Evidence map›Paper›PMID 21997392›Full record

ArticleJournal of the American Society of Nephrology : JASN2011

APOL1 localization in normal kidney and nondiabetic kidney disease.

Sethu M Madhavan, John F O'Toole, Martha Konieczkowski, Santhi Ganesan, Leslie A Bruggeman, John R Sedor

Open access · greenAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 152 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
152citing papers in PubMed, 2 pooled it
9.1field-weighted citation impact, top 1% 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

152 citing papers in PubMed, 2 syntheses or guidelines pooled it, 240 citations in OpenAlex.

  1. Pooled it
  2. Journal of the American Society of Nephrology : JASN · 2019
    Pooled it
  3. Arteriosclerosis, thrombosis, and vascular biology · 2017
    Trial
  4. Update on APOL1 and chronic kidney diseases in children.Pediatric nephrology (Berlin, Germany) · 2026
    Review
  5. Review
  6. A novelRenal failure · 2025
    Article
  7. Article
  8. Review
  9. Article
  10. Mechanisms of podocyte injury in genetic kidney disease.Pediatric nephrology (Berlin, Germany) · 2025
    Review
  11. Article
  12. Heterogeneous afferent arteriolopathy: a key concept for understanding blood pressure-dependent renal damage.Hypertension research : official journal of the Japanese Society of Hypertension · 2024
    Review
  13. Article
  14. Collapsing Glomerulopathy.Advances in kidney disease and health · 2024
    Review
  15. An Update on Viral Infection-Associated Collapsing Glomerulopathy.Advances in kidney disease and health · 2024
    Review
  16. Article
  17. Article
  18. Article
  19. Novel Therapies inKidney international reports · 2023
    Review
  20. The metabolic effects of APOL1 in humans.Pflugers Archiv : European journal of physiology · 2023
    Review

92 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Sethu M MadhavanDepartment of Medicine and the Rammel kamp Center for Education and Research, Metro Health System Campus, Cleveland, Ohio, USA.
John F O'Toole
Martha Konieczkowski
Santhi Ganesan
Leslie A Bruggeman
John R Sedor
MetroHealth · USUniversity School · US

Funding

Mechanisms of Glomerular ScarringR01DK064719 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI SEDOR, JOHN R. · 2003 to 2006
$1.2M
Functional characterization of the novel protein nephrocystin-5K08DK071108 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI O'TOOLE, JOHN F. · 2006 to 2010
$709k
NIDDK NIH HHS DK-064719NIDDK NIH HHS DK-071108NIDDK NIH HHS K08 DK071108NIDDK NIH HHS R01 DK064719
6 · The paper itself

Abstract

In patients of African ancestry, genetic variants in APOL1, which encodes apolipoprotein L1, associate with the nondiabetic kidney diseases, focal segmental glomerulosclerosis (FSGS), HIV-associated nephropathy (HIVAN), and hypertensive nephropathy. Understanding the renal localization of APOL1 may provide clues that will ultimately help elucidate the mechanisms by which APOL1 variants promote nephropathy. Here, we used immunohistology to examine APOL1 localization in normal human kidney sections and in biopsies demonstrating either FSGS (n = 8) or HIVAN (n = 2). Within normal glomeruli, APOL1 only localized to podocytes. Compared with normal glomeruli, fewer cells stained for APOL1 in FSGS and HIVAN glomeruli, even when expression of the podocyte markers GLEPP1 and synaptopodin appeared normal. APOL1 localized to proximal tubular epithelia in normal kidneys, FSGS, and HIVAN. We detected APOL1 in the arteriolar endothelium of normal and diseased kidney sections. Unexpectedly, in both FSGS and HIVAN but not normal kidneys, the media of medium artery and arterioles contained a subset of α-smooth muscle actin-positive cells that stained for APOL1. Comparing the renal distribution of APOL1 in nondiabetic kidney disease to normal kidney suggests that a previously unrecognized arteriopathy may contribute to disease pathogenesis in patients of African ancestry.

Indexed as

AdultAgedAIDS-Associated NephropathyApolipoprotein L1ApolipoproteinsBiopsyCell Line, TransformedDiabetes MellitusEndothelium, VascularFemaleGenetic VariationGenotypeGlomerulosclerosis, Focal SegmentalHumansKidney GlomerulusKidney Tubules, ProximalAPOL1 protein, humanApolipoprotein L1ApolipoproteinsLipoproteins, HDL

Identifiers

PMID21997392
PMCPMC3231786
OpenAlexW2146597955

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.