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Journal articles on the topic 'Hypertensive nephrosclerosis'

Author: Grafiati

Published: 4 June 2021

Last updated: 14 February 2022

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1

Hill, Gary S. "Hypertensive nephrosclerosis." Current Opinion in Nephrology and Hypertension 17, no. 3 (2008): 266–70. http://dx.doi.org/10.1097/mnh.0b013e3282f88a1f.

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2

Fogo, Agnes. "Hypertensive Nephrosclerosis." American Journal of Kidney Diseases 33, no. 6 (1999): E1—E2. http://dx.doi.org/10.1053/s0272-6386(13)90017-2.

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3

Dasgupta, I., C. Porter, A. Innes, and R. Burden. "'Benign' hypertensive nephrosclerosis." QJM 100, no. 2 (2006): 113–19. http://dx.doi.org/10.1093/qjmed/hcl139.

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4

Luft, Friedrich C. "Hypertensive nephrosclerosis: update." Current Opinion in Nephrology and Hypertension 13, no. 2 (2004): 147–54. http://dx.doi.org/10.1097/00041552-200403000-00002.

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5

Tedla, Fasika, and Moro Salifu. "Hypertensive Nephrosclerosis in Kenya." Cardiology 120, no. 3 (2011): 123–24. http://dx.doi.org/10.1159/000334868.

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6

&NA;. "Ramipril preferable in hypertensive nephrosclerosis?" Inpharma Weekly &NA;, no. 1292 (2001): 10. http://dx.doi.org/10.2165/00128413-200112920-00021.

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7

Mujais, Salim K., Dimitrios S. Emmanouel, Balakuntalam S. Kasinath, and Benjamin H. Spargo. "Marked Proteinuria in Hypertensive Nephrosclerosis." American Journal of Nephrology 5, no. 3 (1985): 190–95. http://dx.doi.org/10.1159/000166931.

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8

Luke, Robert G. "Hypertensive nephrosclerosis: pathogenesis and prevalence." Nephrology Dialysis Transplantation 14, no. 10 (1999): 2271–78. http://dx.doi.org/10.1093/ndt/14.10.2271.

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9

Kincaid-Smith, Priscilla. "Clinical diagnosis of hypertensive nephrosclerosis." Nephrology Dialysis Transplantation 14, no. 9 (1999): 2255–56. http://dx.doi.org/10.1093/ndt/14.9.2255.

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10

Toto, Robert B. "Hypertensive nephrosclerosis in African Americans." Kidney International 64, no. 6 (2003): 2331–41. http://dx.doi.org/10.1046/j.1523-1755.2003.00333.x.

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11

Krishnan, R., T. P. Naushad, and N. Biju. "HYPERURICEMIA - A MARKER OF HYPERTENSIVE NEPHROSCLEROSIS IN ESSENTIAL HYPERTENSION?" Journal of Hypertension 22, Suppl. 2 (2004): S360. http://dx.doi.org/10.1097/00004872-200406002-01260.

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12

&NA;. "ACE inhibitors best in hypertensive nephrosclerosis?" Inpharma Weekly &NA;, no. 1366 (2002): 15. http://dx.doi.org/10.2165/00128413-200213660-00030.

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13

Bleyer, Anthony J., and Richard G. Appel. "Risk Factors Associated with Hypertensive Nephrosclerosis." Nephron 82, no. 3 (1999): 193–98. http://dx.doi.org/10.1159/000045402.

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14

Wang, G., F. M. M. Lai, B. C. H. Kwan, et al. "Podocyte Loss in Human Hypertensive Nephrosclerosis." American Journal of Hypertension 22, no. 3 (2009): 300–306. http://dx.doi.org/10.1038/ajh.2008.360.

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15

NAKAYA, HIDEAKI, HIROYUKI SASAMURA, MATSUHIKO HAYASHI, and TAKAO SARUTA. "Temporary Treatment of Prepubescent Rats with Angiotensin Inhibitors Suppresses the Development of Hypertensive Nephrosclerosis." Journal of the American Society of Nephrology 12, no. 4 (2001): 659–66. http://dx.doi.org/10.1681/asn.v124659.

