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When a hydrogel layer is compressed by a fluid flow normal to it, the flow rate may exhibit hysteresis when the imposed pressure drop varies, and we may observe bistability between a relaxed and a compressed state for the hydrogel. 

Two aspects of hydrogel mechanics have been studied separately in the past. The first is the swelling and deswelling of gels in a quiescent solvent bath triggered by an environmental stimulus such as a change in temperature or pH, and the second is the solvent flow around and into a gel domain, driven by an external pressure gradient or moving boundary. The former neglects convection due to external flow, whereas the latter neglects solvent diffusion driven by a gradient in chemical potential. Motivated by engineering and biomedical applications where both aspects coexist and potentially interact with each other, this work presents a poroelasticity model that integrates these two aspects into a single framework, and demonstrates how the coupling between the two gives rise to novel physics in relatively simple one-dimensional and two-dimensional flows. 

Boundary conditions between a porous solid and a fluid has been a long-standing problem in modeling porous media. For deformable poroelastic materials such as hydrogels, the question is further complicated by the elastic stress from the solid network. Recently, an interfacial permeability condition has been developed from the principle of positive energy dissipation on the hydrogel–fluid interface. Although this boundary condition has been used in flow computations and yielded reasonable predictions, it contains an interfacial permeability g as a phenomenological parameter. In this work, we use porescale models of flow into a periodic array of solid cylinders or parallel holes to determine g as a function of the pore size and porosity. This provides a means to evaluate the interfacial permeability for a wide range of poroelastic materials, including hydrogels, foams and biological tissues, to enable realistic flow simulations. 

Albuminuria occurs when albumin leaks abnormally into the urine. Its mechanism remains unclear. A gel-compression hypothesis attributes the glomerular barrier to compression of the glomerular basement membrane (GBM) as a gel layer. Loss of podocyte foot processes would allow the gel layer to expand circumferentially, enlarge its pores and leak albumin into the urine. To test this hypothesis, we develop a poroelastic model of the GBM. It predicts GBM compression in healthy glomerulus and GBM expansion in the diseased state, essentially confirming the hypothesis. However, by itself, the gel compression and expansion mechanism fails to account for two features of albuminuria: the reduction in filtration flux and the thickening of the GBM. A second mechanism, the constriction of flow area at the slit diaphragm downstream of the GBM, must be included. The cooperation between the two mechanisms produces the amount of increase in GBM porosity expected in vivo in a mutant mouse model, and also captures the two in vivo features of reduced filtration flux and increased GBM thickness. Finally, the model supports the idea that in the healthy glomerulus, gel compression may help maintain a roughly constant filtration flux under varying filtration pressure.