIV. Co-receptors are found on CD4 in
the process of binding, fusion, and the entry of HIV-1 into the target cell. HIV
uses two main co-receptors, CCR5 and CXCR4 so they can fuse and enter. This
co-receptor is also the main receptor of the chemoattractive cytokine called
chemokine. A number of mechanisms responsible for cell depletion and/or CD4+
T cell immune dysfunction have been demonstrated in vitro including direct
infection and destruction of cells by HIV, and indirect effects such as cleaning
infected immune cells, cell death associated with aberrant activities and immune
fatigue which causes cellular dysfunction. Patients with CD4 + T cell levels below
a certain threshold are at high risk of developing opportunistic diseases, especially
infections and neoplasms defined as AIDS. Some features of AIDS, such as
Kaposi's sarcoma and certain neurological disorders, cannot be fully explained by
immune deficiencies caused by HIV infection, because these complications can
occur before severe immunological abnormalities occur.4

7
 Figure 2. The HIV Infection4

The combination of viral and immunopathogenic pathogen events that

occur during the course of HIV from initial (primary) infection to advanced
disease is a complex and varied event. It should be understood that the pathogenic
mechanisms of HIV are multifactorial and multifaceted and can differ at various
stages of the disease. Therefore, it is very important to consider the typical clinical
course of people infected with HIV.4
The CDC has recommended screening for HIV infection in routine clinical
practice. The diagnosis of HIV infection depends on the demonstration of
antibodies to HIV and/or the direct detection of HIV or one of its components.
Antibodies to HIV generally appear in circulation 3-12 weeks following infection.
The standard blood screening test for HIV infection is based on detection of
antibodies to HIV. The commonly used platform is ELISA, also reffered to as
enzyme immunoassay (EIA). This solid-phase assay is an extremely good
screening test with a sensitivity of >99.5%. EIA tests generally have a positive
value (very reactive), negative (nonreactive), or uncertain (partially reactive).
Although EIA is a very sensitive test, its not optimal with regard to specificity.
This greatly affects especially the low-risk individuals, such as voluntary blood
donors. In this population, only 10% of EIA positive individuals were confirmed
to have HIV infection. Among the factors associated with false positive EIA tests

8
are antibodies to class II antigens, autoantibodies, liver disease, influenza
vaccinations, and acute viral infections. For this reason, anyone suspected of
having HIV infection based on positive or inconclusive EIA results must have
confirmed results with more specific tests such as Western blot.4,12
The most commonly used confirmatory test is Western blot. This assay
uses HIV antigens with different molecular weights that produce specific
antibodies. These antigens can be separated based on molecular weight, and
antibodies for each component can be detected as bands on Western blots. A
negative Western blot is one in which no bands are present at molecular weights
Corresponding to HIV gene products. In a patient with a positive or indeterminate
EIA and a negative Western blot, one can conclude with certainty that the EIA
reactivity was a false positive. On the other hand, a Western blot demonstrating
antibodies to products of all three of the major genes of HIV (gag, pol, and env) is
conclusive evidence of infection with HIV. Criteria established by the U.S. Food
and Drug Administration (FDA) in 1993 for a positive Western blot state that a
result is considered positive if antibodies exist to two of the three HIV proteins:
p24, gp41, and gp120/160. Compared with other risk populations, routine HIV
testing in ESRD patients is associated with an increase in false-positive EIA
findings and intermediate-positive Western blot results.4, 13
CD4 + counts are generally accepted laboratory tests as the best indicator
in directly describing patients' immunological competencies for HIV infection.
Patients with CD4 + T cells <200 / μL have a high risk of P. jiroveci infection,
while patients with CD4 T cell counts <50 / μL are at high risk of CMV infection,
mycobacteria from M. Avium complex (MAC), and/or T. gondii. After CD4 T
cell counts + <200 / μL, patients should be placed on a regimen for P. Jiroveci
prophylaxis, and once the count is <50/μL, primary prophylaxis for MAC
infection is indicated. Patients with HIV infection must take CD4 + T cell
measurements taken at the time of diagnosis and every 3-6 months thereafter.
More frequent measurements should be taken if declined tren is noted.4, 14
The clinical consequences of HIV infection include a spectrum that starts
from the acute syndrome associated with primary infection, prolonged
asymptomatic to advanced disease. Active viral replication and progressive

9
immunological disorders occur throughout the course of HIV infection in most
patients. Since the mid-1990s, cART has had a major impact on preventing and
controlling disease progression.4

Acute HIV Infection

It is estimated that 50-70% of HIV-infected individuals experience acute
clinical syndrome around 3-6 weeks after primary infection. Varying degrees of
clinical severity have been reported, and although it has been suggested that
symptomatic seroconversion leading to the seeking of medical attention indicates
an increased risk for an accelerated course of disease, there does not appear to be
a correlation between the level of the initial burst of viremia in acute HIV
infection and the subsequent course of disease. It has been reported that several
symptoms of the acute HIV syndrome (fever, skin rash, pharyngitis, and myalgia)
occur less frequently in those infected by injection drug use compared with those
infected by sexual contact. The syndrome is typical of an acute viral syndrome
and has been likened to acute infectious mononucleosis. Symptoms usually persist
for one to several weeks and gradually subside as an immune response to HIV
develops and the levels of plasma viremia decrease. Opportunistic infections have
also been reported during this stage which reflect immune deficiencies resulting
from a reduced number of CD4 + T cells and from the dysfunction of CD4+ T
cells owing to viral protein and endogenous cytokine-induced perturbations of
cells associated with the extremely high levels of plasma viremia. A number of
immunological abnormalities accompany acute HIV syndromes, including
multiphase disorders of the circulating subset of lymphocytes. The total number of
lymphocytes and subset of T cells (CD4 + and CD8 +) initially decreases.
Increasing the ratio of CD4 + / CD8 + T cells occurs due to an increase in the
number of CD8 + T cells. The total number of circulating CD8 + T cells can
increase or be normal but the level of CD4 + T cells is usually depressed even
though there is a slight rebound towards normal. Lymphadenopathy occurs in
about 70% of individuals with primary HIV infection. Most patients recover
spontaneously from this syndrome and most patients experience only a slight
suppression of the number of CD4 T cells.4,11

10
 Asymptomatic Stage
Although the length of time from initial infection to the appearance of
clinical diseases varies greatly. The median time of occurrence of disease in
untreated patients is around 10 years. In this asymptomatic state, HIV is active
and progressively replicating. The rate of development of the disease correlates
directly with the level of HIV RNA. Patients with high plasma HIV viral load
experience symptoms faster than patients with low HIV viral load. Some patients
remain symptomatic regardless of the number of CD4 + T cells that decline
progressively to very low levels. In these patients, the appearance of opportunistic
infections may be the first manifestation of HIV infection. During the
asymptomatic period of HIV infection, the average reduction in CD4 + T cells is
around 50 / μL per year. When the number of CD4 + T cells drops to <200 / μL,
the immunodeficiency conditions produced are severe enough to place patients at
a high risk of opportunistic infections and neoplasms and therefore the disease
becomes clinically apparent.4
In this patient, CD4 + level count was 292/μL. This finding shows the
immunity of patients who are still competent so that patients do not complain of
symptoms related to HIV or other opportunistic infections. From physical
examination there are also no opportunistic infections found in the oral mucosa,
lymph nodes or lung infections.

Symptomatic Disease
Symptoms of HIV disease can occur at any time during the course of HIV
infection. In general, the spectrum of diseases we observe changes when the
number of CD4 + T cells decreases. The more severe and life-threatening
complications of HIV infection occur in patients with CD4 + T counts <200 / μL.
An AIDS diagnosis is made on people aged 6 years and older with HIV infection
and CD4 + T <200 / μL and in anyone with HIV infection who has one HIV-
related disease that indicates severe damage from cell-mediated immunity. While
the secondary infectious agents are typical opportunistic organisms such as P.
jiroveci, atypical mycobacteria, CMV, and other organisms that usually cannot
cause disease without a disruption of the immune system. These pathogens also

11
include common bacterial and mycobacterial pathogens. Overall, the clinical
spectrum of HIV continues to change when patients live longer and when new and
improved approaches to treatment and prophylaxis occur. In addition to classic
AIDS, patients with HIV infection also experience an increased risk of serious
non-AIDS diseases, including non-AIDS related cancers and cardiovascular,
kidney and liver disease. Non-AIDS events dominate the disease burden in
patients with HIV infection who receive ART.4
The management of patients with HIV infection requires not only
comprehensive knowledge about the possible disease processes and experience of
using ART, but also the ability to deal with chronic problems, which are
potentially life-threatening.4,15
Combination of antiretroviral therapy (cART), also referred to as highly
active antiretroviral therapy (HAART), is the cornerstone of managing patients
with HIV infection. Emphasis on HIV replication is an important component in
prolonging survival and in improving the quality of life for patients with HIV
infection. Adequate emphasis requires strict adherence to prescribed antiretroviral
drug regimens.4,11
Currently the drugs used for the treatment of HIV infection are
incorporated in a combination regimen that is divided into four categories: drugs
that inhibit reverse transcriptase enzyme (nucleoside and nucleotide reverse
transcriptase inhibitors; nonnucleoside reverse transcriptase inhibitors), drugs that
inhibit viral protease enzymes (protease inhibitors) , drugs that inhibit viral
integrase enzymes (integrase inhibitors), and which interfere with the entry of
viruses (fusion inhibitors; CCR5 antagonists).4

12
 Table 2. Antiretroviral Drugs Used in the Treatment of HIV Infection.4
Drug Dose in Combination Toxicity
Nucleoside or Nucleotide Reverse Transcriptase Inhibitors

Anemia, granulocytopenia, myopathy,

Zidovudine (AZT,
lactic acidosis, hepatomegaly with
azidothymidine, Retrovir, 200 mg q8h or 300 mg
steatosis, headache, nausea, nail
3‘azido-3‘- bid
pigmentation, lipid abnormalities,
deoxythymidine)
lipoatrophy, hyperglycemia

Lamivudine (Epivir, 2‘3‘-

Flare of hepatitis in HBV-coinfected
dideoxy-3‘- thiacytidine, 150 mg bid or 300 mg qd
patients who discontinue drug
3TC)

Hepatotoxicity in
Emtricitabine (FTC,
200 mg qd HBV-co-infected patients who
Emtriva)
discontinue drug, skin discoloration

Hypersensitivity reaction In HLA-

B5701+ individuals (can be fatal); fever,
Abacavir (Ziagen) 300 mg bid
rash, nausea, vomiting, malaise or
fatigue, and loss of appetite

Renal, osteomalacia, flare of hepatitis in

Tenofovir (Viread) 300 mg qd HBV-co-infected patients who
discontinue drug
Non-Nucleoside Reverse Transcriptase Inhibitors
200 mg/d × 14 days then
Nevirapine (Viramune) 200 mg bid or 400 mg Skin rash, hepatotoxicity
extended release qd

Rash, dysphoria, elevated liver function

tests, drowsiness, abnormal dreams,
Efavirenz (Sustiva) 600 mg qhs
depression, lipid abnormalities,
potentially teratogenic
Etravirine (Intelence) 200 mg bid Rash, nausea, hypersensitivity reactions
Nausea, dizziness, somnolence,
Rilpivirine (Edurant) 25 mg qd vertigo, less CNS toxicity
and rash than Efavirenz
Protease Inhibitors
Nausea, abdominal pain, hyperglycemia,
600 mg bid (also used in
fat redistribution, lipid abnormalities,
Ritonavir (Norvir) lower doses as
may alter levels of many other drugs,
pharmacokinetic booster)
paresthesias, hepatitis

13
 400 mg qd or 300 mg qd Hyperbilirubinemia, PR prolongation,
+ ritonavir 100 mg qd nausea, vomiting, hyperglycemia, fat
Atazanavir (Reyataz)
when given with maldistribution, rash transaminase
efavirenz elevations, renal stones

600 mg + 100 mg Diarrhea, nausea, headache, skin rash,

Darunavir (Prezista) ritonavir twice daily with hepatotoxicity, hyperlipidemia,
food hyperglycemia
Entry Inhibitors
Local injection reactions,
Enfuvirtide (Fuzeon) 90 mg SC bid hypersensitivity reactions, increased rate
of bacterial pneumonia

Hepatotoxicity, nasopharyngitis,
150–600 mg bid
fever, cough, rash, abdominal
Maraviroc (Selzentry) depending on
pain, dizziness, musculoskeletal
concomitant medications
symptoms
Integrase Inhibitor
Nausea, headache, diarrhea, CPK
Raltegravir (Isentress) 400 mg bid elevation, muscle weakness,
rhabdomyolysis
Diarrhea, nausea, upper respiratory
Elvitegravir 1 tablet daily
infections, headache
50 mg daily for
treatment-naïve patients
50 mg twice daily for
Insomnia, headache, hypersensitivity
Dolutegravir (Tivicay) treatment-experienced
reactions, hepatotoxicity
patients or those also
receiving efavirenz or
rifampin

Table 3. Dosing of antiretroviral drugs for HIV-infected adults with chronic

kidney disease (CKD) or end-stage renal disease (ESRD).9
Antiretroviral drug, dosing category
Nucleoside reverse-transcriptase inhibitors
Zidovudine 300 mg po b.i.d.
Usual dosage
Dosage for patients with CKD or ESRD
Cretinine Clearance ≥ 15 mL/min No adjusment
Cretinine Clearance < 15 mL/min 100 mg po q6–8h
Receaiving hemodialysis 100 mg po q6–8h
Receaiving peritoneal dialysis 100 mg po q6–8h
Lamivudine
Usual dosage 150 mg po b.i.d./300 mg po q.d.
Dosage for patients with CKD or ESRD

14
 Creatinine clearance ≥ 50 mL/min No adjustment
Creatinine clearance 30-49 mL/min 150 mg po q.d.
Creatinine clearance 15-29 mL/min 150 mg po first dose, then 100 mg po q.d.
Creatinine clearance 5-14 mL/min 150 mg po first dose, then 50 mg po q.d.
Creatinine clearance <5mL/min 50 mg po first dose, then 25 mg po q.d.
Receiving hemodyalisis 50 mg po first dose, then 25 mg po q.d
Receiving peritoneal dyalisis 50 mg po first dose, then 25 mg po q.d.
Abacavir
Usual dosage 300 mg po b.i.d./600 mg po q.d.
Dosage for patients with CKD or ESRD
All creatinine clearances No adjustment
Receiving hemodyalisis No adjustment
Receiving peritoneal dyalisis Unknown, use with caution
Stavudine immediate release (IIR)
Body weight ≥60 kg
Usual dosage 40 mg po b.i.d.
Dosage for patients with CKD or ESRD
Creatinine clearance >50mL/min No adjustment
Creatinine clearance 26-50mL/min 20 mg po b.i.d.
Creatinine clearance ≤25mL/min 20 mg po q.d.
Receiving hemodialysis 20 mg po q.d.
Receiving peritoneal dialysis Unknown, use with caution
Body weight <60 kg
Usual dosage 30 mg po b.i.d.
Dosage for patients with CKD or ESRD
Creatinine clearance >50mL/min No adjustment
Creatinine clearance 26-50mL/min 15 mg po b.i.d.
Creatinine clearance ≤25mL/min 15 mg po b.i.d.
Receiving hemodialysis 15 mg po b.i.d.
Receiving peritoneal dialysis Unknown, use with caution
Stavudine XR
Body weight ≥60 kg
Usual dosage 100 mg po q.d.
Dosage for patients with CKD or ESRD
Creatinine clearance >50mL/min No dose adjustment
Creatinine clearance ≤50mL/min Unknown, use stavudine IR
Body weight <60 kg
Usual dosage 75 mg po q.d.
Dosage for patients with CKD or ESRD
Creatinine clearance >50mL/min No dose adjustment
Creatinine clearance ≤50mL/min Unknown, use stavudine IR
Didanosine buffered tablets
Body weight ≥60 kg
Usual dosage 200 mg po b.i.d.

