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Occupational toxicology of the kidney
Published in Chris Winder, Neill Stacey, Occupational Toxicology, 2004
Toxicants can alter the glomerular filtration rate (GFR) and the size and/or charge selective properties of the glomerulus. These alterations can be induced by changes in blood pressure as well as by structural or functional changes to the components of the glomerular capillary tuft. In addition, chemically induced immunological injury (see Chapter 3) can lead to glomerular injury due to trapping of circulating immune complexes in the glomerulus (for example, gold, HgCl, cadmium, silica) (Fenwick and Main 2000; Schnellmann 2001; Stratta et al. 2001). Immune complex deposition may also occur following chemically induced autoimmune disease that affects components of the glomerulus such as the basement membrane (for example, volatile hydrocarbons, solvents) (Schnellmann 2001). This type of injury to the glomerulus is called glomerulonephritis. Glomerular disease that affects blood flow through the glomerular capillaries has an adverse effect on the tubules since their blood supply is from the efferent arteriole.
Urology
Published in David A Lisle, Imaging for Students, 2012
Other clinical symptoms and signs, such as acute flank pain and fever, usually accompany haematuria caused by urinary tract infection and ureteric calculi. Glomerulonephritis is suspected where haematuria is accompanied by heavy proteinuria and red cell casts. Glomerulonephritis is confirmed with renal biopsy, best done under imaging guidance, usually US. Patients with glomerulonephritis should have a CXR to search for cardiac enlargement and pulmonary oedema, plus a renal US to screen for underlying renal morphological abnormalities.
Glossary of scientific and technical terms in bioengineering and biological engineering
Published in Megh R. Goyal, Scientific and Technical Terms in Bioengineering and Biological Engineering, 2018
Glomerulonephritis is a type of glomerular kidney disease in which the kidneys’ filters become inflamed and scarred, and slowly lose their ability to remove wastes and excess fluid from the blood to make urine.
Mine-site derived particulate matter exposure exacerbates neurological and pulmonary inflammatory outcomes in an autoimmune mouse model
Published in Journal of Toxicology and Environmental Health, Part A, 2021
Alexis Wilson, Carmen A. Velasco, Guy W. Herbert, Selita N. Lucas, Bethany N. Sanchez, José M. Cerrato, Michael Spilde, Quan-Zhen Li, Matthew J. Campen, Katherine E. Zychowski
Mice were randomly assigned to one of three groups (n = 8/treatment) and subjected to either 4 weekly doses (100 µg/50 µl) of Claim 28 PM, St. Anthony mine PM or dispersion media control (DM) starting at 8 weeks old via oropharyngeal aspiration, as described in Figure 1, based upon previous studies (Bates et al. 2018, 2015). Dispersion media consisted of 600 µl albumin stock (1 mg albumin/1 ml PBS), 399 µL USP Grade PBS, 1 µL dipalmitoylphosphatidylcholine (DPPC) stock (1 mg DPPC/10 µl 10% ethanol). Mice were then aged several weeks until a lupus-like phenotype developed and were euthanized at 24 weeks, as NZBWF1 mice develop glomerulonephritis around this timeframe. Urinary proteinuria suggestive of renal injury and glomerulonephritis was confirmed at > 300 mg/dl to confirm disease development (Chang et al. 2011; Wang et al. 2009).
Two Co(II)-based coordination polymers: structural diversity and treatment activity on chronic primary glomerulonephritis by reducing ROS accumulation and inflammatory response in glomerular epithelial cells
Published in Inorganic and Nano-Metal Chemistry, 2020
Li-Jun Yu, Dong-Song Bai, Wen-Li Tang, Fu-Long Bi, Qing-Shan Zhang
Chronic primary glomerulonephritis (CPGN) is an immunological inflammatory disease that originates in the glomerulus caused by one or more causes. CPGN has the character of disease insidious, long disease course, and potentially progressive kidney damage, which eventually will develop into end-stage renal disease (ESRD), and must rely on dialysis or kidney transplantation to maintain life. CPGN has become a global public health problem after cardiovascular disease and diabetes.[1,2] The etiology and pathogenesis of CPGN are still unclear. Increased production or reduced clearance of free radical in the kidney; release of anticoagulant substances, anti-inflammatory factors and expression of cell adhesion molecules after endothelial cells damaged would all lead to the kidney damage.
An Ag(I)-pyridyl-triazole coordination polymer: treatment effect on HBV-associated glomerulonephritis via inhibiting inflammatory genes expression
Published in Inorganic and Nano-Metal Chemistry, 2020
Hepatitis B virus-associated glomerulonephritis (HBV-associated glomerulonephritis, HBV-GN) refers to kidney damage caused by hepatitis B virus, which is the most important pathological type.[1] Chronic hepatitis B virus infection can lead to glomerular disease caused by deposition of antigen-antibody immune complexes.[2] The main clinical features of hematuria, proteinuria, edema, and HBV markers are positive, and can even progress to end-stage renal failure.[3] The pathogenesis, clinical manifestations and diagnosis of this disease are not yet clear.[4] According to recent reports, the main cause of the disease is adolescents, and males are mostly.