Evidence map›Paper›PMID 31566426›Full record

ArticleAmerican journal of physiology. Renal physiology2019

Progression of diabetic kidney disease in T2DN rats.

Oleg Palygin, Denisha Spires, Vladislav Levchenko, Ruslan Bohovyk, Mykhailo Fedoriuk, Christine A Klemens, Olga Sykes, John D Bukowy, Allen W Cowley, Jozef Lazar and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 2 pooled it
4.2field-weighted citation impact, top 5% 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

42 citing papers in PubMed, 2 syntheses or guidelines pooled it, 54 citations in OpenAlex.

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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

12 authors at 1 institution in 1 country.

Oleg PalyginDepartment of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin.
Denisha SpiresDepartment of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin.
Vladislav LevchenkoDepartment of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin.
Ruslan BohovykDepartment of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin.
Mykhailo FedoriukDepartment of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin.
Christine A KlemensDepartment of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin.ORCID 0000-0002-0812-824X
Olga SykesDepartment of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin.
John D BukowyDepartment of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin.ORCID 0000-0002-4411-3643
Allen W CowleyDepartment of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin.
Jozef LazarDepartment of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin.
Daria V IlatovskayaDepartment of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin.
Alexander StaruschenkoDepartment of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin.ORCID 0000-0002-5190-8356
Medical College of Wisconsin · US

Funding

TRANSGENIC COREP60DK020595 · NIDDK · UNIVERSITY OF CHICAGO · PI BELL, GRAEME I · 1985 to 2012
$25.5M
Pilot and Feasibility ProgramP30DK020595 · NIDDK · UNIVERSITY OF CHICAGO · PI Raghavendra G Mirmira · 2013 to 2026
$20.9M
ZONISMIDE IN THE TREATMENT OF SEIZURES IN PATIENTSM01RR000058 · NCRR · MEDICAL COLLEGE OF WISCONSIN · PI PELECH, ANDREW N · 1985 to 2006
$19.9M
Therapeutic Effects of mTOR Inhibition in Salt-Sensitive HypertensionP01HL116264 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI MATTSON, DAVID L. · 2013 to 2021
$18.7M
INTEGRATED PHYSIOLOGY TRAINING--MOLECULE TO ORGANISMT32HL007852 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI Matthew Robert Hodges · 1996 to 2026
$6.5M
Training in Signature Transdisciplinary Cardiovascular SciencesT32HL134643 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI Justin L Grobe, Jacquelyn P Kulinski · 2017 to 2026
$4.2M
Renal ion channels in the control of blood pressureR35HL135749 · NHLBI · UNIVERSITY OF SOUTH FLORIDA · PI STARUSCHENKO, ALEXANDER · 2017 to 2023
$3.6M
The involvement of ATP-dependent inhibition of ENaC in ARPKD cystogenesisR00DK105160 · NIDDK · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI ILATOVSKAYA, DARIA · 2018 to 2020
$747k
The involvement of ATP-dependent inhibition of ENaC in ARPKD cystogenesisK99DK105160 · NIDDK · MEDICAL COLLEGE OF WISCONSIN · PI ILATOVSKAYA, DARIA · 2015 to 2016
$180k
Transport and metabolism in the kidneyI01BX004024 · VA · JAMES A. HALEY VA MEDICAL CENTER · PI STARUSCHENKO, ALEXANDER · 2019 to 2025
–
BLRD VA I01 BX004024NCRR NIH HHS M01 RR000058NHLBI NIH HHS P01 HL116264NHLBI NIH HHS R35 HL135749NHLBI NIH HHS T32 HL007852NHLBI NIH HHS T32 HL134643NIDDK NIH HHS K99 DK105160NIDDK NIH HHS P30 DK020595NIDDK NIH HHS P60 DK020595NIDDK NIH HHS R00 DK105160
6 · The paper itself

Abstract

Diabetic kidney disease (DKD) is one of the leading pathological causes of decreased renal function and progression to end-stage kidney failure. To explore and characterize age-related changes in DKD and associated glomerular damage, we used a rat model of type 2 diabetic nephropathy (T2DN) at 12 wk and older than 48 wk. We compared their disease progression with control nondiabetic Wistar and diabetic Goto-Kakizaki (GK) rats. During the early stages of DKD, T2DN and GK animals revealed significant increases in blood glucose and kidney-to-body weight ratio. Both diabetic groups had significantly altered renin-angiotensin-aldosterone system function. Thereafter, during the later stages of disease progression, T2DN rats demonstrated a remarkable increase in renal damage compared with GK and Wistar rats, as indicated by renal hypertrophy, polyuria accompanied by a decrease in urine osmolarity, high cholesterol, a significant prevalence of medullary protein casts, and severe forms of glomerular injury. Urinary nephrin shedding indicated loss of the glomerular slit diaphragm, which also correlates with the dramatic elevation in albuminuria and loss of podocin staining in aged T2DN rats. Furthermore, we used scanning ion microscopy topographical analyses to detect and quantify the pathological remodeling in podocyte foot projections of isolated glomeruli from T2DN animals. In summary, T2DN rats developed renal and physiological abnormalities similar to clinical observations in human patients with DKD, including progressive glomerular damage and a significant decrease in renin-angiotensin-aldosterone system plasma levels, indicating these rats are an excellent model for studying the progression of renal damage in type 2 DKD.

Indexed as

AgingAlbuminuriaAnimalsBlood GlucoseDiabetes Mellitus, Type 2Diabetic NephropathiesDisease ProgressionHypertrophyKidney GlomerulusMaleMembrane ProteinsOrgan SizePolyuriaRatsRats, WistarRenin-Angiotensin SystemBlood GlucoseMembrane Proteinsnephrindiabetic glomerular diseasediabetic nephropathypodocyte pathologyrenin-angiotensin-aldosterone systemscanning ion microscopytype 2 diabetic nephropathy

Identifiers

PMID31566426
PMCPMC6960784
OpenAlexW2977599454

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.