Evidence map›Paper›PMID 21358326›Full record

ReviewCurrent opinion in nephrology and hypertension2011

HIV-associated nephropathy: pathogenesis.

Raj K Medapalli, John C He, Paul E Klotman

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in nephrology and hypertension, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
3.7field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

52 citing papers in PubMed, 86 citations in OpenAlex.

  1. Review
  2. Review
  3. Nephrotic Syndrome: Beyond Common Causes.Nephrology (Carlton, Vic.) · 2025
    Article
  4. Review
  5. Review
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  8. Review
  9. Article
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  11. Review
  12. Review
  13. Article
  14. Inhibition of apoptosis signal-regulating kinase 1 mitigates the pathogenesis of human immunodeficiency virus-associated nephropathy.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2021
    Article
  15. Article
  16. Viral Nephropathies, Adding SARS-CoV-2 to the List.International journal of nephrology and renovascular disease · 2021
    Review
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Raj K MedapalliDivision of Nephrology, Department of Medicine, Mount Sinai School of Medicine, New York, New York, USA.
John C He
Paul E Klotman
Icahn School of Medicine at Mount Sinai · USBaylor College of Medicine · US

Funding

VIRAL PATHOGENESIS OF HIV ASSOCIATED NEPHROPATHYP01DK056492 · NIDDK · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI HE, JOHN CIJIANG · 1999 to 2021
$27.8M
Role of HIPK2 in Kidney Tubulointerstitial InjuryR01DK088541 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HE, JOHN CIJIANG · 2010 to 2019
$4.0M
Cellular and molecular mechanisms of retinoids in podocytesR01DK078897 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HE, JOHN CIJIANG · 2007 to 2018
$3.6M
RNA profiling of HIV-associated nephropathy in patients with the MYH9 risk alleleRC4DK090860 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI KLOTMAN, PAUL EVAN · 2010 to 2010
$1.9M
NIDDK NIH HHS P01 DK056492NIDDK NIH HHS P01DK056492NIDDK NIH HHS R01 DK078897NIDDK NIH HHS R01DK078897NIDDK NIH HHS R01 DK088541NIDDK NIH HHS R01DK088541NIDDK NIH HHS RC4 DK090860NIDDK NIH HHS RC4DK090860
6 · The paper itself

Abstract

purpose of reviewHIV-associated nephropathy (HIVAN) is characterized histologically by a collapsing form of focal segmental glomerulosclerosis (FSGS), microcystic tubular dilation, interstitial inflammation and fibrosis. In this review, we provide a summary of the current state of knowledge about the mechanisms involved in the pathogenesis of HIVAN. RECENT

findingsTwo variants in the ApoL1 gene have been identified as the susceptibility alleles that account for a majority of the increased risk of FSGS and nondiabetic end-stage renal disease in blacks. HIVAN1 and HIVAN2 are the other host susceptibility genes that have been identified in animal models for HIVAN. HIV infects renal tubular epithelial cells likely through direct cell-cell transmission. Both in-vivo and in-vitro evidence suggests that Nef and Vpr are the key viral genes mediating HIVAN. Nef induces podocyte dysfunction, whereas Vpr induces renal tubular epithelial cell apoptosis. SUMMARY: HIVAN results from direct infection by HIV-1 and expression of viral genes, especially Nef and Vpr, in renal epithelial cells in a genetically susceptible host. The infected renal epithelium acts as a separate viral compartment from the blood and facilitates evolution of strains distant from blood. Dysregulation of several host cellular pathways, including those involved in cell cycle and apoptosis, ultimately results in the unique histopathological syndrome of HIVAN.

Indexed as

AIDS-Associated NephropathyAnimalsApolipoprotein L1ApolipoproteinsCell DifferentiationCell ProliferationHumansLipoproteins, HDLMolecular Motor ProteinsMyosin Heavy ChainsNephritis, InterstitialPodocytesAPOL1 protein, humanApolipoprotein L1ApolipoproteinsLipoproteins, HDLMolecular Motor ProteinsMYH9 protein, humanMyosin Heavy Chains

Identifiers

PMID21358326
PMCPMC3153858
OpenAlexW2068804282

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.