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Abstract. Hypertensive nephrosclerosis is a leading cause of end-stage renal disease; therefore, strategies to prevent the development of renal disease require close study. Here it is demonstrated that transient treatment of prepubescent rats with angiotensin inhibitors attenuated their susceptibility to the development of hypertensive nephrosclerosis after maturation. Stroke-prone spontaneously hypertensive Izumo strain rats were divided into four groups, treated with vehicle, the angiotensin-converting enzyme inhibitor (ACEI) delapril (40 mg/kg per d), the angiotensin receptor antagonist (AT

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16

Razzaque, M. S., T. Harada та T. Taguchi. "Significance of Increased Accumulation of Type VI Collagen and Transforming Growth Factor βi in Tubulointerstitial Damage in Hypertensive Nephrosclerosis: An Immunohistochemical Study". Journal of International Medical Research 24, № 2 (1996): 199–208. http://dx.doi.org/10.1177/030006059602400204.

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The distribution of type VI collagen and transforming growth factor β1 (TGF β1) was studied by immunohistochemistry in 12 renal biopsy specimens of hypertensive nephrosclerosis and five control cases. In control kidneys, the immunostaining of type VI collagen was found in the mesangium, glomerular basement membrane and tubular basement membrane. For TGF β, mesangium, glomerular basement membrane, tubular basement membrane and tubular epithelial cells stained positively in the control kidneys. In contrast to the control cases, markedly increased immunostaining for both type VI collagen and TGF

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17

Haruhara, Kotaro, Nobuo Tsuboi, Go Kanzaki, et al. "Glomerular Density in Biopsy-Proven Hypertensive Nephrosclerosis." American Journal of Hypertension 28, no. 9 (2015): 1164–71. http://dx.doi.org/10.1093/ajh/hpu267.

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18

Hill, G. S. "Response to ‘Hypertensive nephrosclerosis: Pathogenesis and prevalence’." Kidney International 70, no. 7 (2006): 1383–84. http://dx.doi.org/10.1038/sj.ki.5001720.

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19

Freedmana, Barry I., Samy S. Iskandarb, Vardaman M. Buckalew Jr., John M. Burkarta, and Richard G. Appela. "Renal Biopsy Findings in Presumed Hypertensive Nephrosclerosis." American Journal of Nephrology 14, no. 2 (1994): 90–94. http://dx.doi.org/10.1159/000168695.

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20

Toto, Robert D. "Proteinuria and hypertensive nephrosclerosis in African Americans." Kidney International 66 (November 2004): S102—S104. http://dx.doi.org/10.1111/j.1523-1755.2004.09224.x.

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21

Zucchelli, Pietro, and Alessandro Zuccalá. "Progression of renal failure and hypertensive nephrosclerosis." Kidney International 54 (December 1998): S55—S59. http://dx.doi.org/10.1046/j.1523-1755.1998.06814.x.

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22

Marcantoni, Carmelita, Li-Jun Ma, Charles Federspiel, and Agnes B. Fogo. "Hypertensive nephrosclerosis in African Americans versus Caucasians." Kidney International 62, no. 1 (2002): 172–80. http://dx.doi.org/10.1046/j.1523-1755.2002.00420.x.

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23

Wenzel, Ulrich O., Marlies Bode, Jörg Köhl, and Heimo Ehmke. "A pathogenic role of complement in arterial hypertension and hypertensive end organ damage." American Journal of Physiology-Heart and Circulatory Physiology 312, no. 3 (2017): H349—H354. http://dx.doi.org/10.1152/ajpheart.00759.2016.

