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Articles de revues sur le sujet « Kidney Pathophysiology »

Auteur : Grafiati

Publié le 4 juin 2021

Mis à jour le 1 février 2022

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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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2

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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3

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Bird, Louise, and David Walker. "Pathophysiology of chronic kidney disease." Companion Animal 20, no. 1 (January 2, 2015): 15–19. http://dx.doi.org/10.12968/coan.2015.20.1.15.

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12

Bird, Louise, and David Walker. "Pathophysiology of acute kidney injury." Companion Animal 20, no. 3 (March 2, 2015): 142–47. http://dx.doi.org/10.12968/coan.2015.20.3.142.

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13

Kiss-Tóth, Éva, та Tamás Rőszer. "PPARγin Kidney Physiology and Pathophysiology". PPAR Research 2008 (2008): 1–9. http://dx.doi.org/10.1155/2008/183108.

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Involvement of the nuclear receptor peroxisome proliferator-activated receptor gamma (PPARγ) in kidney physiology has been explored recently. Synthetic PPARγligands can ameliorate the diabetic kidney disease through different mechanisms, involving inhibition of mesangial cell growth, reduction of mesangial matrix, and cytokine production of glomerular cells as well as promoting endothelial cell survival within the kidney glomeruli. Activation of PPARγhas additional profibrotic consequences, which can contribute to wound healing in diabetic glomerulonephritis. Beside many beneficial effects, PP

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14

Radi, Zaher A. "Kidney Pathophysiology, Toxicology, and Drug-Induced Injury in Drug Development." International Journal of Toxicology 38, no. 3 (March 7, 2019): 215–27. http://dx.doi.org/10.1177/1091581819831701.

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Anatomically, the kidneys are paired, bean-shaped (in most mammals), excretory organs that lie in the retroperitoneum. High blood flow to the kidneys, together with high oxygen consumption, makes them more vulnerable to exposure, via the circulation, and subsequent injury related to high concentrations of xenobiotics and chemicals. In preclinical drug development and safety assessment of new investigational drugs, changes in kidney structure and/or function following drug administration in experimental laboratory animals need to be put in context with interspecies differences in kidney functio

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15

Paliouras, Christos, Eirini Tsampikaki, Polichronis Alivanis, and Georgios Aperis. "Pathophysiology of Nephrolithiasis." Nephrology Research & Reviews 4, no. 2 (January 2012): 58–65. http://dx.doi.org/10.4081/nr.2012.e14.

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The incidence of nephrolithiasis has risen over the last twenty years and continues to rise. Although it is often referred to as a disease, recent advances in the understanding of the pathophysiology suggest that it is a systemic disorder. We conducted a PubMed based literature review on the recent advances in the pathophysiology of kidney stone formation. There is a link between diabetes, metabolic syndrome, obesity, insulin resistance and nephrolithiasis. Along with the aging population and a Western diet, these are the main reasons for the rising incidence and prevalence of nephrolithiasis.

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16

Lewis, Robert. "The pathophysiology underlying chronic kidney disease." Primary Care Cardiovascular Journal (PCCJ) 2, no. 1 (2009): 11. http://dx.doi.org/10.3132/pccj.2009.028.

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17

Cunningham, Priscilla, Helen Noble, Abdul-Kadhum Al-Modhefer, and Ian Walsh. "Kidney stones: pathophysiology, diagnosis and management." British Journal of Nursing 25, no. 20 (November 10, 2016): 1112–16. http://dx.doi.org/10.12968/bjon.2016.25.20.1112.

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18

Moe, Orson W. "Kidney stones: pathophysiology and medical management." Lancet 367, no. 9507 (January 2006): 333–44. http://dx.doi.org/10.1016/s0140-6736(06)68071-9.

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19

Sharfuddin, Asif A., and Bruce A. Molitoris. "Pathophysiology of ischemic acute kidney injury." Nature Reviews Nephrology 7, no. 4 (March 1, 2011): 189–200. http://dx.doi.org/10.1038/nrneph.2011.16.

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20

Epstein, Franklin H. "Book ReviewThe Kidney: Physiology and pathophysiology." New England Journal of Medicine 314, no. 7 (February 13, 1986): 453–54. http://dx.doi.org/10.1056/nejm198602133140721.

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21

Kanagasundaram, Nigel Suren. "Pathophysiology of ischaemic acute kidney injury." Annals of Clinical Biochemistry 52, no. 2 (March 2015): 193–205. http://dx.doi.org/10.1177/0004563214556820.

