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Published in Valerio Voliani, Nanomaterials and Neoplasms, 2021
The previous understanding of the renal clearance pathway of NPs was centered on healthy kidneys, and in this regard the clearance criteria for clinically applicable contrast agents were determined based upon the unique anatomical structure and biochemical composition of the normal glomerular capillary wall (GCW; Fig. 14.1A,B) [1b]. The GCW consists of three layers: a fenestrated glomerular endothelium filled with functionalized glycocalyx surfaces (diameter of fenestrae = 60–80 nm) [4]; the glomerular basement membrane, which is a non-cellular layer made of a network of collagen fibrils and other structural proteins (network pores ≈ 10 nm); and podocytes and their foot processes, which wrap around capillaries and are interbridged by the slit diaphragm (4–11 nm) [1b]. In healthy states, it is generally accepted that the in vivo hydrodynamic diameter (HD) of a NP (i.e., the NP-protein corona) less than 6 nm can be efficiently filtered by the glomerulus, whereas NPs with HDs greater than 8 nm cannot primarily undergo renal clearance [1c, 5]. For those NPs that have a HD range from 6–8 nm, a properly modified net surface charge is crucial for optimal renal excretion since the GCW is both size- and charge-selective (Fig. 14.1 B) [1b, 4]. At any given NP HD, negatively charged NPs can experience greater resistance to cross through the GCW than neutral ones [6], whereas the positively charged NPs suffer less restriction to glomerular filtration than neutral NPs of same size. Also, NPs with net surface charges can be more subject to serum protein adsorption and nonspecific cellular uptake than the neutral ones [4]. Therefore, employing zwitterionic or neutral organic coatings (such as glutathione-coating and PEGylation) is preferable so as to achieve both minimal in vivo HD and MPS/RES uptake for the efficient urinary elimination of NPs from the body.
Coordination polymers constructed from 5-nitro-1,2,3-benzenetricarboxylic acid: crystal structures and treatment effect on nephrotic syndrome by regulating intestinal flora and recovering Th17/Treg balances
Published in Inorganic and Nano-Metal Chemistry, 2020
Tingting Qiu, Xin Yi, Lulu Xu, Lifeng Wang, Xihui Hu, Xiaozhong Li
Nephrotic syndrome (NS) is a group of clinical syndromes in which the permeability of the glomerular basement membrane is increased by a variety of causes, resulting in the loss of large amounts of protein from the plasma through the urine.[1,2] NS is a common chronic kidney disease and a major primary disease that could induce the production of renal failure. The etiology and pathogenesis of nephrotic syndrome are complex and involve many factors such as infection, autoimmunity, drugs, genetics, and the environment. The etiology and pathogenesis of NS are still unclear.[3] Although glucocorticoids and immunosuppressive agents can alleviate the symptoms, the side effects and the high recurrence rate limit its application, which may eventually develop into chronic glomerular sclerosis.