HIV AND THE KIDNEYS

• HIV infection can involve different parts of the

kidneys –
• Pre renal- eg Diarrhoea, Sepsis
• Vascular – Thrombotic thrombocytopenic
purpura[TTP]
• Infiltrative – Kaposis sarcoma, Lymphoma.
• Glomerula - HIVAN, HIVIKD
• Tubular –Tenofovir, Amphotericin B,
Forscarnet, Pentamidine
• Interstitium – Plasmocytic infiltrative
nephropathy[specific to HIV], Diffuse
interstitial lymphocytosis syndrome[specific to
HIV], Drugs like rifampicin and septrin
• Post renal Tumors, Indinavir, Fungus balls,
Retroperitoneal fibrosis
 INTRODUCTION
• HIV infection in the kidneys can be broadly
divided into 3 categories-
• The direct effect of the virus on the cells of the
kidneys
• The nephrotoxic effects of antiretroviral drugs
and other drugs used in treating HIV and
associated comorbidities.
• Renal effects of comorbid conditions.
• Route of entry of HIV into renal cells is
debatable, because the renal cells lack the usual
cellular receptors of the HIV virus.
• However, HIV RNA is detectable in the renal
cells. Indeed, the kidneys may be a reservoir for
HIV.
• HIV RNA/DNA have been detected in patients
kidney cells, even when viral loads are
undetectable in the blood.
• Therefore, renal tubular cells may be a
separate compartment for HIV cells, separate
from blood.
• Renal cells may support mutation of new viral
strains that may differ from the strain in the
blood.
 RISK FACTORS
• Impaired renal function is relatively common
among most cohorts of HIV patients, involving
up to 10%.
• Common risk factors include-
• Hypertension, Diabetes, Black race, Hepatitis
virus, Low CD4 count, Some HAART
medications[ Tenofovir, Indinavir, Atazanavir
etc], Old age, Low muscle mass, Preexisting CKD
• As in all patients with CKD, patients with HIV
and renal disease have an increased risk of
atherosclerosis and vasculopathy and death,
when compared with those with HIV without
renal disease.
HIV ASSOCIATED NEPHROPATHY[HIVAN]

• Initially described in 1984 in USA.

• 90% of cases occur in blacks. Also seen in
hispanics.
• Infects glomerular and tubular cells, causing
collapsing FSGS and cystic tubular dilatation.
• Most common cause of ESRD in HIV patients.
• Commoner in long standing infection[several
years] and very low CD4 count.
• Clinical presentation of HIVAN has undergone dramatic
changes since the post HAART era,
• Incidence has dramatically reduced in the USA by more
than 300%.
• Proteinuria has reduced from nephrotic to non nephrotic
range in most cases.
• Renal size by ultrasound has reduced from large,
echogenic kidneys to normal sized kidneys in many cases.
• Time to ESRD has changed from 3-4 months to several
years.
• HIVAN is the most common cause of ESRD in HIV
patients.
• It occurs almost exclusively in blacks due to the
presence of APOL 1 gene.
• It is one of the commonest causes of ESRD in
Africans especially the younger sexually active
age groups.
• It is an indication to start HAART, no matter the
viral load.
 MANAGEMENT
• Biopsy, This shows collapsing FSGS, marked
microcystic dilatation of renal tubules, Lymphocytic
interstitial infiltrates and Interstitial fibrosis.
• HAART-This is the most important treatment. It has
been shown to reduce incidence of HIVAN and cause
reversibility of CKD.
• ACE inhibitors
• ? Prednisolone- Some studies suggest renal benefits
when no coexisting infection.
• Manage hyperlipidemia
• Look out for encapsulated organisms and
hypercoagulability as in other nephrotics.
• Treat hypertension to a target of 130/80.
• Manage comorbidities eg DM.
• Discourage smoking and illicit drug use.
 HIV IMMUNE KIDNEY DISEASE[HIVIKD]
• IgA nephropathy[commoner in caucasians]
• Post infectious GN[commoner in Africans]
• ‘Lupus like’ GN without other evidence of lupus.
• MPGN[Hep C with cryoglobulin]
• Membranous GN[with Hep B]
• Immunotactoid GN
• IgA levels are commonly elevated in HIV patients.
Autopsy on caucasians with HIV showed increased
incidence of mesangial deposition of IgA on
immunoflorescence.
 CLINICAL PRESENTATION
• Unlike HIVAN, these patients present with
nephritic syndrome –
• Hematuria, Proteinuria, AKI or CKD,
Hypertension, Fluid overload.
• Investigations may include ANA, RF,
Cryoglobulins[in hep C], C3[low in post
infectious GN], C4[low in cryoglobulins],
hepatitis serology.
 MANAGEMENT
• In the past, it was thought that HIVAN was almost
exclusive to blacks, while HIVIKD was almost
exclusive to non blacks. More recently, many blacks
have been shown to have HIVIKD.
• Biopsy is a good start [60% of patients thought to
have HIVAN eventually had HIVIKD in some reports]
• Efficacy of HAART is not clear in this cohort.
• Consider immunossupressives depending on type of
GN and comorbidities.
 HAART NEPHROTOXICITY
• Tenofovir – Fanconi syndrome
• Indinavir –Stones, Interstitial nephritis
• Atanavir – Stones, CKD