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Podocyte Density and Albuminuria in Aging Diabetic Ins2± Mice with or Without Adenosine A1 Receptor Signaling

Authors Faulhaber-Walter R, Jiang L, Mizel D, Zerfas PM, Kopp JB, Schnermann JB, Chen L, Schiffer M

Received 5 February 2019

Accepted for publication 27 November 2019

Published 21 February 2020 Volume 2020:13 Pages 19—26

DOI https://doi.org/10.2147/IJNRD.S203810

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 3

Editor who approved publication: Professor Pravin Singhal


Robert Faulhaber-Walter, 1–3 Lanping Jiang, 4 Diane Mizel, 2 Patricia M Zerfas, 2 Jeffrey B Kopp, 2 Jurgen B Schnermann, 2 Limeng Chen, 2, 4 Mario Schiffer 3, 5

1Facharztzentrum Aarberg, Waldshut-Tiengen, Germany; 2NIDDK, National Institutes of Health, Bethesda, MD, USA; 3Department of Nephrology, Medical School Hannover, Hannover, Germany; 4Peking Union Medical College Hospital, Beijing, People’s Republic of China; 5Department of Nephrology, University of Erlangen, Erlangen, Germany

Correspondence: Robert Faulhaber-Walter
Facharztzentrum Aarberg, Tannenstrasse 4, Waldshut-Tiengen 79761, Germany
Tel +49-151-27164882
Fax +49-321-21036268
Email rofaulhaber@web.de

Aim of Study: To investigate podocyte density in aging diabetic Ins2± and Ins2±, A1AR-/- mouse models in C57Bl/6 background.
Methods: Ins2± mice and especially Ins2±, adenosine A1 receptor knockout mice (Ins2±, A1AR-/-) are mouse models with a phenotype of diabetic nephropathy. Aged mice (at ∼ 40 weeks) were assessed for glomerular filtration barrier function by measuring albuminuria, glomerular filtration, glomerular damage by electron microscopy, and podocyte numbers by Wilms Tumor protein (WT-1) staining.
Results: Compared to healthy wild-type mice, both diabetic mouse models developed diabetic nephropathy, including hyperfiltration (p< 0.01) and albuminuria (p< 0.05). Typical diabetic structural glomerular and podocyte damage was visualized by electron microscopy. Podocyte count per glomerular area (podocyte density) was significantly decreased in both diabetic mouse models (p< 0.01). In contrast, no significant correlation was detected between albuminuria and absolute podocyte count per glomerulus.
Conclusion: The amount of albuminuria as marker of diabetic nephropathy does not correlate with the podocytes density; however, a relative podocyte deficiency became evident with an increase in glomerular area in the diabetic animals, suggesting a relative podocytopenia.

Keywords: diabetes nephropathy podocyte mouse Akita WT-1


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