ckd pada b20

Upload: meldy-muzada-elfa

Post on 04-Nov-2015

217 views

Category:

Documents


0 download

DESCRIPTION

Infeksi

TRANSCRIPT

CKD pada B20

CKD pada B20HIV-associated nephropathy (HIVAN), formerly known as AIDS-associated nephropathy, is characterized by the following findings:Nephrotic range proteinuriaAzotemiaNormal to large kidneys on ultrasound imagesNormal pressureFocal segmental glomerulosclerosis (FSGS) on renal biopsy findings

Moro O Salifu et al, HIV-associated Nephropathy, 2014Guidelines for the Management of Chronic Kidney Disease in HIV-Infected Patients: Recommendations of the HIV Medicine Association of the Infectious Diseases Society of AmericaUp to 60% of all renal biopsies performed for patients with CKD reveal characteristic histological findings designated as HIVAN, 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 HIV-Infected Patients: Recommendations of the HIV Medicine Association of the Infectious Diseases Society of AmericaFollow-up urine analyses are recommended to screen for newly developed kidneydamage for the following groups, which are at higher risk for the development of proteinuria and poor renal outcome:African American personsPatients with diabetesPatients with hypertensionPatients with hepatitis C virus coinfection, andPatients with HIV RNA levels 14000 copies/mL or absolute CD4+ lymphocyte counts < 200 cells/mLManagementRecommendation 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 (B-III).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 ofrenal function (B-II).

HAART: Highly active antiretroviral therapyInvasive 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 infectionthe 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 E7Inaktivasi 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