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Relevant bibliographies by topics / Kidney Pathophysiology

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Academic literature on the topic 'Kidney Pathophysiology'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Kidney Pathophysiology"

1

Hewitt, Stephen M., and Robert A. Star. "Enlightening kidney pathophysiology." Nature Materials 18, no. 10 (September 19, 2019): 1034–35. http://dx.doi.org/10.1038/s41563-019-0490-5.

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McCullough, Peter A. "Cardiorenal Syndromes: Pathophysiology to Prevention." International Journal of Nephrology 2011 (2011): 1–10. http://dx.doi.org/10.4061/2011/762590.

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There is a strong association between both acute and chronic dysfunction of the heart and kidneys with respect to morbidity and mortality. The complex interrelationships of longitudinal changes in both organ systems have been difficult to describe and fully understand due to a lack of categorization of the common clinical scenarios where these phenomena are encountered. Thus, cardiorenal syndromes (CRSs) have been subdivided into five syndromes which represent clinical vignettes in which both the heart and the kidney are involved in bidirectional injury and dysfunction via a final common pathw

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Noda, Yumi, Eisei Sohara, Eriko Ohta, and Sei Sasaki. "Aquaporins in kidney pathophysiology." Nature Reviews Nephrology 6, no. 3 (January 26, 2010): 168–78. http://dx.doi.org/10.1038/nrneph.2009.231.

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4

Su, Wen, Rong Cao, Xiao-yan Zhang, and Youfei Guan. "Aquaporins in the kidney: physiology and pathophysiology." American Journal of Physiology-Renal Physiology 318, no. 1 (January 1, 2020): F193—F203. http://dx.doi.org/10.1152/ajprenal.00304.2019.

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The kidney is the central organ involved in maintaining water and sodium balance. In human kidneys, nine aquaporins (AQPs), including AQP1–8 and AQP11, have been found and are differentially expressed along the renal tubules and collecting ducts with distinct and critical roles in the regulation of body water homeostasis and urine concentration. Dysfunction and dysregulation of these AQPs result in various water balance disorders. This review summarizes current understanding of physiological and pathophysiological roles of AQPs in the kidney, with a focus on recent progress on AQP2 regulation

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Che, Ruochen, Yanggang Yuan, Songming Huang, and Aihua Zhang. "Mitochondrial dysfunction in the pathophysiology of renal diseases." American Journal of Physiology-Renal Physiology 306, no. 4 (February 15, 2014): F367—F378. http://dx.doi.org/10.1152/ajprenal.00571.2013.

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Mitochondrial dysfunction has gained recognition as a contributing factor in many diseases. The kidney is a kind of organ with high energy demand, rich in mitochondria. As such, mitochondrial dysfunction in the kidney plays a critical role in the pathogenesis of kidney diseases. Despite the recognized importance mitochondria play in the pathogenesis of the diseases, there is limited understanding of various aspects of mitochondrial biology. This review examines the physiology and pathophysiology of mitochondria. It begins by discussing mitochondrial structure, mitochondrial DNA, mitochondrial

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Gilbert, Bruce R., and E. Darracott Vaughan. "Pathophysiology of the Aging Kidney." Clinics in Geriatric Medicine 6, no. 1 (February 1990): 13–30. http://dx.doi.org/10.1016/s0749-0690(18)30631-1.

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Nakano, Daisuke, and Akira Nishiyama. "Multiphoton imaging of kidney pathophysiology." Journal of Pharmacological Sciences 132, no. 1 (September 2016): 1–5. http://dx.doi.org/10.1016/j.jphs.2016.08.001.

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Anderson, Carl F. "The Kidney: Physiology and Pathophysiology." Mayo Clinic Proceedings 60, no. 8 (August 1985): 563. http://dx.doi.org/10.1016/s0025-6196(12)60580-1.

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Dunea, George. "The Kidney: Physiology and Pathophysiology." JAMA: The Journal of the American Medical Association 254, no. 23 (December 20, 1985): 3373. http://dx.doi.org/10.1001/jama.1985.03360230105035.

