Log in

Relevant bibliographies by topics / Glomerular Damage / Journal articles

To see the other types of publications on this topic, follow the link: Glomerular Damage.

Journal articles on the topic 'Glomerular Damage'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Glomerular Damage.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

11

Schindler, Maximilian, Antje Blumenthal, Marcus Johannes Moeller, Karlhans Endlich, and Nicole Endlich. "Adriamycin does not damage podocytes of zebrafish larvae." PLOS ONE 15, no. 11 (2020): e0242436. http://dx.doi.org/10.1371/journal.pone.0242436.

Full text

Abstract:

Podocytes are highly specialized epithelial cells that are essential for an intact glomerular filtration barrier in the kidney. Several glomerular diseases like focal segmental glomerulosclerosis (FSGS) are initially due to podocyte injury and loss. Since causative treatments for FSGS are not available until today, drug screening is of great relevance. In order to test a high number of drugs, FSGS needs to be reliably induced in a suitable animal model. The zebrafish larva is an ideal model for kidney research due to the vast amount of offsprings, the rapid development of a simple kidney and a

APA, Harvard, Vancouver, ISO, and other styles

12

Stavniichuk, A., O. Savchuk, Abdul Hye Khan, Wojciech K. Jankiewicz, and John D. Smith. "A sorafenib-induced model of glomerular kidney disease." Bulletin of Taras Shevchenko National University of Kyiv. Series: Biology 81, no. 2 (2020): 25–31. http://dx.doi.org/10.17721/1728_2748.2020.81.25-31.

Full text

Abstract:

Glomerular damage and proteinuria are important pathophysiological signs of chronic kidney disease. This study provides data obtained using a model developed based on the use of the anti-cancer drug sorafenib. Sorafenib is a tyrosine kinase inhibitor that acts through the signaling pathway associated with vascular endothelial growth factor and is widely used to treat various types of cancer. Sorafenib, on the other hand, causes serious side effects in patients, including the development of chronic kidney disease. This study was aimed at using the nephrotoxic properties of sorafenib to model ch

APA, Harvard, Vancouver, ISO, and other styles

13

Bazzi, Claudio, Teresa M. Seccia, Pietro Napodano, et al. "High Blood Pressure Is Associated with Tubulointerstitial Damage along with Glomerular Damage in Glomerulonephritis. A large Cohort Study." Journal of Clinical Medicine 9, no. 6 (2020): 1656. http://dx.doi.org/10.3390/jcm9061656.

Full text

Abstract:

The key role of arterial hypertension in chonic kidney disease (CKD) progression is widely recognized, but its contribution to tubulointerstitial damage (TID) in glomerulonephritis (GN) remains uncertain. Hence, the objective of this study is to clarify whether TID is associated with glomerular damage, and whether the damage at the tubulointerstitial compartment is more severe in hypertensive patients. The study included retrospectively consecutive patients referred to the Nephrology Unit with diagnoses of primary glomerulonephritis, lupus nephritis (LN), and nephroangiosclerosis (NAS) at biop

APA, Harvard, Vancouver, ISO, and other styles

14

Couser, W. "Pathogenesis of glomerular damage in glomerulonephritis." Nephrology Dialysis Transplantation 13, no. 90001 (1998): 10–15. http://dx.doi.org/10.1093/ndt/13.suppl_1.10.

Full text

APA, Harvard, Vancouver, ISO, and other styles

15

Rayego-Mateos, S., R. Rodrigues-Diez, R. R. Rodrigues-Diez, et al. "Mechanisms and targets of glomerular damage." Nephrology Dialysis Transplantation 27, suppl 2 (2012): ii9—ii10. http://dx.doi.org/10.1093/ndt/gfs229.

Full text

APA, Harvard, Vancouver, ISO, and other styles

16

Schenk, Heiko, Anna Masseli, Patricia Schroder, et al. "Sulfatases, in Particular Sulf1, Are Important for the Integrity of the Glomerular Filtration Barrier in Zebrafish." BioMed Research International 2019 (July 22, 2019): 1–11. http://dx.doi.org/10.1155/2019/4508048.

