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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.
Mechanisms of Chemically Induced Glomerular Injury
Published in Robin S. Goldstein, Mechanisms of Injury in Renal Disease and Toxicity, 2020
The location and properties of the glomerular mesangial cells confer a central role for these cells in the regulation of renal function. Mesangium is composed of mesangial cells and MM.17 Mesangial cells are located within the central portion of the glomerular tuft between capillary loops3,18 and connect through gap junctions with each other as well as with the lacis cells of the extraglomerular mesangium, and with the juxtaglomerular granular cells. The glomerular MM and mesangial cells are separated from the capillary lumen by a fenestrated endothelium (Figure 4). Thus mesangial cells are constantly percolated by plasma from glomerular capillaries and are continuously exposed to various types of cells, macromolecules, immune complexes, and circulating or locally released hormones and mediators.19
Functions of the Kidneys and Functional Anatomy
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The renal corpuscles, in the cortex of the kidney, comprise tufts of glomerular capillaries in distinct loops that invaginate Bowman's capsules. Fluid is filtered from the glomerular capillaries into Bowman's space under the action of opposing hydrostatic and oncotic pressures. The glomerular capillaries are supplied by an afferent arteriole and are drained by a second, efferent, arteriole. The filtration barrier to the movement of fluid and solutes from the glomerular capillary to Bowman's space comprises the capillary endothelium, a layer of basement membrane, and the capsular epithelial cells, the podocytes. The capillary endothelium has many perforations, or fenestrae. The podocytes have many lengthened foot processes, which overlap and are embedded in the basement membrane layer. There are slits between the foot processes, and these are covered by very thin diaphragms. Mesangial cells are found in close association with the capillary loops of the glomerulus. The glomerular mesangial cells have a phagocytic function and remove trapped material from the basement membrane. Myofilaments in the mesangial cells enable the cells to contract or relax in response to stimuli, similar to vascular smooth muscle, thereby altering the surface area available for diffusion across the glomerular capillary membrane.
Budesonide delayed-release capsules to reduce proteinuria in adults with primary immunoglobulin A nephropathy
Published in Expert Review of Clinical Immunology, 2023
Jonathan Barratt, Richard A Lafayette, Brad H Rovin, Bengt Fellström
The first ‘hit’ refers to an excess of poorly O-galactosylated IgA1 in the circulation. Gd-IgA1 is prone to self-aggregation and formation of circulating IgA immune complexes with other serum proteins. In susceptible individuals, the presence of Gd-IgA1 elicits an autoimmune response with the production of specific anti-Gd-IgA1 IgG and IgA antibodies (the second ‘hit’), which amplifies the formation of circulating immune complexes, constituting the third ‘hit’ [12–14]. The fourth and final ‘hit’ is the deposition of these circulating IgA-containing immune complexes in the glomerular mesangium, which occurs due to a combination of mesangial trapping and an increased affinity of IgA immune complex constituents for the extracellular mesangial matrix [12–14]. The accumulation of IgA-containing immune complexes in the mesangium leads to mesangial cell activation with release of proinflammatory and profibrotic mediators, which in turn promote glomerular inflammation and subsequent scarring. Simultaneous glomerular complement activation through both the lectin and alternative pathways amplifies these inflammatory and fibrotic responses and promotes glomerular and downstream tubulointerstitial injury. The extent of the mesangial reaction to IgA immune complex deposition is highly variable for uncertain reasons, but this variability likely explains the marked heterogeneity in rates of disease progression seen in patients with IgAN [13].
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).