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22

Greenwald, J. E., P. Needleman, M. R. Wilkins, and G. F. Schreiner. "Renal synthesis of atriopeptin-like protein in physiology and pathophysiology." American Journal of Physiology-Renal Physiology 260, no. 4 (April 1, 1991): F602—F607. http://dx.doi.org/10.1152/ajprenal.1991.260.4.f602.

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Atriopeptin is synthesized in mammalian atria as a 126-amino acid (14 kDa) prohormone, but it is secreted and circulates as a 28-amino acid (2.5 kDa) peptide. We have demonstrated the synthesis and secretion of an atriopeptin-like peptide in neonatal and adult rat kidney cell cultures. In this study, we evaluated the site of renal synthesis of this protein and its expression in normal rats and rats made nephrotic with puromycin aminonucleoside. The major form of atriopeptin in normal kidneys comigrated with an apparent molecular mass of 2.5 kDa assessed by gel filtration chromatography. Howeve

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23

Masood, Humaira, Ruochen Che, and Aihua Zhang. "Inflammasomes in the Pathophysiology of Kidney Diseases." Kidney Diseases 1, no. 3 (2015): 187–93. http://dx.doi.org/10.1159/000438843.

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Background: The inflammasome is a complex of proteins in the cytoplasm that consists of three main components: a sensor protein (receptor), an adapter protein and caspase-1. Inflammasomes are the critical components of innate immunity and have been gradually recognized as a critical mediator in various autoimmune diseases; also, their role in chronic kidney disease and acute kidney injury has been gradually accepted. Summary: Inflammasomes triggered by infectious or sterile injuries transfer proinflammatory mediators into mature ones through innate danger-signaling platforms. Information on in

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24

Ozkok, Abdullah, and Charles L. Edelstein. "Pathophysiology of Cisplatin-Induced Acute Kidney Injury." BioMed Research International 2014 (2014): 1–17. http://dx.doi.org/10.1155/2014/967826.

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Cisplatin and other platinum derivatives are the most widely used chemotherapeutic agents to treat solid tumors including ovarian, head and neck, and testicular germ cell tumors. A known complication of cisplatin administration is acute kidney injury (AKI). The nephrotoxic effect of cisplatin is cumulative and dose-dependent and often necessitates dose reduction or withdrawal. Recurrent episodes of AKI may result in chronic kidney disease. The pathophysiology of cisplatin-induced AKI involves proximal tubular injury, oxidative stress, inflammation, and vascular injury in the kidney. There is p

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25

Agarwal, Rajiv. "Diabetic kidney disease: pathophysiology, implications and management." Trends in Endocrinology & Metabolism 17, no. 2 (March 2006): 38–39. http://dx.doi.org/10.1016/j.tem.2005.12.001.

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26

Sałata, Daria, and Barbara Dołęgowska. "Bioactive lipids in kidney physiology and pathophysiology." Postępy Higieny i Medycyny Doświadczalnej 68 (January 24, 2014): 73–83. http://dx.doi.org/10.5604/17322693.1086412.

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27

Srinivas, Rashmi, and S. Vishwanath. "Pathophysiology of Hypertension in Chronic Kidney Disease." Hypertension Journal 4, no. 3 (2018): 166–69. http://dx.doi.org/10.15713/ins.johtn.0126.

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28

Schnaper, H. William. "The Tubulointerstitial Pathophysiology of Progressive Kidney Disease." Advances in Chronic Kidney Disease 24, no. 2 (March 2017): 107–16. http://dx.doi.org/10.1053/j.ackd.2016.11.011.

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29

Kohan, Donald E. "Endothelins in the Kidney: Physiology and Pathophysiology." American Journal of Kidney Diseases 22, no. 4 (October 1993): 493–510. http://dx.doi.org/10.1016/s0272-6386(12)80920-6.

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30

Toth-Manikowski, Stephanie, and Mohamed G. Atta. "Diabetic Kidney Disease: Pathophysiology and Therapeutic Targets." Journal of Diabetes Research 2015 (2015): 1–16. http://dx.doi.org/10.1155/2015/697010.