Full text

Abstract:

The 6-O-endosulfatases (sulfs) are important enzymatic components involved in the regulation of heparan sulfate by altering the sulfatation pattern. Specifically in the kidney, sulfs have been implicated in the glomerular podocyte-endothelial cell crosstalk and in the preservation of the glomerular filtration barrier (GFB) in different mouse models. Since it has been shown that in zebrafish larvae, Sulf1, Sulf2a, and Sulf2b are expressed in the pronephric kidney we set out to establish if a reduction in sulf expression leads to GFB dysfunction. Here, we show that a reduced sulf expression foll

APA, Harvard, Vancouver, ISO, and other styles

17

Bellucci, Linda, Giovanni Montini, Federica Collino, and Benedetta Bussolati. "Mesenchymal Stromal Cell-Derived Extracellular Vesicles Pass through the Filtration Barrier and Protect Podocytes in a 3D Glomerular Model under Continuous Perfusion." Tissue Engineering and Regenerative Medicine 18, no. 4 (2021): 549–60. http://dx.doi.org/10.1007/s13770-021-00374-9.

Full text

Abstract:

Abstract Background: Dynamic cultures, characterized by continuous fluid reperfusion, elicit physiological responses from cultured cells. Mesenchymal stem cell-derived EVs (MSC-EVs) has been proposed as a novel approach in treating several renal diseases, including acute glomerular damage, by using traditional two-dimensional cell cultures and in vivo models. We here aimed to use a fluidic three-dimensional (3D) glomerular model to study the EV dynamics within the glomerular structure under perfusion. Methods: To this end, we set up a 3D glomerular model culturing human glomerular endothelial

APA, Harvard, Vancouver, ISO, and other styles

18

Cojocaru, Manole, Inimioara Cojocaru, Isabela Silosi, and Camelia Vrabie. "Kidney Damage in Autoimmune Diseases." Journal of Medical Biochemistry 29, no. 2 (2010): 61–65. http://dx.doi.org/10.2478/v10011-010-0007-x.

Full text

Abstract:

Kidney Damage in Autoimmune DiseasesRenal involvement in autoimmunity has many facets. Glomerular, tubular and vascular structures are targeted and damaged as a consequence of autoimmune processes. Immunologically mediated kidney diseases represent the third most common cause of end-stage renal failure (after diabetic and hypertensive nephropathies). Appropriate evalution of patients with immune-mediated kidney diseases requires a meticulous history and physical examination, with particular attention to the urinalysis, tests of renal function and often renal biopsy. The thorough clinician shou

APA, Harvard, Vancouver, ISO, and other styles

19

Atchison, Douglas K., Christopher L. O’Connor, Rajasree Menon та ін. "Hypertension induces glomerulosclerosis in phospholipase C-ε1 deficiency". American Journal of Physiology-Renal Physiology 318, № 5 (2020): F1177—F1187. http://dx.doi.org/10.1152/ajprenal.00541.2019.

Full text

Abstract:

Loss-of-function mutations in phospholipase C-ε1 (PLCE1) have been detected in patients with nephrotic syndrome, but other family members with the same mutation were asymptomatic, suggesting additional stressor are required to cause the full phenotype. Consistent with these observations, we determined that global Plce1-deficient mice have histologically normal glomeruli and no albuminuria at baseline. Angiotensin II (ANG II) is known to induce glomerular damage in genetically susceptible individuals. Therefore, we tested whether ANG II enhances glomerular damage in Plce1-deficient mice. ANG II

APA, Harvard, Vancouver, ISO, and other styles

20

Hartner, Andrea, Nada Cordasic, Carlos Menendez-Castro та ін. "Lack of α8-integrin aggravates podocyte injury in experimental diabetic nephropathy". American Journal of Physiology-Renal Physiology 299, № 5 (2010): F1151—F1157. http://dx.doi.org/10.1152/ajprenal.00058.2010.

Full text

Abstract:

Development of diabetic nephropathy is accompanied by changes in integrin-mediated cell-matrix interactions. The α8-integrin chain is specifically expressed in mesangial cells of the glomerulus. During experimental hypertension, α8-integrin plays a protective role in the glomerulus. We hypothesized that α8-integrin is involved in maintaining the integrity of the glomerulus in diabetic nephropathy. Experimental streptozotocin (STZ) diabetes led to an increased expression and glomerular deposition of α8-integrin. To test the functional role of α8-integrin, STZ diabetes was induced in mice with a

APA, Harvard, Vancouver, ISO, and other styles

21

Stojimirovic, Biljana, and Dejan Petrovic. "Proteinuria inducing tubulointerstitial damage." Medical review 56, no. 7-8 (2003): 351–54. http://dx.doi.org/10.2298/mpns0308351s.