15
 Dosage for patients with CKD or ESRD
Creatinine clearance ≥60 mL/min No adjustment
Creatinine clearance 30-59 mL/min 200 mg po q.d.
Creatinine clearance 10-29 mL/min 150 mg po q.d.
Creatinine clearance <10 mL/min 100 mg po q.d.
Receiving hemodialysis 100 mg po q.d.
Receiving peritoneal dialysis 100 mg po q.d.
Body weight <60 kg
Usual dosage 125 mg po b.i.d.
Dosage for patients with CKD or ESRD
Creatinine clearance ≥60 mL/min No adjustment
Creatinine clearance 30-59 mL/min 150 mg po q.d.
Creatinine clearance 10-29 mL/min 100 mg po q.d.
Creatinine clearance <10 mL/min 75 mg po q.d.
Receiving hemodialysis 75 mg po q.d.
Receiving peritoneal dialysis 75 mg po q.d.
Didanosine EC
Body weight ≥60 kg
Usual dosage 400 mg po q.d.
Dosage for patients with CKD or ESRD
Creatinine clearance ≥60 mL/min No adjustment
Creatinine clearance 30-59 mL/min 200 mg po q.d.
Creatinine clearance 10-29 mL/min 125 mg po q.d.
Creatinine clearance <10 mL/min 125 mg po q.d.
Receiving hemodialysis 125 mg po q.d.
Receiving peritoneal dialysis 125 mg po q.d.
Body weight <60 kg
Usual dosage 250 mg po q.d.
Dosage for patients with CKD or ESRD
Creatinine clearance ≥60 mL/min No adjustment
Creatinine clearance 30-59 mL/min 125 mg po q.d.
Creatinine clearance 10-29 mL/min 125 mg po q.d.
Creatinine clearance <10 mL/min Do not use; use buffered tablets instead
Receiving hemodialysis Do not use; use buffered tablets instead
Receiving peritoneal dialysis Do not use; use buffered tablets instead
Zalcitabine
Usual dosage 0.75 mg po t.i.d.
Dosage for patients with CKD or ESRD
Creatinine clearance ≥40 mL/min No adjustment
Creatinine clearance 10-40 mL/min 0.75 mg po q12h
Creatinine clearance <10 mL/min 0.75 mg po q24h
Receiving hemodyalisis Unknown, use with caution
Receiving peritoneal dyalisis Unknown, use with caution
Emtricitabine

16
 Usual dosage 200 mg po q.d.
Dosage for patients with CKD or ESRD
Creatinine clearance ≥50 mL/min No adjustment
Creatinine clearance 30-49 mL/min 200 mg po q48h
Creatinine clearance 10-29 mL/min 200 mg po q72h
Creatinine clearance <10 mL/min 200 mg po q96h
Receiving hemodialysis 200 mg po q96h
Receiving peritoneal dialysis Unknown, use with caution
Tenofovir
Usual dosage 300 mg po q.d.
Dosage for patients with CKD or ESRD
Creatinine clearance ≥50 mL/min No adjustment
Creatinine clearance 30-49 mL/min 300 mg po q48h
Creatinine clearance 10-29 mL/min 300 mg po q72h
Receiving hemodialysis 300 mg po every 7 days
Receiving peritoneal dialysis Unknown, use with caution
Emtricitabine/tenofovir
Usual dosage 200 mg/300 mg po q.d.
Dosage for patients with CKD or ESRD
Creatinine clearance ≥50 mL/min No adjustment
Creatinine clearance 30-49 mL/min One tab po q48h
Unknown, should not use combination
Creatinine clearance <30 mL/min tablet

Nonnucleoside reverse-transcriptase inhibitors

Nevirapine
Usual dosage 200 mg po b.i.d.
Dosage for patients with CKD or ESRD
Creatinine clearance >20 mL/min No adjustment
Receiving hemodialysis No adjustment
Receiving peritoneal dialysis Unknown, use with caution
Efavirenz
Usual dosage 600 mg po q.d.
Dosage for patients with CKD or ESRD No adjustment
Delavirdine
Usual dosage 400 mg po t.i.d.
Dosage for patients with CKD or ESRD No adjustment

Protease Inhibitors
Indinavir
Usual dosage 800 mg po t.i.d.
Dosage for patients with CKD or ESRD No adjustment
Saquinavir soft gel
Usual dosage 1200 mg po t.i.d.
Dosage for patients with CKD or ESRD No adjustment

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 Saquinavir hard gel
Usual dosage 600 mg po t.i.d.
Dosage for patients with CKD or ESRD No adjustment
Nelfinavir
Usual dosage 1250 mg po b.i.d.
Dosage for patients with CKD or ESRD No adjustment
Amprenavir
Usual dosage 1200 mg po b.i.d.
Dosage for patients with CKD or ESRD No adjustment
Fosampenavir
Usual dosage 1400 mg po q.d./700 mg po b.i.d.
Dosage for patients with CKD or ESRD No adjustment
Ritonavir
Usual dosage 600 mg po b.i.d.
Dosage for patients with CKD or ESRD No adjustment
Lopinavir/ritonavir
Usual dosage 400 mg/100 mg po b.i.d.
Dosage for patients with CKD or ESRD No adjustment
Ataznavir
Usual dosage 400 mg po q.d.
Dosage for patients with CKD or ESRD No adjustment