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Diabetes is a worldwide epidemic that has led to a rise in diabetic kidney disease (DKD). Over the past two decades, there has been significant clarification of the various pathways implicated in the pathogenesis of DKD. Nonetheless, very little has changed in the way clinicians manage patients with this disorder. Indeed, treatment is primarily centered on controlling hyperglycemia and hypertension and inhibiting the renin-angiotensin system. The purpose of this review is to describe the current understanding of how the hemodynamic, metabolic, inflammatory, and alternative pathways are all ent

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31

Akilesh, Shreeram, Noemie Juaire, Jeremy S. Duffield, and Kelly D. Smith. "Chronic Ifosfamide Toxicity: Kidney Pathology and Pathophysiology." American Journal of Kidney Diseases 63, no. 5 (May 2014): 843–50. http://dx.doi.org/10.1053/j.ajkd.2013.11.028.

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32

Bonventre, Joseph V., and Li Yang. "Cellular pathophysiology of ischemic acute kidney injury." Journal of Clinical Investigation 121, no. 11 (November 1, 2011): 4210–21. http://dx.doi.org/10.1172/jci45161.

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33

Rosa, Ciro Dalla. "Book Review: The Kidney: Physiology and Pathophysiology." Urologia Journal 59, no. 1 (February 1992): 111–12. http://dx.doi.org/10.1177/039156039205900136.

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34

Geenen, Remy W. F., Hylke Jan Kingma, and Aart J. van der Molen. "Pathophysiology of Contrast-Induced Acute Kidney Injury." Interventional Cardiology Clinics 3, no. 3 (July 2014): 363–67. http://dx.doi.org/10.1016/j.iccl.2014.03.007.

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35

Bansal, Shweta, and Rahul N. Patel. "Pathophysiology of Contrast-Induced Acute Kidney Injury." Interventional Cardiology Clinics 9, no. 3 (July 2020): 293–98. http://dx.doi.org/10.1016/j.iccl.2020.03.001.

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36

Bhatt, Kirti, Mitsuo Kato, and Rama Natarajan. "Mini-review: emerging roles of microRNAs in the pathophysiology of renal diseases." American Journal of Physiology-Renal Physiology 310, no. 2 (January 15, 2016): F109—F118. http://dx.doi.org/10.1152/ajprenal.00387.2015.

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MicroRNAs (miRNA) are endogenously produced short noncoding regulatory RNAs that can repress gene expression by posttranscriptional mechanisms. They can therefore influence both normal and pathological conditions in diverse biological systems. Several miRNAs have been detected in kidneys, where they have been found to be crucial for renal development and normal physiological functions as well as significant contributors to the pathogenesis of renal disorders such as diabetic nephropathy, acute kidney injury, lupus nephritis, polycystic kidney disease, and others, due to their effects on key ge

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37

Martin, Rhonda K. "Acute Kidney Injury." AACN Advanced Critical Care 21, no. 4 (October 1, 2010): 350–56. http://dx.doi.org/10.4037/nci.0b013e3181f9574b.

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Acute kidney injury (AKI) is a common disease in the acutely ill patient population, as a singular diagnosis or a complication of sepsis, causing significant mortality and morbidity. Progress in diagnosis, treatment, and research in AKI has been limited by the lack of a universally accepted clinical definition. The clinical definition of AKI onset and progression, early diagnostic indicators, and understanding the unique pathophysiology of AKI are requisite to early treatment and management and ultimately positive patient outcomes. This article reviews the advances in defining and staging AKI

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38

Neki, NS. "Cardiorenal Syndrome - A Review Article." Journal of Medicine 16, no. 1 (February 25, 2015): 39–45. http://dx.doi.org/10.3329/jom.v16i1.22400.

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Cardiorenal syndromes (CRS) describe the dynamic inter-relationship between heart and kidney malfunction. Recent studies have clearly defined its various types and pathophysiology. Improved survival, cardiovascular risk factors (diabetes, hypertension, dyslipidemia), diagnostic and therapeutic intervention are some contributors in its causation. Types 1 and 2 CRS involve acute and chronic cardiovascular disease (CVD) scenarios leading to acute kidney injury or accelerated chronic kidney disease. Types 3 and 4 CRS describe acute and chronic kidney disease leading primarily to heart failure, alt

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39

Kinaan, Mustafa, Hanford Yau, Suzanne Quinn Martinez, and Pran Kar. "Concepts in Diabetic Nephropathy: From Pathophysiology to Treatment." Journal of Renal and Hepatic Disorders 1, no. 2 (June 29, 2017): 10–24. http://dx.doi.org/10.15586/jrenhep.2017.17.

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Since the 1930s when Kimmelstiel and Wilson first described the classic nodular glomerulosclerosis lesions in diabetic kidneys, nephropathy has been recognized as a major and common complication of diabetes. Nearly 40% of diabetics around the world have microalbuminuria, a marker of progression to chronic kidney disease (CKD). Diabetic kidney disease (DKD) is also considered a leading cause of CKD worldwide. Given the significant morbidity, mortality, and health-care burden, several clinical and scientific societies continue to seek a better understanding of this disease. Screening for microal

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40

Kadir, Akmarawita. "Hubungan Patofisiologi Hipertensi dan Hipertensi Renal." Jurnal Ilmiah Kedokteran Wijaya Kusuma 5, no. 1 (February 13, 2018): 15. http://dx.doi.org/10.30742/jikw.v5i1.2.

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Introduction : Hypertension is a disease with an incidence rate is still high around the world, most of the causes of hypertension is unknown (essential hypertension / primary hypertension), a small portion of hypertension caused by diseases acquired (secondary hypertension). The unknown cause of Hypertension causing complications of diseases that worsen it, eg kidney disease (renal disease), and can be a disease that actually cause hypertension becomes more severe (secondary hypertension). Pathophysiology of essential hypertension has been a lot of discussed, but the pathophysiology of renal

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41

Horino, Taro, and Yoshio Terada. "II. Epidemiology and Pathophysiology of Acute Kidney Injury." Nihon Naika Gakkai Zasshi 103, no. 5 (2014): 1055–60. http://dx.doi.org/10.2169/naika.103.1055.

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42

Tamura, Kouichi. "2. Pathophysiology of Atherosclerosis in Chronic Kidney Disease." Nihon Naika Gakkai Zasshi 105, no. 5 (2016): 802–10. http://dx.doi.org/10.2169/naika.105.802.

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43

Vlachopanos, Georgios, Dimitrios Schizas, Natasha Hasemaki, and Argyrios Georgalis. "Pathophysiology of Contrast-Induced Acute Kidney Injury (CIAKI)." Current Pharmaceutical Design 25, no. 44 (January 9, 2020): 4642–47. http://dx.doi.org/10.2174/1381612825666191210152944.

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: Contrast-induced acute kidney injury (CIAKI) is a severe complication associated with the use of iodinated contrast media (CM); a sudden but potentially reversible fall in glomerular filtration rate (GFR) typically occurring 48-72 hours after CM administration. Principal risk factors related with the presentation of CIAKI are preexisting chronic kidney disease and diabetes mellitus. Studies on CIAKI present considerable complexity because of differences in CM type and dose, controversies in definition and baseline comorbidities. Despite that, it should be noted that CIAKI poses a serious hea

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44

Coe, Fredric L., Andrew Evan, and Elaine Worcester. "Pathophysiology-Based Treatment of Idiopathic Calcium Kidney Stones." Clinical Journal of the American Society of Nephrology 6, no. 8 (August 2011): 2083–92. http://dx.doi.org/10.2215/cjn.11321210.

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45

Dawson, Charlotte H., and Charles RV Tomson. "Kidney stone disease: pathophysiology, investigation and medical treatment." Clinical Medicine 12, no. 5 (October 2012): 467–71. http://dx.doi.org/10.7861/clinmedicine.12-5-467.

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46

Campese, Vito M. "Pathophysiology of Resistant Hypertension in Chronic Kidney Disease." Seminars in Nephrology 34, no. 5 (September 2014): 571–76. http://dx.doi.org/10.1016/j.semnephrol.2014.08.011.

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Rapoport, J. "Autosomal dominant polycystic kidney disease: pathophysiology and treatment." QJM 100, no. 1 (December 17, 2006): 1–9. http://dx.doi.org/10.1093/qjmed/hcl129.

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48

Metzinger-Le Meuth, Valérie, Ophélie Fourdinier, Nathalie Charnaux, Ziad A. Massy, and Laurent Metzinger. "The expanding roles of microRNAs in kidney pathophysiology." Nephrology Dialysis Transplantation 34, no. 1 (May 25, 2018): 7–15. http://dx.doi.org/10.1093/ndt/gfy140.

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49

Coe, Fredric L., and Joan H. Parks. "Pathophysiology of Kidney Stones and Strategies for Treatment." Hospital Practice 23, no. 3 (March 15, 1988): 185–207. http://dx.doi.org/10.1080/21548331.1988.11703444.

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50

Kanasaki, Keizo, Munehiro Kitada, and Daisuke Koya. "Pathophysiology of the aging kidney and therapeutic interventions." Hypertension Research 35, no. 12 (October 18, 2012): 1121–28. http://dx.doi.org/10.1038/hr.2012.159.

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