Full text

Abstract:

Introduction Glomerular basal membrane represents a mechanical and electric barrier for plasma proteins. In physiological conditions only plasma proteins of low molecular weight are completely filtered through basal membrane. Due to damages of glomerular basal membrane there is an increase in filtration of plasma proteins of moderate and high molecular weight. Proteinuria In regard to its etiology proteinuria can be prerenal, renal and postrenal. By analyzing albumin, 1-microglobulin, immunoglobulin G and 2-macroglobulin, together with total protein in urine, it is possible to detect and diffe

APA, Harvard, Vancouver, ISO, and other styles

22

Han, Yingjie, Frank Y. Ma, Greg H. Tesch, Carl L. Manthey, and David J. Nikolic-Paterson. "Role of macrophages in the fibrotic phase of rat crescentic glomerulonephritis." American Journal of Physiology-Renal Physiology 304, no. 8 (2013): F1043—F1053. http://dx.doi.org/10.1152/ajprenal.00389.2012.

Full text

Abstract:

The ability of macrophages to cause acute inflammatory glomerular injury is well-established; however, the role of macrophages in the fibrotic phase of chronic kidney disease remains poorly understood. This study examined the role of macrophages in the fibrotic phase ( days 14 to 35) of established crescentic glomerulonephritis. Nephrotoxic serum nephritis (NTN) was induced in groups of eight Wistar-Kyoto rats that were given a selective c-fms kinase inhibitor, fms-I, or vehicle alone from day 14 until being killed on day 35. Rats killed on day 14 NTN had pronounced macrophage infiltration wit

APA, Harvard, Vancouver, ISO, and other styles

23

Shulman, K., S. Rosen, K. Tognazzi, E. J. Manseau, and L. F. Brown. "Expression of vascular permeability factor (VPF/VEGF) is altered in many glomerular diseases." Journal of the American Society of Nephrology 7, no. 5 (1996): 661–66. http://dx.doi.org/10.1681/asn.v75661.

Full text

Abstract:

Vascular permeability factor (VPF), also known as vascular endothelial growth factor (VEGF), is a potent enhancer of microvascular permeability and a selective endothelial cell growth factor. In normal human kidney, VPF/VEGF mRNA and protein are strongly expressed by visceral glomerular epithelial cells, and VPF/VEGF may be an important regulator of glomerular endothelial cell function. This study examined 47 renal biopsies from patients with a variety of glomerular diseases for expression of VPF/VEGF mRNA and protein by in situ hybridization and immunohisto-chemistry. In many glomerular disea

APA, Harvard, Vancouver, ISO, and other styles

24

Zhai, Limin, Junfei Gu, Di Yang, Wei Wang, and Shandong Ye. "Metformin Ameliorates Podocyte Damage by Restoring Renal Tissue Podocalyxin Expression in Type 2 Diabetic Rats." Journal of Diabetes Research 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/231825.

Full text

Abstract:

Podocalyxin (PCX) is a signature molecule of the glomerular podocyte and of maintaining integrity of filtration function of glomerulus. The aim of this study was to observe the effect of different doses of metformin on renal tissue PCX expression in type 2 diabetic rats and clarify its protection on glomerular podocytes. Type 2 diabetic Sprague-Dawley (SD) rats in which diabetes was induced by high-fat diet/streptozotocin (HFD-STZ) were treated with different doses of metformin (150, 300, and 500 mg/kg per day, resp.) for 8 weeks. Various biochemical parameters, kidney histopathology, and rena

APA, Harvard, Vancouver, ISO, and other styles

25

Toffoli, Barbara, Cristina Zennaro, Carine Winkler, et al. "Hemicentin 1 influences podocyte dynamic changes in glomerular diseases." American Journal of Physiology-Renal Physiology 314, no. 6 (2018): F1154—F1165. http://dx.doi.org/10.1152/ajprenal.00198.2017.

