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Renal Disease; Fluid and Electrolyte Disorders
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Deposition of IgA in the kidney occurs and is associated with inflammation and proliferation of mesangial cells (see Figures 8.12 and 8.13). There are associations with liver disease.
Immunologic Mechanisms in Renal Disease
Published in Robin S. Goldstein, Mechanisms of Injury in Renal Disease and Toxicity, 2020
Brian D. Schreiber, Gerald C. Groggel
Another site of immune deposits within the glomerulus is the mesangium. Deposits are found here in association with subendothelial deposits, but can also be found alone. The mesangium is made up of mesangial cells and matrix. It is separated from the systemic circulation only by the glomerular endothelial cell with its wide fenestrae (Michael et al., 1980). It is readily accessible to circulating macromolecules, including immune complexes (Michael et al., 1980). The complexes may be degraded locally or pass out of the glomerulus through the hilum into the renal lymphatics. Thus, circulating immune complexes may readily deposit in the mesangium. However, deposits may also form here by an in situ mechanism. In classic studies by Mauer et al. (1973), heat-aggregated human IgG was injected into rabbits and deposited in the mesangium of their kidneys. The kidneys were removed and transplanted into normal rabbits which received rabbit anti-human IgG and formed immune deposits in situ. The rabbits developed a mesangial proliferative glomerulonephritis with deposits of human IgG, rabbit IgG, and rabbit complement.
IgA nephropathy
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Jan Novak, Bruce A. Julian, Jiri Mestecky
In IgA nephropathy, Gal-deficient hinge-region glycans with terminal GalNAc on IgA1 represent neoepitopes that are recognized by the previously mentioned autoantibodies, resulting in the formation of circulating immune complexes. These complexes are relatively large, are not efficiently cleared from the circulation, and tend to deposit in the renal mesangium thereby binding and activating mesangial cells to induce glomerular injury.
Targeted drug delivery strategy: a bridge to the therapy of diabetic kidney disease
Published in Drug Delivery, 2023
Xian Chen, Wenni Dai, Hao Li, Zhe Yan, Zhiwen Liu, Liyu He
Glomerular basement membrane (GBM) thickening is considered as the earliest observed pathological feature in patients with DKD, which is appeared within 1–2 years after the onset of DM (Tervaert et al., 2010; Ponchiardi et al., 2013). Endothelial cells play an important role in the progression of DKD. With the development of DKD, the fenestrated ECs are decreased in diabetic patients, which correlates with albuminuria and the loss of GFR (Dou and Jourde-Chiche, 2019). Mesangial expansion, caused by Mesangial cells (MCs) enlargement and accumulation of glomerular matrix protein, is the most common renal pathological change in DKD (Reidy et al., 2014; Zhang et al., 2019). On the glomerular capillary side of MCs, without the surrounding of GBM and podocytes, drugs can be delivered to MCs for treating kidney diseases (Scindia et al., 2008). Podocytes are glomerular epithelial cells which contain 3 separate elements: cell body, extending processes and foot processes (Garg, 2018). Podocytes injury in DKD is induced by many compound factors, such as inflammatory reaction, mechanical stress, oxidative stress, renin angiotensin aldosterone system activation, TGF-β1 induction, and AGEs accumulation, and any part of the pathway is expected to be the target of DKD therapy (Kawanami et al., 2016). The renal tubules consist of the proximal tubules, collecting tubules and distal tubules. The morphological and functional changes of the renal tubules are involved in the pathogenesis and progression of DKD (Duan et al., 2021). Most renal tubular targeted systems are directed at the proximal tubules (Christensen et al., 2012).
Role of advanced glycation end products and insulin resistance in diabetic nephropathy
Published in Archives of Physiology and Biochemistry, 2023
Many growing bodies of evidence suggest the role of AGEs induced ER stress in the development and progression of DN. More specifically, AGEs and advanced oxidation protein products (AOPPs) have been shown to induce ER stress in cultured podocytes leading to apoptosis in murine podocytes (Chen et al. 2008, Rong et al. 2015). Upregulation of ER stress markers was observed in podocytes treated with high glucose concentrations resulting in their cell death (Cao et al. 2014). Mesangial cells are essential to maintain the integrity of glomerulus and also play an important role in maintaining glomerular filtration (Fan et al. 2017). Mesangial cells are the most susceptible to the damage induced due to high glucose along with increased ROS. Exposure to high glucose leads to proliferation of mesangial cells resulting in overproduction of extracellular matrix (ECM), which was suppressed by overexpression of XBP-1s (Shao et al. 2013).
Oxidative stress and histopathological changes in several organs of mice injected with biogenic silver nanoparticles
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2022
Shushanik Kazaryan, Lilit Farsiyan, Juleta Tumoyan, Gayane Kirakosyan, Naira Ayvazyan, Hrachik Gasparyan, Sona Buloyan, Lilit Arshakyan, Ara Kirakosyan, Ashkhen Hovhannisyan
Although the exposure to O. araratum did not affect the overall structure of the liver, the extract caused heavy portal hypertension. In this group, acute congestion of central veins, sinusoidal dilation and hemostasis was observed. These haemodynamic changes lead to liver ischaemia, which in turn caused focal necrosis and pyknosis of the hepatocytes. Along with this, the onset of microvesicular steatosis was observed (Figure 8). Statistical analysis of all parameters in liver tissue showed significant differences between the control group and mice treated with O. araratum (p < .05). Examination of renal tissue showed that exposure to O. araratum extract leads to acute tubular necrosis, which is accompanied by glomerulonephritis. In the glomeruli of the renal tissue, foci of diffuse proliferation of mesangial cells have been revealed. In the lumen of the tubules, sloughed-off necrotic epithelial cells and granular casts were observed (Figure 8). The statistical analysis of these parameters also revealed significant differences compared to control animals (p < .05).