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Journal articles on the topic 'Ischemic nephropathy'

Author: Grafiati

Published: 28 May 2022

Last updated: 30 July 2025

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1

Fergany, Amr F. "Ischemic nephropathy." Urologic Clinics of North America 28, no. 4 (2001): 805–13. http://dx.doi.org/10.1016/s0094-0143(01)80035-5.

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2

Nobert, Craig F., and John A. Libertino. "Ischemic nephropathy." Current Opinion in Urology 8, no. 2 (1998): 129–34. http://dx.doi.org/10.1097/00042307-199803000-00011.

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3

Breyer, Julia A., and Harry R. Jacobson. "Ischemic nephropathy." Current Opinion in Nephrology and Hypertension 2, no. 2 (1993): 216–24. http://dx.doi.org/10.1097/00041552-199303000-00007.

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4

Tuttle, Katherine R. "Ischemic nephropathy." Current Opinion in Nephrology and Hypertension 10, no. 2 (2001): 167–73. http://dx.doi.org/10.1097/00041552-200103000-00003.

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5

Kaul, Anupama, and Harsh Vardhan. "Ischemic nephropathy." Clinical Queries: Nephrology 1, no. 4 (2012): 268–78. http://dx.doi.org/10.1016/j.cqn.2012.10.001.

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6

Chaturvedy, Manish, and Kirti Rana. "Ischemic nephropathy." Clinical Queries: Nephrology 2, no. 2 (2013): 84–90. http://dx.doi.org/10.1016/j.cqn.2013.04.002.

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7

Novick, Andrew C. "ATHEROSCLEROTIC ISCHEMIC NEPHROPATHY." Urologic Clinics of North America 21, no. 2 (1994): 195–200. http://dx.doi.org/10.1016/s0094-0143(21)00937-x.

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8

Luo, Fengbao, Jian Shi, Qianqian Shi, Xianlin Xu, Ying Xia, and Xiaozhou He. "Mitogen-Activated Protein Kinases and Hypoxic/Ischemic Nephropathy." Cellular Physiology and Biochemistry 39, no. 3 (2016): 1051–67. http://dx.doi.org/10.1159/000447812.

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Tissue hypoxia/ischemia is a pathological feature of many human disorders including stroke, myocardial infarction, hypoxic/ischemic nephropathy, as well as cancer. In the kidney, the combination of limited oxygen supply to the tissues and high oxygen demand is considered the main reason for the susceptibility of the kidney to hypoxic/ischemic injury. In recent years, increasing evidence has indicated that a reduction in renal oxygen tension/blood supply plays an important role in acute kidney injury, chronic kidney disease, and renal tumorigenesis. However, the underlying signaling mechanisms,

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9

Lerman, Lilach, and Stephen C. Textor. "Pathophysiology of ischemic nephropathy." Urologic Clinics of North America 28, no. 4 (2001): 793–803. http://dx.doi.org/10.1016/s0094-0143(01)80034-3.

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10

Alcázar, José, and José Rodicio. "Hypertension and ischemic nephropathy." Current Hypertension Reports 2, no. 4 (2000): 343–44. http://dx.doi.org/10.1007/s11906-000-0034-y.

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11

Garovic, Vesna D., and Stephen C. Textor. "Renovascular Hypertension and Ischemic Nephropathy." Circulation 112, no. 9 (2005): 1362–74. http://dx.doi.org/10.1161/circulationaha.104.492348.

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12

Textor, Stephen C., and Lilach Lerman. "Renovascular Hypertension and Ischemic Nephropathy." American Journal of Hypertension 23, no. 11 (2010): 1159–69. http://dx.doi.org/10.1038/ajh.2010.174.

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13

Palmaz, Julio C. "Vascular Intervention in Ischemic Nephropathy." Journal of Vascular and Interventional Radiology 10, no. 2 (1999): 157–60. http://dx.doi.org/10.1016/s1051-0443(99)71075-4.

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14

Matsumoto, Alan H., David J. Spinosa, J. Fritz Angle, and Klaus D. Hagspiel. "Ischemic nephropathy: Recognition and treatment." Techniques in Vascular and Interventional Radiology 2, no. 2 (1999): 74–83. http://dx.doi.org/10.1016/s1089-2516(99)80048-1.

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15

MANN, S. "Diagnostic tests for ischemic nephropathy." American Journal of Hypertension 8, no. 4 (1995): 29A. http://dx.doi.org/10.1016/0895-7061(95)97483-8.