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The self-amplifying cascade of messenger and effector molecules of the complement system serves as a powerful danger-sensing system that protects the host from a hostile microbial environment, while maintaining proper tissue and organ function through effective clearance of altered or dying cells. As an important effector arm of innate immunity, it also plays important roles in the regulation of adaptive immunity. Innate and adaptive immune responses have been identified as crucial players in the pathogenesis of arterial hypertension and hypertensive end organ damage. In line with this view, c

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24

Cordonnier, D., A. R. Rachi, P. Courderc, et al. "Primitive Renal Microarterial Lesions or Pre-Hypertensive Nephrosclerosis." Journal of Hypertension 4, no. 5 (1986): 642–43. http://dx.doi.org/10.1097/00004872-198610000-00028.

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25

Zarif, Linda, Adrian Covic, Sudha Iyengar, Ashwini R. Sehgal, John R. Sedor, and Jeffrey R. Schelling. "Inaccuracy of clinical phenotyping parameters for hypertensive nephrosclerosis." Nephrology Dialysis Transplantation 15, no. 11 (2000): 1801–7. http://dx.doi.org/10.1093/ndt/15.11.1801.

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26

&NA;. "Reversible renal insufficiency with enalapril in hypertensive nephrosclerosis." Inpharma Weekly &NA;, no. 809 (1991): 20. http://dx.doi.org/10.2165/00128413-199108090-00054.

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27

Ying, Wei-Zhong, Pei-Xuan Wang, and Paul W. Sanders. "Induction of apoptosis during development of hypertensive nephrosclerosis." Kidney International 58, no. 5 (2000): 2007–17. http://dx.doi.org/10.1046/j.1523-1755.2000.00373.x.

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28

Koupepidou, P., T. Christophides, C. Comstantinou-Deltas, and A. Pierides. "METHYLENETETRAHYDROFOLATE REDUCTASE (MTHFR). 677TT GENOTYPE PREDICTS HYPERTENSIVE NEPHROSCLEROSIS." Journal of Hypertension 22, Suppl. 2 (2004): S344. http://dx.doi.org/10.1097/00004872-200406002-01200.

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29

Radenkovic, S., M. Milojkovic, and N. Lecic. "MARKERS OF OXIDATIVE STRESS IN BENIGN HYPERTENSIVE NEPHROSCLEROSIS." Journal of Hypertension 22, Suppl. 2 (2004): S356. http://dx.doi.org/10.1097/00004872-200406002-01245.

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30

Allen, Christopher E., and Paul W. Sanders. "Hypertensive nephrosclerosis: not enough of a good thing?" American Journal of Physiology-Renal Physiology 304, no. 6 (2013): F674—F675. http://dx.doi.org/10.1152/ajprenal.00695.2012.

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31

Bidani, A. K., K. A. Griffin, W. Plott, and M. M. Schwartz. "Renal ablation acutely transforms 'benign' hypertension to 'malignant' nephrosclerosis in hypertensive rats." Hypertension 24, no. 3 (1994): 309–16. http://dx.doi.org/10.1161/01.hyp.24.3.309.

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32

Seccia, Teresa, Brasilina Caroccia, Maria Piazza, and Gian Paolo Rossi. "The Key Role of Epithelial to Mesenchymal Transition (EMT) in Hypertensive Kidney Disease." International Journal of Molecular Sciences 20, no. 14 (2019): 3567. http://dx.doi.org/10.3390/ijms20143567.

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Accumulating evidence indicates that epithelial-to-mesenchymal transition (EMT), originally described as a key process for organ development and metastasis budding in cancer, plays a key role in the development of renal fibrosis in several diseases, including hypertensive nephroangiosclerosis. We herein reviewed the concept of EMT and its role in renal diseases, with particular focus on hypertensive kidney disease, the second leading cause of end-stage renal disease after diabetes mellitus. After discussing the pathophysiology of hypertensive nephropathy, the ‘classic’ view of hypertensive nep

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33

Luft, Friedrich C. "Hypertensive nephrosclerosis–a cause of end‐stage renal disease?" Nephrology Dialysis Transplantation 15, no. 10 (2000): 1515–17. http://dx.doi.org/10.1093/ndt/15.10.1515.