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Dunea, George. "The Kidney: Physiology and Pathophysiology." JAMA: The Journal of the American Medical Association 267, no. 23 (June 17, 1992): 3216. http://dx.doi.org/10.1001/jama.1992.03480230116042.

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Dissertations / Theses on the topic "Kidney Pathophysiology"

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Prowle, John Richard. "Renal blood flow and the pathophysiology of acute kidney injury." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607649.

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Gaze, David C. "The pathophysiology of cardiac troponin elevation in chronic kidney disease : proposed mechanisms." Thesis, St George's, University of London, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.656857.

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The measurement of the cardiac troponins has produced a paradigm shift in the management of cardiac disease. Elevation of cTn without acute myocardial infarction (AMI) also occurs in non-cardiac patients including those with chronic kidney disease (CKD). Cardiovascular disease accounts for 50% of mortality in CKD. In this thesis, the prognostic value of cTn elevation in CKD was investigated by meta-analysis of published data and recruitment of a CKD cohort. The relationship between elevated cTn and cardiac imaging; the involvement of inflammation, oxidative stress and platelet activation were

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Prapansilp, Panote. "Molecular pathological investigation of the pathophysiology of fatal malaria." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:e966a2f2-a37d-4586-b09e-2bb616e5dce2.

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Malaria remains one of the world's major health problems, especially in developing countries. A better understanding of the pathology and pathophysiology of severe malaria is key to develop new treatments. Different approaches have been used in malaria research including the in vitro co-culture models with endothelial cells and both murine and simian animal models. However these are open to controversy due to disagreement on their representativeness of human disease. Using human post-mortem tissue in malaria research is another important approach but is practically challenging, limiting the av

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4

Anderson, Paul Hamill. "The regulation of Vitamin D metabolism in the kidney and bone." Title page, contents and abstract only, 2002. http://web4.library.adelaide.edu.au/theses/09PH/09pha5486.pdf.

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Includes bibliographical references (leaves 226-273.) Investigates the regulation of the expression of CYP27B1, CYP24 and vitamin D receptor (VDR) mRNA, both in the bone and in the kidney, with the aim to determine whether the regulation of the vitamin D metabolism in the bone is independent from that in the kidney. The effects of age, dietary calcium and vitamin D status on the expression of these genes in both the kidney and the bone, as well as on a number of biochemical factors known to regulate the renal metabolism of 1,25D, such as PTH, calcium and 1,25D itself, were examined. CYP27B1 mR

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Sevastos, Jacob Prince of Wales Clinical School UNSW. "The role of tissue factor in renal ischaemia reperfusion injury." Awarded by:University of New South Wales. Prince of Wales Clinical School, 2006. http://handle.unsw.edu.au/1959.4/27416.

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Reperfusion injury may mediate renal dysfunction following ischaemia. A murine model was developed to investigate the role of the tissue factor-thrombin-protease activated receptor pathway in renal ischaemia reperfusion injury (IRI). In this model, mice received 25 minutes of ischaemia and subsequent periods of reperfusion. C57BL6, protease activated receptor-1 (PAR-1) knockout mice, and tissue factor (TF) deficient mice were used. Following 24 hours IRI, PAR-1 deficiency resulted in protection against severe renal failure compared to the C57BL6 mice (creatinine, 118.2 ?? 6.3 vs 203 ?? 12 ??mo

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Sousa, Maria Rita Mota de. "Pathophysiology and therapeutic implications of ischemic acute kidney injury." Dissertação, 2016. https://repositorio-aberto.up.pt/handle/10216/89429.

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Sousa, Maria Rita Mota de. "Pathophysiology and therapeutic implications of ischemic acute kidney injury." Master's thesis, 2016. https://repositorio-aberto.up.pt/handle/10216/89429.

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"Mechanisms of angiotensin II-mediated kidney injury: role of TGF-β/Smad signalling". 2012. http://library.cuhk.edu.hk/record=b5549544.

