Evidence map›Paper›PMID 31599090›Full record

ArticleAnatomical record (Hoboken, N.J. : 2007)2020

Progressive Nephron Loss in Aging Kidneys: Clinical-Structural Associations Investigated by Two Anatomical Methods.

Michael D Hughson, Wendy E Hoy, John F Bertram

Open access · hybridAbstract read
In one paragraph

Article in Anatomical record (Hoboken, N.J. : 2007), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
4.4field-weighted citation impact, top 6% 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

9 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Nephrons, podocytes and chronic kidney disease: Strategic antihypertensive therapy for renoprotection.Hypertension research : official journal of the Japanese Society of Hypertension · 2023
    Review
  7. Article
  8. Article
  9. 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 3 institutions in 3 countries.

Michael D HughsonUniversity of Mississippi Medical Center, Jackson, Mississippi.ORCID 0000-0003-1310-707X
Wendy E HoyCentre for Chronic Disease, University of Queensland, Brisbane, Queensland, Australia.
John F BertramCardiovascular Disease Program, Biomedicine Discovery Institute and Department of Anatomy and Developmental Biology, Monash University, Clayton, Victoria, Australia.
American University of Iraq Sulaimani · IQDiscovery Institute · USThe University of Queensland · AU

Funding

Nephron Count, Birth Weight &Hypertensive Renal DiseaseR01DK065970 · NIDDK · UNIVERSITY OF MISSISSIPPI MEDICAL CENTER · PI HUGHSON, MICHAEL DONALD · 2004 to 2006
$659k
Division of Intramural Research, of the NIDDK HHSN26120080001NIDDK NIH HHS R01 DK065970NIH NIDDK R01-DK065970-01
6 · The paper itself

Abstract

Two major studies of structural changes associated with aging in human kidneys are reviewed and new information presented. The studies are the Monash University stereologically analyzed series of 319 autopsy kidneys from the United States in which 44% were white and the Mayo Clinic CT angiogram/biopsy analysis of 1,388 US kidney donors in which 97% were white. Hypertension rates in the Monash series were 48% and included moderate and severe hypertension. In the Mayo Clinic study, 12% had mild hypertension. The studies showed no relationship between glomerular number and hypertension except for a weak relationship with older white women in the Monash series. An inverse relationship was present between glomerular number and glomerular volume, a reciprocity that tended to enhance glomerular mass and by inference filtration capacity with lower nephron numbers. This relationship seemed to be present whether low nephron numbers were intrinsic or acquired. In the Mayo Clinic studies, pretransplant iothalamate clearances demonstrated that single nephron (SN) glomerular filtration rates (GFR) were similar throughout the range of glomerular number in subjects younger than 70 years, but that increased SNGFR correlated with nephron hypertrophy and increased nephrosclerosis particularly at 70 years of age and over. Hypertension at least through middle age cannot be related to a deficiency of glomeruli, but glomeruli are lost with later aging in association with adaptive nephron hypertrophy that can maintain GFR near normal. These studies help define an age-related nephropathy that overlaps with hypertension as a potential cause of end-stage renal disease when glomerulosclerosis is advanced.

Indexed as

AdolescentAdultAgedAged, 80 and overAge FactorsAgingChildChild, PreschoolFemaleGlomerular Filtration RateHumansInfantKidneyKidney GlomerulusMaleMiddle Agedagingbirth weightglomerulosclerosisnephrosclerosisstereology

Identifiers

PMID31599090
PMCPMC9545976
OpenAlexW2979437794

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.