Full text

Abstract:

Different complex mechanisms control the morphology of podocyte foot processes and their interactions with the underlying basement membrane. Injuries to this system often cause glomerular dysfunction and albuminuria. The present study aimed at identifying early markers of glomerular damage in diabetic nephropathy. For this purpose, we performed a microarray analysis on kidneys of 3-wk-old peroxisome proliferator-activated receptor-γ (PPARγ)-null and AZIP/F1 mice, which are two models of diabetic nephropathy due to lipodystrophy. This was followed by functional annotation of the enriched cluste

APA, Harvard, Vancouver, ISO, and other styles

26

Hotz, P., N. Thielemans, A. Bernard, F. Gutzwiller, and R. Lauwerys. "Serum laminin, hydrocarbon exposure, and glomerular damage." Occupational and Environmental Medicine 50, no. 12 (1993): 1104–10. http://dx.doi.org/10.1136/oem.50.12.1104.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

Stahl, R. A., F. Thaiss, U. Wenzel, W. Schoeppe, and U. Helmchen. "A rat model of progressive chronic glomerular sclerosis: the role of thromboxane inhibition." Journal of the American Society of Nephrology 2, no. 11 (1992): 1568–77. http://dx.doi.org/10.1681/asn.v2111568.

Full text

Abstract:

In order to evaluate a possible role of thromboxane A2 (TxA2) in the pathophysiology of chronic glomerular disease, we studied the effect of a 12-wk combined treatment with the thromboxane receptor blocker Daltroban (D) and the thromboxane synthesis inhibitor UK 38485 (UK) on glomerular function and morphology in a rat model of chronic progressive glomerular injury. The glomerular lesion was induced in unilaterally nephrectomized rats by the repeated i.v. injection of an antibody directed against mesangial cells. Control rats were uninephrectomized. Three months after the first antibody inject

APA, Harvard, Vancouver, ISO, and other styles

28

Pavenstädt, Hermann. "Roles of the podocyte in glomerular function." American Journal of Physiology-Renal Physiology 278, no. 2 (2000): F173—F179. http://dx.doi.org/10.1152/ajprenal.2000.278.2.f173.

Full text

Abstract:

The podocyte is the most differentiated cell type in the glomerulum, which forms a crucial component of the glomerular filtration barrier. It has been assumed that podocyte foot processes counteract the elastic force of the glomerular basement membrane and that vasoactive hormones may regulate the contractile state of their foot processes and thereby modulate the ultrafiltration coefficient K f. Podocyte damage leads to proteinuria, and podocyte injury occurs in many glomerular diseases, which may progress to chronic renal failure. The understanding of the regulation of physiological propertie

APA, Harvard, Vancouver, ISO, and other styles

29

Reckelhoff, J. F., and C. Baylis. "Glomerular metalloprotease activity in the aging rat kidney: inverse correlation with injury." Journal of the American Society of Nephrology 3, no. 11 (1993): 1835–38. http://dx.doi.org/10.1681/asn.v3111835.

Full text

Abstract:

Glomerular metalloprotease activity (phenanthroline inhibitable) was measured in cortical homogenates from rat kidneys by use of the rate of degradation of 3H-denatured type I collagen (gelatin). Glomerular metalloprotease activity was similar in male and female kidneys from kidneys from young (4 months) rats (27 +/- 7 and 34 +/- 6 micrograms of [3H]-gelatin degraded/h per milligram of glomerular protein, respectively). Glomerular metalloprotease activity was unaltered by age (18 to 20 months) in intact males but increased two times in old intact females. castrated males, and ovariectomized fe

APA, Harvard, Vancouver, ISO, and other styles

30

Wu, Jiawen, Xiaoyun Min, Li Wang, et al. "Fn14 Deficiency Ameliorates Anti-dsDNA IgG-Induced Glomerular Damage in SCID Mice." Journal of Immunology Research 2018 (December 16, 2018): 1–12. http://dx.doi.org/10.1155/2018/1256379.

Full text

Abstract:

Many studies have demonstrated that anti-dsDNA IgG is closely associated with lupus nephritis. Recently, it was found that activation of the fibroblast growth factor-inducible 14 (Fn14) signaling pathway damages glomerular filtration barrier in MRL/lpr lupus-prone mice. However, MRL/lpr mice have high titers of serum autoantibodies other than anti-dsDNA IgG. The aim of this study was to further explore the effect of Fn14 deficiency on anti-dsDNA IgG-induced glomerular damage in severe combined immunodeficiency (SCID) mice that have no endogenous IgG. Fn14 deficiency was generated in SCID mice.

APA, Harvard, Vancouver, ISO, and other styles

31

Rinschen, Markus M., Oleg Palygin, Carlos Guijas, et al. "Metabolic rewiring of the hypertensive kidney." