Dataset related to article "Role of ultrastructural determinants of glomerular permeability in ultrafiltration function loss".

<em>The files contain the raw data related to the manuscript: "Role of ultrastructural determinants of glomerular permeability in ultrafiltration function loss" available at https://insight.jci.org/articles/view/137249.</em> <strong>Datasets:</strong> <strong>Scripts for CFD simulation of water passage through the glomerular filtration barrier (GFB) of Wistar, MWF and MWF-treated rats:</strong> <strong>STL_models</strong> - contains STL models of the unit cell of GFB reconstructed for the three groups of rats (i.e., WIST, MWF and MWFL). The dimensions assumed are presented in tables 2 and 4 in the main text and well explained in the Supplemental Material. <strong>CFD_cases</strong> – contains cases in .rar archives for each group of rats; each case includes scripts which needed to run a CFD simulation of steady for incompressible, turbulent flow with porosity treatment, using the <strong><em>porousSimpleFoam</em></strong> solver in OpenFOAM. OpenFOAM version 6 (openfoam.org) was used for generating all data presented in this paper, but scripts should run well with updated versions. <strong>Figure 1_Pores morphometrical analysis.xlsx </strong>- dataset for the calculation of distribution of slit pore size. These data are presented in Figure 1. <strong>Figure 2_subpodocyte space morphometry.xlsx </strong>- dataset for the quantification of subpodocyte area. These data are presented in Figure 2. <strong>Figure 5_CD151 and a3 integrin expression.xlsx </strong>- dataset related to the quantification of CD151, a3 integrin and their colocalization. These data are presented in Figure 5. <strong>k_SupplTable2.xlsx</strong> – dataset for the calculation and total and relative permeability of each structural layer of GFB. These data are presented in Supplemental Table 2. <strong>Neal-model_graphs_Figure4_SupplFigure3.xlsx</strong> - dataset for the calculation and of hydraulic resistances of GFB using the models of Neal et al. (2007). These data are presented in Figure 4 and Supplemental Figure 3. <strong>Table 1_Systemic parameters.xlsx </strong>- dataset related to the systemic parameters. These data are presented in Table 1. <strong>Table 2_Morphometric characterization.xlsx </strong>- dataset related to the morphometric characterization of epithelial slit pores and GBM. These data are presented in Table 2. <strong>Abstract of the manuscript</strong> The epithelial filtration slit is a crucial component of the glomerular capillary membrane, which is essential for maintaining glomerular filtration function. Though chronic kidney diseases are an immense clinical problem, the mechanisms through which structural alterations reduce glomerular water filtration have not yet been understood completely. To investigate the mechanisms underlying filtration function loss, we studied rats with spontaneously occurring progressive kidney disease, either treated with angiotensin II antagonist or untreated, combining high-resolution electron microscopy of the glomerular capillary wall with theoretical water filtration modeling. Under pathological conditions, epithelial filtration pores and the extension of the subpodocyte space were larger than in normal controls. Numerical analyses indicated that these ultrastructural changes increased hydraulic resistance of the glomerular capillary wall by extending coverage of the filtration barrier by the subpodocyte space, with the changes in hydrodynamic forces acting on podocytes likely being responsible for their detachment. Angiotensin II inhibition normalized the subpodocyte space's hydraulic resistance, restored mechanical podocyte load, and preserved CD151-α3 integrin complex assembly, improving podocyte adherence and survival. Our results show that ultrastructural changes in podocytes are major determinants of the hydraulic resistance of the glomerular capillary wall and highlight the mechanism of podocyte loss in kidney disease progression, as well as the mechanisms underlying angiotensin II inhibition.