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Relevant bibliographies by topics / Glomerular Damage

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Journal articles

Academic literature on the topic 'Glomerular Damage'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 February 2022

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Journal articles on the topic "Glomerular Damage"

1

Bertani, T., and G. Remuzzi. "Proteinuria and glomerular damage." Journal of Diabetes and its Complications 6, no. 4 (1992): 265. http://dx.doi.org/10.1016/1056-8727(92)90064-r.

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2

Kakimoto, Tetsuhiro, Kinya Okada, Yoshihiro Hirohashi, et al. "Automated image analysis of a glomerular injury marker desmin in spontaneously diabetic Torii rats treated with losartan." Journal of Endocrinology 222, no. 1 (2014): 43–51. http://dx.doi.org/10.1530/joe-14-0164.

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Diabetic nephropathy is a major complication in diabetes and a leading cause of end-stage renal failure. Glomerular podocytes are functionally and structurally injured early in diabetic nephropathy. A non-obese type 2 diabetes model, the spontaneously diabetic Torii (SDT) rat, is of increasing preclinical interest because of its pathophysiological similarities to human type 2 diabetic complications including diabetic nephropathy. However, podocyte injury in SDT rat glomeruli and the effect of angiotensin II receptor blocker treatment in the early stage have not been reported in detail. Therefo

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3

Comper, W. D., A. S. N. Lee, M. Tay, and Y. Adal. "Anionic charge concentration of rat kidney glomeruli and glomerular basement membrane." Biochemical Journal 289, no. 3 (1993): 647–52. http://dx.doi.org/10.1042/bj2890647.

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Estimates of levels of glomerular and glomerular-basement-membrane anion charge should serve as useful quantitative markers for the integrity of the tissues in health and disease. We have developed a simple, rapid, technique to measure this charge through the use of ion exchange with radioisotopes 22Na+ and 36Cl- at low ionic strengths in phosphate buffer. When this technique is used, normal glomeruli isolated from rat have a measured net anion charge concentration of 17.4 +/- 3.7 p-equiv. per glomerulus (n = 20). Perfused rat kidneys that lose approximately half of their glomerular heparan [3

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4

Lambert, Robert, Mark Henry, Brian Howden, et al. "GLOMERULAR DAMAGE AFTER KIDNEY PRESERVATION." Transplantation 42, no. 2 (1986): 125–29. http://dx.doi.org/10.1097/00007890-198608000-00004.

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5

Wang, Pei-Rong, Hiroshi Kitamura, Akira Shimizu, and Nobuaki Yamanaka. "Glomerular Damage in Experimental Proliferative Glomerulonephritis Under Glomerular Capillary Hypertension." Kidney and Blood Pressure Research 40, no. 2 (2015): 188–99. http://dx.doi.org/10.1159/000368494.

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6

Ofstad, Jarle, and Bjarne M. Iversen. "Glomerular and tubular damage in normotensive and hypertensive rats." American Journal of Physiology-Renal Physiology 288, no. 4 (2005): F665—F672. http://dx.doi.org/10.1152/ajprenal.00226.2004.

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Tubular cell damage is an important mediator of interstitial fibrosis in chronic renal diseases. Glomerular and tubular damage in genetic hypertension was therefore studied. Tubular and glomerular damage was investigated in 10-, 40-, and 70-wk-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) and compared with glomerular capillary pressure (PGC) and glomerulosclerosis in superficial (OC) and juxtamedullary (JMC). Tubular vimentin was used as criterion of tubular damage. Variation in tubular diameter was measured during change in perfusion pressure, and ureter ligation was u

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7

Wu, X., J. Pippin, and J. B. Lefkowith. "Attenuation of immune-mediated glomerulonephritis with an anti-CD11b monoclonal antibody." American Journal of Physiology-Renal Physiology 264, no. 4 (1993): F715—F721. http://dx.doi.org/10.1152/ajprenal.1993.264.4.f715.

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Nephrotoxic nephritis (NTN), a model of autoimmune glomerulonephritis, is characterized by glomerular inflammation, which results in both proteinuria and an increase in eicosanoid production. In light of the ability of CD18 integrins to participate in leukocyte adherence (and thereby migration), we examined the role of the integrin CD11b/CD18 in NTN using OX42, a monoclonal antibody directed against rat CD11b. Administration of OX42 30 min before induction of NTN decreased proteinuria (by 50%) but did not affect the number of leukocytes found in the glomerulus or the accompanying increase in g

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8

Valdivielso, José M., Carlos Crespo, José R. Alonso, et al. "Renal ischemia in the rat stimulates glomerular nitric oxide synthesis." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 280, no. 3 (2001): R771—R779. http://dx.doi.org/10.1152/ajpregu.2001.280.3.r771.

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Renal ischemia in humans and in experimental animals is associated with a complex and possibly interrelated series of events. In this study, we have investigated the glomerular nitric oxide (NO) production after renal ischemia. Unilateral or bilateral renal ischemia was induced in Wistar rats by clamping one or both renal arteries. NO production was assessed by measuring glomerular production of nitrite, a stable end product of NO catabolism, and NO-dependent glomerular cGMP production and by assessing the glomerular NADPH diaphorase (ND) activity, an enzymatic activity that colocalizes with N

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9

Saraf, Santosh L., Justin R. Sysol, Alexandru Susma, et al. "Progressive Glomerular Damage in Sickle Cell Trait and Sickle Cell Anemia Mouse Models." Blood 128, no. 22 (2016): 3637. http://dx.doi.org/10.1182/blood.v128.22.3637.3637.

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Abstract Homozygous inheritance of the hemoglobin S mutation (Hb SS; sickle cell anemia) affects 1 in 500 African Americans and is consistently associated with an increased risk for kidney disease, although the mechanisms are poorly understood. Heterozygous inheritance (Hb AS; sickle cell trait) affects 1 in 8 African Americans and has also been associated with an increased risk for kidney disease in some, but not all cohorts. We first investigated whether inheritance of the Hb S mutation resulted in incremental kidney damage in Hb AS and Hb SS mice compared to Hb AA mice using transgenic sick

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10

WAGNER, JÜRGEN, CLAUDIUS DECHOW, CHRISTIAN MORATH, et al. "Retinoic Acid Reduces Glomerular Injury in a Rat Model of Glomerular Damage." Journal of the American Society of Nephrology 11, no. 8 (2000): 1479–87. http://dx.doi.org/10.1681/asn.v1181479.

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Abstract.In the reaction of kidneys to injury, cytokine-driven proliferation plays an important role and precedes the development of glomerulosclerosis. There is great interest in agents that may interfere with such proliferation. Therefore, a rat model of mesangioproliferative glomerulonephritis (induced by anti-Thy1.1) was studied, and the effects of all-trans-retinoic acid (all-trans-RA) and isotretinoin, powerful antiproliferative and anti-inflammatory substances, on glomerular damage and cell proliferation were examined. Vehicle-injected control rats were compared with rats treated with d

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