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16

Chonchol, Michel, and Stuart Linas. "Diagnosis and Management of Ischemic Nephropathy." Clinical Journal of the American Society of Nephrology 1, no. 2 (2006): 172–81. http://dx.doi.org/10.2215/cjn.00940905.

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17

García-Donaire, José A., and José M. Alcázar. "Ischemic nephropathy: Detection and therapeutic intervention." Kidney International 68 (December 2005): S131—S136. http://dx.doi.org/10.1111/j.1523-1755.2005.09924.x.

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18

Joyce, James D., JAMES D. JOYE, SHARZAD ZARGHAMEE, and FREDERICK G. GOAR. "Renal Artery Stenosis and Ischemic Nephropathy." Journal of Interventional Cardiology 14, no. 4 (2001): 451–57. http://dx.doi.org/10.1111/j.1540-8183.2001.tb00357.x.

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19

Ledesma, Y., J. Parekh, T. T. Maw, and A. Webber. "An Unusual Case of Ischemic Nephropathy." American Journal of Transplantation 15, no. 3 (2015): 843–45. http://dx.doi.org/10.1111/ajt.13160.

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20

Hoshide, Satoshi, Kazuomi Kario, and Kazuyuki Shimada. "Ischemic nephropathy in an elderly patient." Geriatrics & Gerontology International 8, no. 2 (2008): 133–35. http://dx.doi.org/10.1111/j.1447-0594.2008.00460.x.

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21

Alcazar, José M., and José L. Rodicio. "Ischemic nephropathy: Clinical characteristics and treatment." American Journal of Kidney Diseases 36, no. 5 (2000): 883–93. http://dx.doi.org/10.1053/ajkd.2000.19077.

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22

Textor, S. C. "Ischemic Nephropathy: Where Are We Now?" Journal of the American Society of Nephrology 15, no. 8 (2004): 1974–82. http://dx.doi.org/10.1097/01.asn.0000133699.97353.24.

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23

Kelly, Katherine J., Jizhong Zhang, Ling Han, Mingsheng Wang, Shaobo Zhang, and Jesus H. Dominguez. "Intravenous renal cell transplantation with SAA1-positive cells prevents the progression of chronic renal failure in rats with ischemic-diabetic nephropathy." American Journal of Physiology-Renal Physiology 305, no. 12 (2013): F1804—F1812. http://dx.doi.org/10.1152/ajprenal.00097.2013.

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Diabetic nephropathy, the most common cause of progressive chronic renal failure and end-stage renal disease, has now reached global proportions. The only means to rescue diabetic patients on dialysis is renal transplantation, a very effective therapy but severely limited by the availability of donor kidneys. Hence, we tested the role of intravenous renal cell transplantation (IRCT) on obese/diabetic Zucker/SHHF F1 hybrid (ZS) female rats with severe ischemic and diabetic nephropathy. Renal ischemia was produced by bilateral renal clamping of the renal arteries at 10 wk of age, and IRCT with g

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24

Delgado Acosta, Fernando, Elvira Jiménez Gómez, Isabel Bravo Rey, Roberto Valverde Moyano, Francisco de Asís Bravo-Rodriguez, and Rafael Oteros Fernández. "Contrast-induced nephropathy: A dilemma between loss of neurons or nephrons in the setting of endovascular treatment of acute ischemic stroke." Interventional Neuroradiology 26, no. 1 (2019): 33–37. http://dx.doi.org/10.1177/1591019919883755.

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Purpose The aim is to report the incidence and risk factors of contrast-induced nephropathy after the use of iodine-based contrast for the endovascular treatment of acute ischemic stroke. Methods Data from patients who underwent neuroendovascular procedures in a center over a period of 22 months were analysed retrospectively. Contrast-induced nephropathy was determined by an increase in serum creatinine level of >25% of baseline or an absolute increase in serum creatinine level of at least 44 µmol/L (0.50 mg/dL) occurring after intravascular administration of contrast media without alternat

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25

Kim, Seo Rin, Amrutesh S. Puranik, Kai Jiang, et al. "Progressive Cellular Senescence Mediates Renal Dysfunction in Ischemic Nephropathy." Journal of the American Society of Nephrology 32, no. 8 (2021): 1987–2004. http://dx.doi.org/10.1681/asn.2020091373.

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BackgroundPeripheral vascular diseases may induce chronic ischemia and cellular injury distal to the arterial obstruction. Cellular senescence involves proliferation arrest in response to stress, which can damage neighboring cells. Renal artery stenosis (RAS) induces stenotic-kidney dysfunction and injury, but whether these arise from cellular senescenceand their temporal pattern remain unknown.MethodsChronic renal ischemia was induced in transgenic INK-ATTAC and wild type C57BL/6 mice by unilateral RAS, and kidney function (in vivo micro-MRI) and tissue damage were assessed. Mouse healthy and

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26

Li, Longling, and Changqing Li. "Microvascular complications of diabetes worsen long-term functional outcomes after acute ischemic stroke." Journal of International Medical Research 46, no. 8 (2018): 3030–41. http://dx.doi.org/10.1177/0300060517734743.

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Objective This study was performed to evaluate the potential predictors of poor outcomes associated with diabetes-specific microvascular pathologies and to analyze their influence on clinical outcomes by adjusting for other well-known prognostic factors in patients with acute ischemic stroke. Methods We analyzed 1389 consecutive adult patients with acute ischemic stroke and explored the relationship among clinical characteristics, laboratory measurements, imaging findings, and 6-month functional outcomes. Results The final study population comprised 216 patients with both acute ischemic stroke

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27

BOGDANOVA, ALINA R., and ROZALIYA R. SHARIPOVA. "modern principles of pharmacoloGical treatment ischemic nephropathy." Bulletin of Contemporary Clinical Medicine 8, no. 6 (2015): 120–26. http://dx.doi.org/10.20969/vskm.2015.8(6).120-126.

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28

DEAN, RICHARD H., REID W. TRIBBLE, KIMBERLEY J. HANSEN, ELIZABETH OʼNEIL, TIMOTHY E. CRAVEN, and JOHN F. REDDING. "Evolution of Renal Insufficiency in Ischemic Nephropathy." Annals of Surgery 213, no. 5 (1991): 446–56. http://dx.doi.org/10.1097/00000658-199105000-00010.

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29

Hansen, Kimberley J., R. Bradley Thomason, Timothy E. Craven, et al. "Surgical management of dialysis-dependent ischemic nephropathy." Journal of Vascular Surgery 21, no. 2 (1995): 197–211. http://dx.doi.org/10.1016/s0741-5214(95)70262-8.

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30

Gheith, Osama, Torki Al-Otaibi, Nabil Elserwy, et al. "Reversible Ischemic Nephropathy in a Deceased Donor Renal Transplant Recipient With BK Nephropathy." Experimental and Clinical Transplantation 20, Suppl 1 (2022): 132–35. http://dx.doi.org/10.6002/ect.mesot2021.p64.

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31

Dugbartey, George J., and Andrew N. Redington. "Prevention of contrast-induced nephropathy by limb ischemic preconditioning: underlying mechanisms and clinical effects." American Journal of Physiology-Renal Physiology 314, no. 3 (2018): F319—F328. http://dx.doi.org/10.1152/ajprenal.00130.2017.

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Contrast-induced nephropathy (CIN) is an important complication following diagnostic radiographic imaging and interventional therapy. It results from administration of intravascular iodinated contrast media (CM) and is currently the third most common cause of hospital-acquired acute kidney injury. CIN is associated with increased morbidity, prolonged hospitalization, and higher mortality. Although the importance of CIN is widely appreciated, and its occurrence can be mitigated by the use of pre- and posthydration protocols and low osmolar instead of high osmolar iodine-containing CM, specific

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32

Kelly, K. J., James L. Burford, and Jesus H. Dominguez. "Postischemic inflammatory syndrome: a critical mechanism of progression in diabetic nephropathy." American Journal of Physiology-Renal Physiology 297, no. 4 (2009): F923—F931. http://dx.doi.org/10.1152/ajprenal.00205.2009.

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Diabetes is a major epidemic, and diabetic nephropathy is the most common cause of end-stage renal disease. Two critical components of diabetic nephropathy are persistent inflammation and chronic renal ischemia from widespread vasculopathy. Moreover, acute ischemic renal injury is common in diabetes, potentially causing chronic kidney disease or end-stage renal disease. Accordingly, we tested the hypothesis that acute renal ischemia accelerates nephropathy in diabetes by activating proinflammatory pathways. Lean and obese-diabetic ZS rats (F1 hybrids of spontaneously hypertensive heart failure

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33

Akhundova, A. A. "Evaluation of the state of tubular epithelium in low birth weight infants with ischemic nephropathy." Kazan medical journal 100, no. 6 (2019): 877–84. http://dx.doi.org/10.17816/kmj2019-877.

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Aim. The study of the diagnostic value of KIM-1 and NGAL in urine and cystatin C in the blood plasma of low birth weight infants with ischemic nephropathy. Methods. 150 newborns were divided into 3 groups: main group 72 low birth weight infants with manifestations of ischemic nephropathy divided into three subgroups: group 1A mild (n=36), 1B moderate (n=20), 1C severe (n=16); comparioson group 28 low birth weight infants without the evidence of ischemic nephropathy; control group 50 healthy newborns (20 full-term and 30 preterm).To assess the state of tubular epithelium of the kidneys, t

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34

Rivoli, Laura, Francesca Di Mario, Giuseppe Coppolino, et al. "Pharmacological Effects of RAAS Blockade in Ischemic Nephropathy." Current Drug Metabolism 17, no. 6 (2016): 550–58. http://dx.doi.org/10.2174/1389200217666160219114443.

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35

Hansen, Kimberley J. "Prevalence of Ischemic Nephropathy in the Atherosclerotic Population." American Journal of Kidney Diseases 24, no. 4 (1994): 615–21. http://dx.doi.org/10.1016/s0272-6386(12)80222-8.

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36

Piercy, K. Todd, Kian Mostafavi, Timothy E. Craven, et al. "Open operative management of dialysis-dependent ischemic nephropathy." Dialysis & Transplantation 36, no. 4 (2007): 192–204. http://dx.doi.org/10.1002/dat.20118.

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37

Textor, Stephen C., Abdu Abumoawad, Ahmed Saad, Christopher Ferguson, and Allan Dietz. "Stem Cell Therapy for Microvascular Injury Associated with Ischemic Nephropathy." Cells 10, no. 4 (2021): 765. http://dx.doi.org/10.3390/cells10040765.

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Ischemic nephropathy reflects progressive loss of kidney function due to large vessel atherosclerotic occlusive disease. Recent studies indicate that this process is characterized by microvascular rarefaction, increased tissue hypoxia and activation of inflammatory processes of tissue injury. This review summarizes the rationale and application of functional MR imaging to evaluate tissue oxygenation in human subjects that defines the limits of renal adaptation to reduction in blood flow, development of increasingly severe tissue hypoxia and recruitment of inflammatory injury pathways in ischem

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38

Sampathkumar, Krishnaswamy, and Ratchagan Saravanan. "A Randomized Controlled Study of Remote Ischemic Preconditioning for Prevention of Contrast-Induced Nephropathy." Open Urology & Nephrology Journal 12, no. 1 (2019): 72–76. http://dx.doi.org/10.2174/1874303x01912010072.

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Introduction: Remote Ischemic Preconditioning (RIPC) is a technique which applies brief periods of reversible ischemia and reperfusion to limbs provoking adaptive protective responses to distant organs like Heart, Kidneys and Brain. Methods: Its efficacy in the prevention of Contrast Nephropathy was tested in our open-label, randomized and sham- controlled study. 100 patients with Chronic Kidney Disease Stages 1-3a requiring Contrast agent for Percutaneous Coronary Interventions were included. Subjects were randomized in a 1:1 ratio to receive either Remote Ischemic Preconditioning (RIPC) or s

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39

Afrin, Syeda Fahmida, Md Hasanur Rahman, Md Asadul Millat, Md Shafiul Alam Quarashi, Asma Begum, and Meherunnesa Begum. "Minor Myocardial Injury: An Early Post Intervention Complication." Delta Medical College Journal 5, no. 2 (2017): 94–98. http://dx.doi.org/10.3329/dmcj.v5i2.33348.

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Percutaneous Coronary Intervention (PCI) is the most commonly performed invasive therapeutic cardiac procedure and plays an important role in the treatment of ischemic heart disease. Complications of Percutaneous Coronary Intervention (PCI) are relatively infrequent. The most common complications include discomfort and bleeding at the puncture site where the catheter was inserted. Major complications include death, MI, or stroke and other infrequent complications include transient ischemic attacks (minor myocardial injury), vascular complication and contrast induced nephropathy, transient isch

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40

Ratliff, B. B., T. Ghaly, P. Brudnicki, et al. "Endothelial progenitors encapsulated in bioartificial niches are insulated from systemic cytotoxicity and are angiogenesis competent." American Journal of Physiology-Renal Physiology 299, no. 1 (2010): F178—F186. http://dx.doi.org/10.1152/ajprenal.00102.2010.

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Intrinsic stem cells (SC) participate in tissue remodeling and regeneration in various diseases and following toxic insults. Failure of tissue regeneration is in part attributed to lack of SC protection from toxic stress of noxious stimuli, thus prompting intense research efforts to develop strategies for SC protection and functional preservation for in vivo delivery. One strategy is creation of artificial SC niches in an attempt to mimic the requirements of endogenous SC niches by generating scaffolds with properties of extracellular matrix. Here, we investigated the use of hyaluronic acid (H

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41

Bahadoram, Sara, Bijan Keikhaei, Mohammad Bahadoram, Mohammad-Reza Mahmoudian-Sani, and Shakiba Hassanzadeh. "Renal complications of sickle cell disease." Journal of Renal Endocrinology 7, no. 1 (2021): e20-e20. http://dx.doi.org/10.34172/jre.2021.20.

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The nephropathy and renal complications of sickle cell disease are associated with various events such as hypoxic or ischemic conditions and reperfusion injury. Erythrocyte sickling occurs following these events and renal medullary acidosis.

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42

Hansen, Kimberley J., Gregory S. Cherr, and Richard H. Dean. "Dialysis-Free Survival after Surgical Repair of Ischemic Nephropathy." Cardiovascular Surgery 10, no. 4 (2002): 400–404. http://dx.doi.org/10.1177/096721090201000421.

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43

Coen, Giorgio, Micaela Manni, Maria Fabrizia Giannoni, et al. "Ischemic Nephropathy in an Elderly Nephrologic and Hypertensive Population." American Journal of Nephrology 18, no. 3 (1998): 221–27. http://dx.doi.org/10.1159/000013340.

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44

Textor, Stephen C. "Issues in renovascular disease and ischemic nephropathy: beyond ASTRAL." Current Opinion in Nephrology and Hypertension 20, no. 2 (2011): 139–45. http://dx.doi.org/10.1097/mnh.0b013e328342bb35.

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45

Palmaz, Julio C. "The Current Status of Vascular Intervention in Ischemic Nephropathy." Journal of Vascular and Interventional Radiology 9, no. 4 (1998): 539–43. http://dx.doi.org/10.1016/s1051-0443(98)70318-5.

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46

Er, Fikret, Amir M. Nia, Henning Dopp, et al. "Ischemic Preconditioning for Prevention of Contrast Medium–Induced Nephropathy." Circulation 126, no. 3 (2012): 296–303. http://dx.doi.org/10.1161/circulationaha.112.096370.

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47

Kiberd, Bryce A. "Use of magnetic resonance angiography to treat ischemic nephropathy." American Journal of Kidney Diseases 26, no. 5 (1995): 873. http://dx.doi.org/10.1016/0272-6386(95)90458-1.

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48

Hansen, K. "Dialysis-free survival after surgical repair of ischemic nephropathy." Cardiovascular Surgery 10, no. 4 (2002): 400–404. http://dx.doi.org/10.1016/s0967-2109(02)00040-6.

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49

Cheungpasitporn, Wisit, Stephen L. Kopecky, Ulrich Specks, Kharmen Bharucha, and Fernando C. Fervenza. "Non-ischemic cardiomyopathy after rituximab treatment for membranous nephropathy." Journal of Renal Injury Prevention 6, no. 1 (2016): 18–25. http://dx.doi.org/10.15171/jrip.2017.04.

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50

Shi, Lang, Zhixia Song, Chenglong Li, et al. "HDAC6 Inhibition Alleviates Ischemia- and Cisplatin-Induced Acute Kidney Injury by Promoting Autophagy." Cells 11, no. 24 (2022): 3951. http://dx.doi.org/10.3390/cells11243951.

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Histone deacetylase (HDAC) 6 exists exclusively in cytoplasm and deacetylates cytoplasmic proteins such as α-tubulin. HDAC6 dysfunction is associated with several pathological conditions in renal disorders, including UUO-induced fibrotic kidneys and rhabdomyolysis-induced nephropathy. However, the role of HDAC6 in ischemic acute kidney injury (AKI) and the mechanism by which HDAC6 inhibition protects tubular cells after AKI remain unclear. In the present study, we observed that HDAC6 was markedly activated in kidneys subjected to ischemia- and cisplatin (cis)-induced AKI treatment. Pharmacolog

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