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血管紧张素II(Ang II)在慢性肾脏病中起重要的致病作用，尽管体外研究证实TGF-β/Smad3起正调控，Smad7起负调控作用，但Smad3在Ang II 诱导的肾脏损害中的作用仍不清楚。因此，本论文在Smad3基因敲除的小鼠中通过Ang II诱导的高血压肾损伤模型研究TGF-β/Smad3通路的作用及机制。如第三章所述，敲除Smad3的小鼠不发生Ang II诱导的高血压肾损伤如尿白蛋白，血肌酐升高，肾脏炎症（如IL-1, TNFα上调，F4/80+ 巨噬细胞浸润）及肾脏纤维化（包括α-SMA+肌成纤维细胞聚集，和胶原基质沉积）。敲除Smad3对高血压肾病起保护作用是因为抑制了肾脏TGF-β1表达及Smurf2 依赖的Smad7泛素化降解，从而抑制TGF-β/Smad3介导的肾脏纤维化和NF-B介导的炎症。<br>越来越多的证据显示Ang II产生和降解的平衡在高血压肾病的发展中起重要作用。在这篇论文中，我们假设ACE2的降解可能会引起Ang II代谢通路的失衡，从而加重其介导的高血压肾病。这一假设在第四章得到验证，在单侧输尿管梗阻小鼠模型敲除ACE2加重肾内Ang II介导的肾脏纤维化和炎症。这一变化与肾内高水平的Ang II和降低的血管紧张素1-7，上调的血管紧张素受体1，及激活的TGF-β/Smad3 和 NF-κB 信号通路有关。另外，升高的Smurf2介导的Smad

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Psotka, Mitchell Adam. "The pathophysiology of renal failure in a shiga toxin plus lipopolysaccharide induced murine model of hemolytic uremic syndrome." 2008. http://proquest.umi.com/pqdweb?did=1805440271&sid=3&Fmt=2&clientId=3507&RQT=309&VName=PQD.

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Corridon, Peter R. "Hydrodynamic delivery for the study, treatment and prevention of acute kidney injury." Thesis, 2014. http://hdl.handle.net/1805/4603.

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Indiana University-Purdue University Indianapolis (IUPUI)<br>Advancements in human genomics have simultaneously enhanced our basic understanding of the human body and ability to combat debilitating diseases. Historically, research has shown that there have been many hindrances to realizing this medicinal revolution. One hindrance, with particular regard to the kidney, has been our inability to effectively and routinely delivery genes to various loci, without inducing significant injury. However, we have recently developed a method using hydrodynamic fluid delivery that has shown substantial pr

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Books on the topic "Kidney Pathophysiology"

1

Pathophysiology of renal disease. 2nd ed. New York: McGraw-Hill, 1987.

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2

Leaf, Alexander. Renal pathophysiology. 3rd ed. New York: Oxford University Press, 1985.

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3

M, Denker Bradley, and Rose Burton David 1942-, eds. Renal pathophysiology: The essentials. 2nd ed. Philadelphia: Lippincott Williams & Wilkins, 2007.

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M, Denker Bradley, ed. Renal pathophysiology: The essentials. 3rd ed. Baltimore, MD: Lippincott Williams & Wilkins, 2010.

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5

Fuminori, Sakai, Berliner Robert W. 1915-, Honda Nishio, and Ullrich K. J, eds. The frontiers of nephrology: Proceedings of the International Forum "The Frontiers of Nephrology", honoring Fuminori Sakai, held in Tokyo, Japan, 24-25 August 1989. Amsterdam: Excerpta Medica, 1990.

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6

G, Rennke Helmut, ed. Renal pathophysiology: The essentials. Baltimore: Williams & Wilkins, 1994.

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7

Dixhoorn, Mieneke G. A. van. IgA in experimental kidney disease. [Leiden: University of Leiden, 1998.

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8

Höper, J. Influence of local oxygen deficiency on function and integrity of liver, kidney, and heart. Stuttgart: G. Fischer, 1991.

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9

Eleftheriadis, Theodoros. Vitamin D receptor agonists and kidney diseases. Hauppauge, N.Y: Nova Science Publishers, 2010.