Entry/fusion inhibitors
Enfuvirtide
Usual dosage 90 mg sc b.i.d.
Dosage for patients with CKD or ESRD
Creatinine clearance ≥35 mL/min No adjustment
Creatinine clearance <35 mL/min Unknown, use with caution

Patients in this case report received cART therapy, Tenofovir 300 mg

every Wednesday post Hemodialysis, Lamivudin 1x100 mg, and Efaviren 1x600
mg.
Dialysis and kidney transplantation have extended the life span of CKD
patients worldwide. The indications for starting renal replacement therapy in
patients with CKD include uremic pericarditis, intractable muscle cramping
encephalopathy, anorexia, and unclear causes of nausea, nutritional deficiencies,
and fluid and electrolyte disorders.4,8
HIV transmission on dialysis units can be avoided by strict application of
standard infection control procedures. The Center for Disease Control and
Prevention (CDC) does not recommend routine isolation or special machines for

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HIV-infected patients undergoing hemodialysis, given the low probability of
transmission from patient to patient and/or from patient to staff. In the United
States, transmission of HIV infection from patients to patients has not been
reported on the dialysis unit. However, at least four well-documented outbreaks of
HIV transmission have occurred since 1990 in hemodialysis units outside the
United States, including Argentina, Colombia and Egypt. The most likely cause of
transmission is a violation of the infection control protocol. However, there is no
single etiology that can be identified. Possibilities include reuse of dialyzer, blood
lines and needles in different patients, use of weak chemical germicides
(benzalkonium chloride); port contamination connecting the dialysis machine to
the blood line; and the use of contaminated heparin vials. The risk of HIV
seroconversion after injection needle injury is estimated to be 3 out of 1000 or 0.3
percent. Post-exposure prophylaxis with antiretroviral therapy should be given to
exposed health workers.4
Death among dialysis patients infected with HIV is closely related to the
course of HIV infection. Increased survival is associated with the early stages of
HIV infection at the start of kidney replacement therapy, younger age, higher CD4
cell count, and use of ART. Long-term exposure to ART is associated with an
increased risk of cardiovascular disease in HIV-positive dialysis patients.
Regulations containing protease inhibitors and nucleoside reverse transcriptase
inhibitors (NRTIs) are associated with metabolic disorders and endothelial
dysfunction. 16

4. CONCLUSION
1. A case of an HIV-positive patient with CKD which undergo routine
hemodialysis has been reported. Patients do not have risk factors for HIV
transmission unless blood transfusions. Patients without HIV symptoms and
currently receiving Tenofovir 300 mg every Wednesday post Hemodialysis,
Lamivudin 1x100 mg, Efaviren 1x600 mg and Cotrimoxazol 1x960 mg.
2. CKD risk factors include low birth weight, history of childhood obesity,
hypertension, diabetes mellitus, autoimmune disease, elderly, African, family
history with kidney disease, previous acute kidney injury, and the findings of

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 proteinuria, abnormal urine sediment, or urinary tract structural
abnormalities. This patient only has one risk factor, hypertension.
3. The risk of HIV infection in the United States through blood transfusion is
about 1 in 2 million units of blood. Patients cannot completely eliminate the
risk of HIV-related transmission through transfusion. The high risk of HIV
transmission through blood transfusion is a major cause of HIV transmission
to patients. Allegations are also reinforced by the absence of unsafe sexual
contact by patients.
4. Death among dialysis patients infected with HIV is closely related to the
course of HIV infection. Increased survival is associated with the early stages
of HIV infection at the start of kidney replacement therapy, younger age,
higher CD4 cell count, and use of ART. Long-term exposure to ART is
associated with an increased risk of cardiovascular disease in HIV-positive
dialysis patients. Regulations containing protease inhibitors and nucleoside
reverse transcriptase inhibitors (NRTIs) are associated with metabolic
disorders and endothelial dysfunction.

Reference

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