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34

Wang, G., B. C. H. Kwan, F. M. M. Lai, et al. "Intrarenal Expression of miRNAs in Patients With Hypertensive Nephrosclerosis." American Journal of Hypertension 23, no. 1 (2010): 78–84. http://dx.doi.org/10.1038/ajh.2009.208.

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35

Zucchelli, Pietro, and Alessandro Zuccalà. "The Diagnostic Dilemma of Hypertensive Nephrosclerosis: The Nephrologist's View." American Journal of Kidney Diseases 21, no. 5 (1993): 87–91. http://dx.doi.org/10.1016/0272-6386(93)70100-d.

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36

Pan, Xiaoqing, Xuemei Geng, Yong Liu, et al. "Transfer RNA Fragments in the Kidney in Hypertension." Hypertension 77, no. 5 (2021): 1627–37. http://dx.doi.org/10.1161/hypertensionaha.121.16994.

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Small noncoding RNAs (sncRNAs) are important regulators of gene expression. In contrast with well-studied microRNAs, transfer RNA-derived RNA fragments (tRFs) are a new class of sncRNAs that has not been studied in hypertension. This study aims to characterize renal tRFs and identify dysregulation and potential role of renal tRFs in hypertension. We analyzed sncRNA-sequencing and mRNA-sequencing data from the kidneys of Dahl salt-sensitive rats and sncRNA-sequencing data from kidney biopsy specimens from hypertensive nephrosclerosis patients. Over 300 tRFs were identified in the rat renal oute

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37

Ono, Yuko, Hidehiko Ono, and Edward D. Frohlich. "Hydrochlorothiazide exacerbates nitric oxide-blockade nephrosclerosis with glomerular hypertension in spontaneously hypertensive rats." Journal of Hypertension 14, no. 7 (1996): 823–28. http://dx.doi.org/10.1097/00004872-199607000-00004.

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38

Joshi, Keshab Raj, Ashish Gautam, Dipendra Raj Pandeya, and Keshab Poudel. "Serum Creatinine and Urine Microalbumin Level in Hypertensive and Non hypertensive Patients." Medical Journal of Shree Birendra Hospital 12, no. 2 (2015): 27–30. http://dx.doi.org/10.3126/mjsbh.v12i2.12923.

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Introduction: Hypertension is one of the most common cardiovascular disorders, more likely to accelerateatherosclerosis causing cardiovascular complications and benign arteriolar nephrosclerosis for an extendedperiod of time may manifest as a mild to moderate elevation of serum creatinine and/or microalbuminuria.Methods: The present study was carried out on total 100 subjects. Which were divided into two groups. Firstgroup of experimental group consist of 50 subjects with known Hypertensive Subjects. Another group is controlgroup consist of 50 Non-Hypertensive Subjects with no present and past

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39

Ono, Hidehiko, Yuko Ono, and Edward D. Frohlich. "L-Arginine reverses severe nephrosclerosis in aged spontaneously hypertensive rats." Journal of Hypertension 17, no. 1 (1999): 121–28. http://dx.doi.org/10.1097/00004872-199917010-00018.

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40

Wang, Gang, Fernand Mac-Moune Lai, Bonnie C. H. Kwan, et al. "Expression of ACE and ACE2 in Patients with Hypertensive Nephrosclerosis." Kidney and Blood Pressure Research 34, no. 3 (2011): 141–49. http://dx.doi.org/10.1159/000324521.

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41

Caetano, Edna Regina Silva Pereira, Roberto Zatz, Luís Balthazar Saldanha, and José Nery Praxedes. "Hypertensive Nephrosclerosis as a Relevant Cause of Chronic Renal Failure." Hypertension 38, no. 2 (2001): 171–76. http://dx.doi.org/10.1161/01.hyp.38.2.171.

