Evidence map›Paper›PMID 25949944›Full record

ReviewWorld journal of nephrology2015

African origins and chronic kidney disease susceptibility in the human immunodeficiency virus era.

Alex N Kasembeli, Raquel Duarte, Michèle Ramsay, Saraladevi Naicker

Open access · hybridAbstract readReview
In one paragraph

Review in World journal of nephrology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 36 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Kidney disease and APOL1.Human molecular genetics · 2021
    Review
  11. A focus on the association of Apol1 with kidney disease in children.Pediatric nephrology (Berlin, Germany) · 2021
    Review
  12. Article
  13. Kidney international reports · 2019
    Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Review
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

4 authors at 1 institution in 1 country.

Alex N KasembeliAlex N Kasembeli, Raquel Duarte, Saraladevi Naicker, Department of Internal Medicine, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg 2193, South Africa.
Raquel DuarteAlex N Kasembeli, Raquel Duarte, Saraladevi Naicker, Department of Internal Medicine, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg 2193, South Africa.
Michèle RamsayAlex N Kasembeli, Raquel Duarte, Saraladevi Naicker, Department of Internal Medicine, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg 2193, South Africa.
Saraladevi NaickerAlex N Kasembeli, Raquel Duarte, Saraladevi Naicker, Department of Internal Medicine, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg 2193, South Africa.
University of the Witwatersrand · ZA

Funding

Wits Non-communicable Disease Research Leadership ProgramD43TW008330 · FIC · WITS HEALTH CONSORTIUM (PTY), LTD · PI CROWTHER, NIGEL JOHN, KLIPSTEIN-GROBUSCH, KERSTIN · 2010 to 2014
$985k
FIC NIH HHS D43 TW008330
6 · The paper itself

Abstract

Chronic kidney disease (CKD) is a major public health problem worldwide with the estimated incidence growing by approximately 6% annually. There are striking ethnic differences in the prevalence of CKD such that, in the United States, African Americans have the highest prevalence of CKD, four times the incidence of end stage renal disease when compared to Americans of European ancestry suggestive of genetic predisposition. Diabetes mellitus, hypertension and human immunodeficiency virus (HIV) infection are the major causes of CKD. HIV-associated nephropathy (HIVAN) is an irreversible form of CKD with considerable morbidity and mortality and is present predominantly in people of African ancestry. The APOL1 G1 and G2 alleles were more strongly associated with the risk for CKD than the previously examined MYH9 E1 risk haplotype in individuals of African ancestry. A strong association was reported in HIVAN, suggesting that 50% of African Americans with two APOL1 risk alleles, if untreated, would develop HIVAN. However these two variants are not enough to cause disease. The prevailing belief is that modifying factors or second hits (including genetic hits) underlie the pathogenesis of kidney disease. This work reviews the history of genetic susceptibility of CKD and outlines current theories regarding the role for APOL1 in CKD in the HIV era.

Indexed as

African ancestryAPOL1Chronic kidney diseaseGeneticsHuman immunodeficiency virusHuman immunodeficiency virus-associated nephropathyMYH9

Identifiers

PMID25949944
PMCPMC4419140
OpenAlexW2058464043

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.