Evidence map›Paper›PMID 32739206›Full record

ReviewKidney international2020

The role of renal hypoxia in the pathogenesis of diabetic kidney disease: a promising target for newer renoprotective agents including SGLT2 inhibitors?

Anne C Hesp, Jennifer A Schaub, Pottumarthi V Prasad, Volker Vallon, Gozewijn D Laverman, Petter Bjornstad, Daniël H van Raalte

Open access · greenAbstract readReview
In one paragraph

Review in Kidney international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed, 1 pooled it
16.5field-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

104 citing papers in PubMed, 1 synthesis or guideline pooled it, 178 citations in OpenAlex.

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

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

7 authors at 6 institutions in 2 countries.

Anne C HespDiabetes Center, Department of Internal Medicine, Amsterdam University Medical Centers, location VUMC, Amsterdam, The Netherlands. Electronic address: a.c.hesp@amsterdamumc.nl.
Jennifer A SchaubDivision of Nephrology, University of Michigan, Ann Arbor, Michigan, USA.
Pottumarthi V PrasadDepartment of Radiology, NorthShore University Health System, Evanston, Illinois, USA; Pritzker School of Medicine, University of Chicago, Chicago, Illinois, USA.
Volker VallonDepartment of Medicine, University of California San Diego and Veterans Affairs San Diego Healthcare System, San Diego, California, USA.
Gozewijn D LavermanDepartment of Internal Medicine, Ziekenhuis Groep Twente, Almelo, The Netherlands.
Petter BjornstadDepartment of Medicine, Division of Nephrology, and Section of Endocrinology, Department of Pediatrics, University of Colorado School of Medicine, Aurora, Colorado, USA.
Daniël H van RaalteDiabetes Center, Department of Internal Medicine, Amsterdam University Medical Centers, location VUMC, Amsterdam, The Netherlands.
Amsterdam University Medical Centers · NLNorthShore University HealthSystem · USUniversity of Colorado Denver · USUniversity of Michigan–Ann Arbor · USVA San Diego Healthcare System · USZiekenhuis Groep Twente · NL

Funding

UAB-UCSD O'Brien Core Center for Acute Kidney Injury ResearchP30DK079337 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI AGARWAL, ANUPAM · 2008 to 2022
$18.3M
Glomerular and Tubular Function in the Diabetic KidneyR01DK112042 · NIDDK · VETERANS MEDICAL RESEARCH FDN/SAN DIEGO · PI SCOTT Culver THOMSON, Volker Vallon · 2017 to 2026
$4.1M
The Contribution of Kidney Disease to Age-Associated Cognitive DeclineRF1AG061296 · NIA · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI MAHER, PAMELA ANNE · 2019 to 2019
$3.2M
Role of tubuloglomerular feedback in the development of hypertension in diabetesR01HL142814 · NHLBI · UNIVERSITY OF SOUTH FLORIDA · PI LIU, RUISHENG · 2019 to 2022
$2.4M
Unraveling Kidney Physiology, Pathophysiology & Therapeutics: A Modeling ApproachR01DK106102 · NIDDK · DUKE UNIVERSITY · PI LAYTON, ANITA · 2016 to 2019
$1.4M
Renal HEIR Study: Renal Hemodynamics, Energetics and Insulin Resistance in Youth Onset Type 2 Diabetes StudyK23DK116720 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI BJORNSTAD, PETTER · 2018 to 2022
$963k
Intrarenal Oxygenation: An Early Marker for Risk of Developing AKIR01DK106557 · NIDDK · ENDEAVOR HEALTH CLINICAL OPERATIONS · PI PRASAD, POTTUMARTHI V · 2016 to 2018
$717k
NHLBI NIH HHS R01 HL142814NIA NIH HHS RF1 AG061296NIDDK NIH HHS K23 DK116720NIDDK NIH HHS P30 DK079337NIDDK NIH HHS R01 DK106102NIDDK NIH HHS R01 DK106557NIDDK NIH HHS R01 DK112042
6 · The paper itself

Abstract

Diabetic kidney disease is the most common cause of end-stage kidney disease and poses a major global health problem. Finding new, safe, and effective strategies to halt this disease has proven to be challenging. In part that is because the underlying mechanisms are complex and not fully understood. However, in recent years, evidence has accumulated suggesting that chronic hypoxia may be the primary pathophysiological pathway driving diabetic kidney disease and chronic kidney disease of other etiologies and was called the chronic hypoxia hypothesis. Hypoxia is the result of a mismatch between oxygen delivery and oxygen demand. The primary determinant of oxygen delivery is renal perfusion (blood flow per tissue mass), whereas the main driver of oxygen demand is active sodium reabsorption. Diabetes mellitus is thought to compromise the oxygen balance by impairing oxygen delivery owing to hyperglycemia-associated microvascular damage and exacerbate oxygen demand owing to increased sodium reabsorption as a result of sodium-glucose cotransporter upregulation and glomerular hyperfiltration. The resultant hypoxic injury creates a vicious cycle of capillary damage, inflammation, deposition of the extracellular matrix, and, ultimately, fibrosis and nephron loss. This review will frame the role of chronic hypoxia in the pathogenesis of diabetic kidney disease and its prospect as a promising therapeutic target. We will outline the cellular mechanisms of hypoxia and evidence for renal hypoxia in animal and human studies. In addition, we will highlight the promise of newer imaging modalities including blood oxygenation level-dependent magnetic resonance imaging and discuss salutary interventions such as sodium-glucose cotransporter 2 inhibition that (may) protect the kidney through amelioration of renal hypoxia.

Indexed as

Diabetes Mellitus, Type 2Diabetic NephropathiesHyperglycemiaSodium-Glucose Transporter 2 InhibitorsAnimalsHumansHypoglycemic AgentsHypoxiaKidneyHypoglycemic AgentsSodium-Glucose Transporter 2 InhibitorsBOLD-MRIchronic hypoxia hypothesischronic kidney diseasediabetes mellitusdiabetic kidney diseasehypoxiarenoprotectionsodium–glucose cotransporter 2 inhibition

Identifiers

PMID32739206
PMCPMC8397597
OpenAlexW3020088156

What OpenQuestion holds

Textmetadata
LicenceTDM
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.