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42

Qiu, Changbin, Patrick Bruneval, Andree Roeckel, Didier Heudes, Jean-Paul Duong Van Huyen, and Sebastien Roux. "Mibefradil prevents L-NAME-exacerbated nephrosclerosis in spontaneously hypertensive rats." Journal of Hypertension 17, no. 10 (1999): 1489–95. http://dx.doi.org/10.1097/00004872-199917100-00018.

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43

FOGO, Agnes, Julia A. BREYER, Michael C. SMITH, et al. "Renal histopathology in US African-Americans with presumed hypertensive nephrosclerosis." Nephrology 4, s2 (1998): S54—S58. http://dx.doi.org/10.1111/j.1440-1797.1998.tb00473.x.

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44

Caetano, E. "The clinical diagnosis of hypertensive nephrosclerosis - how reliable is it?" Nephrology Dialysis Transplantation 14, no. 2 (1999): 288–90. http://dx.doi.org/10.1093/ndt/14.2.288.

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45

Roldan, C., C. Campo, J. Segura, et al. "HYPERTENSIVE NEPHROSCLEROSIS IS RELATED WITH SUBCLINICAL LEFT VENTRICULAR DIASTOLIC DYSFUNCTION." Journal of Hypertension 22, Suppl. 2 (2004): S35—S36. http://dx.doi.org/10.1097/00004872-200406002-00113.

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46

Segura, Julián, Carlos Campo, José L. Rodicio, and Luis M. Ruilope. "ACE Inhibitors and Appearance of Renal Events in Hypertensive Nephrosclerosis." Hypertension 38, no. 3 (2001): 645–49. http://dx.doi.org/10.1161/hy09t1.096184.

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47

Lee, Hing-Chung, Helen C. Mitchell, Paul Van Dreal, and William A. Pettinger. "Hyperfiltration and Conservation of Renal Function in Hypertensive Nephrosclerosis Patients." American Journal of Kidney Diseases 21, no. 4 (1993): 68–74. http://dx.doi.org/10.1016/0272-6386(93)70076-b.

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48

FABBIAN, F. "Metabolic alterations associated to nephrosclerosis in elderly essential hypertensive patients." American Journal of Hypertension 9, no. 4 (1996): 55A. http://dx.doi.org/10.1016/0895-7061(96)81621-9.

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49

Carriazo, Sol, Maria Vanessa Perez-Gomez, and Alberto Ortiz. "Hypertensive nephropathy: a major roadblock hindering the advance of precision nephrology." Clinical Kidney Journal 13, no. 4 (2020): 504–9. http://dx.doi.org/10.1093/ckj/sfaa162.

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Abstract In the 2017 Annual Report of the ERA-EDTA Registry, hypertension continues to be the second or third most common cause of renal replacement therapy (RRT) in Europe, tied with glomerulonephritis. There is, however, one little issue: hypertension-induced end-stage renal disease (ESRD) might not exist at all as currently understood, that is, as hypertensive nephrosclerosis. In this regard, the incidence of RRT due to hypertensive nephropathy is related to the incidence of other causes of ESRD but not to the burden of hypertension per country. The current definition of hypertensive nephro

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50

Han, Lin, Yan Ma, Jian-guo Qin, et al. "The Renal Protective Effect of Jiangya Tongluo Formula, through Regulation of Adrenomedullin and Angiotensin II, in Rats with Hypertensive Nephrosclerosis." Evidence-Based Complementary and Alternative Medicine 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/428106.

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We investigated the effect of Jiangya Tongluo (JYTL) formula on renal function in rats with hypertensive nephrosclerosis. A total of 21 spontaneously hypertensive rats (SHRs) were randomized into 3 groups: valsartan (10 mg/kg/d valsartan), JYTL (14.2 g/kg/d JYTL), and a model group (5 mL/kg/d distilled water); Wistar Kyoto rats comprised the control group (n= 7, 5 mL/kg/d distilled water). Treatments were administered by gavage every day for 8 weeks. Blood pressure, 24-h urine protein, pathological changes in the kidney, serum creatinine, and blood urea nitrogen (BUN) levels were estimated. Th

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