CKD pada B20

HIV-associated nephropathy (HIVAN), formerly known

as AIDS-associated nephropathy, is characterized by
the following findings:
1. Nephrotic range proteinuria
2. Azotemia
3. Normal to large kidneys on ultrasound images
4. Normal pressure
5. Focal segmental glomerulosclerosis (FSGS) on renal
biopsy findings

Moro O Salifu et al, HIV-associated Nephropathy, 2014

Guidelines for the Management of

Chronic Kidney Disease in HIVInfected Patients:
Recommendations of the HIV
Medicine Association of the
Infectious
Diseases
Society
of with CKD
Up
to 60% of all renal
biopsies performed
for patients
reveal
characteristic histological findings designated as HIVAN,
America
which is a collapsing form of focal glomerulosclerosis (FSGS)
with tubulointersitial injury, most often presenting as the
nephrotic
syndrome.
Even in patients
with normal kidney function, the presence of
proteinuria may indicate early kidney disease.

Guidelines for the Management of

Chronic Kidney Disease in HIVInfected Patients:
Recommendations of the HIV
Medicine Association of the
Infectious
Diseases
Society
of
Follow-up urine analyses are recommended to screen for newly
developed kidney
America
damage for the following groups, which are at higher risk for the
development of proteinuria and poor renal outcome:
1. African American persons
2. Patients with diabetes
3. Patients with hypertension
4. Patients with hepatitis C virus coinfection, and
5. Patients with HIV RNA levels 14000 copies/mL or absolute CD4+
lymphocyte counts < 200 cells/mL

Management
Recommendation 1. In HIV-infected patients with evidence of
nephropathy, blood pressure should be controlled to a level no
higher than 125/75 mm Hg (B-III), with the initial preferential use of
ACE inhibitors or ARBs for those patients with proteinuria (B-II).
Calcium channel blockers should be avoided in patients receiving
protease inhibitors (D-II).
Recommendation 2. Dialysis and the placement of arterio-venous
fistulae (native fistulae preferred [A-II]) should not be withheld for
patients solely because of HIV infection (A-II).
Recommendation 3. Renal transplantation may be considered for
patients with ESRD if provided in a supervised clinical trial or at
centers with adequate experience in this area (C-III).
Recommendation 4. Patients with HIVAN should be treated with
HAART at diagnosis (B-II). HAART should not be withheld from
patients simply because of the severity of their renal dysfunction (BIII).
Recommendation 5. Addition of ACE inhibitors, ARBs, and/or
prednisone should be considered in patients with HIVAN if HAART
alone does not result in improvement of
renal function (B-II).
HAART: Highly active antiretroviral therapy

Invasive Cervical Cancer Risk

Among HIV-infected Women
Abraham GA et al, J Acquir Immune Defic
Syndr.2013;62(4):405-413.
HIV infection and low CD4+T-cell count are associated with an
increased risk of persistent oncogenic human papillomavirus infection
the major risk factor for cervical cancer.
Data from large prospective study of ICC in HIV-infected women
suggest that maintaining CD4 at higher counts could lower ICC risk.

Human immunodefisiensi virus(HIV) diduga berhubungan dengan lesi

prakanker dan kanker serviks atas dasar bahwa sistem imunitas
berperan penting pada proses keganasan yang multi faktorial. Sistem
imunitas yang tertekan merupakan predisposisi infeksi virus onkogenik,
apalagi dengan keadaan mekanisme regulalasi sel yang sudah
terganggu akan mempercepat perkembangan keganasan. Insiden NIS
meningkat pada kasus HIV yaitu NIS didapatkan sebanyak 13% pada
HIV seronegatif, 17% pada HIV seropositif tanpa AIDS, dan 42% pasien
HIV seropositif dengan AIDS (Wrightet al., 1999).

Patofisiologi Human Papillomavirus

pada kanker serviks

Human papillomavirus berkontribusi dalam perkembangan

lesi neoplastik melalui onkoprotein virus yang disebut dengan
E6 dan E7.
Onkoprotein yang disandikan oleh gen E6 dan E7 memiliki
kemampuan mengikat protein pengatur sel host, khususnya
produk dari tumor suppressor gene p53 dan protein
retinoblastoma (pRB) yang terhipofosforilasi. Perubahan ini
menyebabkan degradasi p53 oleh onkoprotein E6 dan
inaktivasi fungsi pRB oleh produk gen E7
Inaktivasi pRB oleh protein E7 dari HPV dapat menyebabkan
upregulation P16INK4a pada lesi servikal. Gangguan
pengaturan jalur siklus sel pRB-P16INK4a menghasilkan
proliferasi sel yang tidak terbatas yang pada akhirnya
berkontribusi terhadap transformasi sel ke arah keganasan