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Personalized Nutrition in Chronic Kidney Disease
Published in Nilanjana Maulik, Personalized Nutrition as Medical Therapy for High-Risk Diseases, 2020
A specific form of focal segmental glomerulosclerosis is associated with morbid obesity, with nephrotic proteinuria and slow progression towards end-stage kidney disease (Ritz, Koleganova et al. 2011; Amann and Benz 2013). This condition often merges with proteinuric diabetic nephropathy. The latter, at least in Western countries, is also increasingly being found in the absence of proteinuria and its hallmark has shifted to diffuse vascular disease (Packham, Ivory et al. 2011; Amann and Benz 2013; de Vries, Ruggenenti et al. 2014; Robles, Villa et al. 2015; Bolignano and Zoccali 2017; Friedman, Wahed et al. 2018; Jonker, de Heer et al. 2018).
The urinary tract and male reproductive system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Luis Beltran, Daniel M. Berney
There may be a history of recurrent urinary infection, failure to thrive in early childhood, or nocturnal enuresis. In bilateral cases the condition usually presents with the features of chronic renal failure or hypertension. The diagnosis of chronic pyelonephritis is most easily confirmed radiologically, with typical findings comprising asymmetrical shrinkage of the kidney, irregularity of the renal outlet due to cortical scarring, and dilatation or disturbance of the calyces adjacent to the scarred areas. In some patients, heavy proteinuria approaching that seen in the nephrotic syndrome may develop. These patients show secondary focal segmental glomerulosclerosis and its presence suggests the likelihood of a more rapid deterioration of renal function.
Renal medicine
Published in Shibley Rahman, Avinash Sharma, A Complete MRCP(UK) Parts 1 and 2 Written Examination Revision Guide, 2018
Shibley Rahman, Avinash Sharma
Approximately 50% of subjects with focal segmental glomerulosclerosis do not respond to steroid therapy but ACE inhibitors are a recognised strategy to slow the progression of renal disease. Such a patient is in fact at high risk of cardiovascular disease with a very high cholesterol but the question specifically asks about renal disease.
Electron microscopy in renal pathology: overall applications and guidelines for tissue, collection, preparation, and stains
Published in Ultrastructural Pathology, 2021
David N. Howell, Guillermo A. Herrera
Real-time imaging allows in most instances a good visualization of the kidney to be biopsied. The normal renal cortex is about 10 mm in thickness, but it can become significantly thinner in disease processes with cortical damage resulting in interstitial fibrosis. The idea of the renal biopsy is to reach the outer cortex to obtain representative tissue with glomeruli and also to sample the corticomedullary junction, as in some instances, this area may be of value for the diagnosis of glomerular diseases which begin in this location, such as focal segmental glomerulosclerosis. If the needle is pushed farther, then only medulla may be obtained, making it impossible to evaluate glomerular pathology. A renal biopsy that does not provide adequate tissue for evaluation using the three diagnostic techniques, that is, LM, IF, and EM, may be difficult to interpret and the final diagnosis may be compromised in certain instances.
Bradykinin receptor in immune-mediated renal tubular injury in trichloroethylene-sensitized mice: Impact on NF-κB signaling pathway
Published in Journal of Immunotoxicology, 2018
Ling Yang, Jiaxiang Zhang, Na Li, Haibo Xie, Shuangping Chen, Hui Wang, Tong Shen, Qi-xing Zhu
The present study also reflected how if B1R/B2R was increased, this was accompanied by renal dysfunction/pathological damage in TCE-sensitized mice. Once again, however, defined mechanisms for how B1R and B2R contribute to TCE-induced immune renal injury remain unclear. The broad spectrum of KKS action are mediated by B1R and B2R, which have been classified as trans-membrane G protein-coupled receptors (GPCR) (da Costa et al. 2014). These two receptors are expressed not only on structural cells but on inflammatory cells (Ricciardolo et al. 2016). Using double immunofluorescence staining with CK-18 (specifically expressed in renal epithelial cells), the present study showed B1R and B2R were mainly expressed on tubular epithelial cells (Djudjaj et al. 2016). The present study also showed that highly selective antagonists against B1R and B2R exerted protective (albeit not completely mitigative) effects against TCE-induced renal injury. Most of these effects were similar to those noted in studies of experimental focal segmental glomerulosclerosis (Pereira et al. 2014) and renal ischemia/re-perfusion injury (Kakoki et al. 2007). Still, the current results also conflict with findings of some previous studies. For example, Sang et al. (2016) indicated there were opposite effects of antagonists against B1R and B2R in experimental diabetic rats. Such contradictory results in the different studies reflect upon the complicated functions of B1R and B2R and their impact on the kidneys.
Focal and segmental glomerulosclerosis in murine models: a histological and ultrastructural characterization with immunohistochemistry correlation of glomerular CD44 and WT1 expression
Published in Ultrastructural Pathology, 2018
Sufia Husain, Ibrahim Ginawi, Abdelhafiz Ibrahim Bashir, Hala Kfoury, Tariq Eid Al Johani, Hanan Hagar, Lama Raddaoui, Mohammed Al Ghonaim, Abdulkareem Alsuwaida
Focal segmental glomerulosclerosis (FSGS) is a common progressive chronic renal disease.3 It is a group of podocytopathies of variable etiology in which there is glomerulosclerosis in the tuft of at least one glomerulus often with adhesion to the Bowman’s capsule (Figure 1c). The term glomerulosclerosis is defined as the obliteration of the glomerular capillary lumina by sclerotic matrix. The lesions are characterized by focal and segmental pattern of involvement. It typically presents with moderate to heavy proteinuria and usually manifests as nephrotic syndrome that generally responds poorly to standard steroid therapy. FSGS can be primary, characterized by primary/idiopathic podocyte injury or secondary occurring secondarily to a specific type of insult to the kidney. Etiologically, various congenital and acquired factors play a role in the development of FSGS. FSGS is sub-classified according to the Columbia classification and is one of the most common causes of nephrotic syndrome in adults world over and has the potential to progress to end-stage renal disease.3 The renal biopsy typically shows focal and segmental type of glomerulosclerosis in at least one glomerulus. There is no deposition of immunoglobulins or complements in the glomerulus, therefore on immunofluorescence (IF) study there is no positivity for IgA, IgG, IgM, C3, and C1q. Occasionally, there may be some non-specific uptake of IgM and C3 in the sclerotic areas. Electron microscopy (EM) study shows effacement of the podocyte foot processes, ranging from patchy to diffuse effacement depending on the type of FSGS but no electron dense immune deposits are identified.