Evidence map›Paper›PMID 32670095›Full record

ReviewFrontiers in physiology2020

Physiology and Pathophysiology of Compensatory Adaptations of a Solitary Functioning Kidney.

Zoe McArdle, Michiel F Schreuder, Karen M Moritz, Kate M Denton, Reetu R Singh

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
12.7field-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

36 citing papers in PubMed, 72 citations in OpenAlex.

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  18. Glomerular hyperfiltration: part 2-clinical significance in children.Pediatric nephrology (Berlin, Germany) · 2023
    Review
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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

5 authors at 3 institutions in 2 countries.

Zoe McArdleCardiovascular Program, Monash Biomedicine Discovery Institute and Department of Physiology, Monash University, Melbourne, VIC, Australia.
Michiel F SchreuderDepartment of Pediatric Nephrology, Amalia Children's Hospital, Radboud University Medical Center, Nijmegen, Netherlands.
Karen M MoritzChild Health Research Centre and School of Biomedical Sciences, University of Queensland, Brisbane, QLD, Australia.
Kate M DentonCardiovascular Program, Monash Biomedicine Discovery Institute and Department of Physiology, Monash University, Melbourne, VIC, Australia.
Reetu R SinghCardiovascular Program, Monash Biomedicine Discovery Institute and Department of Physiology, Monash University, Melbourne, VIC, Australia.
Monash University · AURadboud University Nijmegen · NLUniversity of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Children born with a solitary functioning kidney (SFK) have an increased risk of hypertension and kidney disease from early in adulthood. In response to a reduction in kidney mass, the remaining kidney undergoes compensatory kidney growth. This is associated with both an increase in size of the kidney tubules and the glomeruli and an increase in single nephron glomerular filtration rate (SNGFR). The compensatory hypertrophy and increase in filtration at the level of the individual nephron results in normalization of total glomerular filtration rate (GFR). However, over time these same compensatory mechanisms may contribute to kidney injury and hypertension. Indeed, approximately 50% of children born with a SFK develop hypertension by the age of 18 and 20-40% require dialysis by the age of 30. The mechanisms that result in kidney injury are only partly understood, and early biomarkers that distinguish those at an elevated risk of kidney injury are needed. This review will outline the compensatory adaptations to a SFK, and outline how these adaptations may contribute to kidney injury and hypertension later in life. These will be based largely on the mechanisms we have identified from our studies in an ovine model of SFK, that implicate the renal nitric oxide system, the renin angiotensin system and the renal nerves to kidney disease and hypertension associated with SFK. This discussion will also evaluate current, and speculate on next generation, prognostic factors that may predict those children at a higher risk of future kidney disease and hypertension.

Indexed as

compensatory hypertrophyglomerular hyperfiltrationnitric oxiderenal sympathetic nervesrenin angiotensin systemsolitary functioning kidney

Identifiers

PMID32670095
PMCPMC7332829
OpenAlexW3037522617

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.