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10

Hikaru, Koide, and Hayashi T, eds. Extracellular matrix in the kidney: 6th International Symposium on Basement Membrane, Shizuoka, May 29-June 1, 1993. Basel: Karger, 1994.

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Book chapters on the topic "Kidney Pathophysiology"

1

Sanders, P. W. "Pathophysiology of myeloma kidney." In Monoclonal Gammopathies and the Kidney, 53–60. Dordrecht: Springer Netherlands, 2003. http://dx.doi.org/10.1007/978-94-017-0191-4_5.

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Ren, Jiafa, and Chunsun Dai. "Pathophysiology of Chronic Kidney Disease." In Chronic Kidney Disease, 13–32. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-32-9131-7_2.

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Loeffler, Ivonne. "Pathophysiology of Diabetic Nephropathy." In Diabetes and Kidney Disease, 45–61. Oxford, UK: Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781118494073.ch4.

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Yasuda, Hideo. "Pathophysiology of AKI." In Acute Kidney Injury and Regenerative Medicine, 33–45. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-1108-0_3.

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Bruno, M., and M. Marangella. "Cystinuria: Recent Advances in Pathophysiology and Genetics." In Hereditary Kidney Diseases, 173–77. Basel: KARGER, 1997. http://dx.doi.org/10.1159/000059896.

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6

Worcester, Elaine M. "Pathophysiology of Kidney Stone Formation." In Nutritional and Medical Management of Kidney Stones, 21–42. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-15534-6_2.

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7

Tonnesen, A. S. "The Kidney in Sepsis." In Pathophysiology of Shock, Sepsis, and Organ Failure, 973–95. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-76736-4_66.

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Thurau, K. "Pathophysiology of the Acutely Failing Kidney." In Endocrine Regulation of Electrolyte Balance, 73–80. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71405-4_8.

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Busch, Martin. "Cardiovascular Disease in Diabetic Nephropathy: Pathophysiology and Treatment." In Diabetes and Kidney Disease, 83–100. Oxford, UK: Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781118494073.ch7.

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Murlidharan, Praveen, Sreelekshmi Kamaladevan, Satish Balan, and Chandrasekharan C. Kartha. "Mechanisms for Obesity Related Kidney Disease." In Pathophysiology of Obesity-Induced Health Complications, 193–216. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-35358-2_12.

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Conference papers on the topic "Kidney Pathophysiology"

1

Bao, Guangyu, Xiaomin Chen, and Ramesh K. Agarwal. "Optimization of Anastomotic Geometry for Vascular Access Fistula." In ASME/JSME/KSME 2015 Joint Fluids Engineering Conference. American Society of Mechanical Engineers, 2015. http://dx.doi.org/10.1115/ajkfluids2015-26130.

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Arteriovenous fistula (AVF) is one type of vascular access which is a surgically created vein used to remove and return blood during hemodialysis [1]. It is a long-term treatment for kidney failure. Although clinical treatment and technology have both achieved great improvements in recent years, the vascular access for hemodialysis still has significant early failure rates after the insertion of AVF in patients [2]. Studies have shown that stenosis in the vascular access circuit is the single major cause for access morbidity. Majority of efforts to understand the mechanisms of stenosis formati

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2

Bao, Guangyu, Xiaomin Chen, and Ramesh K. Agarwal. "Optimization of Anastomotic Geometry for Vascular Access Fistula." In ASME 2016 Fluids Engineering Division Summer Meeting collocated with the ASME 2016 Heat Transfer Summer Conference and the ASME 2016 14th International Conference on Nanochannels, Microchannels, and Minichannels. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/fedsm2016-7612.

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Arteriovenous fistula (AVF) is one type of vascular access which is a surgically created vein used to remove and return blood during hemodialysis [1]. It is a long-term treatment for kidney failure. Although clinical treatment and technology have both achieved great improvements in recent years, the vascular access for hemodialysis still has significant early failure rates after the insertion of AVF in patients [2]. Studies have shown that stenosis in the vascular access circuit is the single major cause for access morbidity. Majority of efforts to understand the mechanisms of stenosis formati

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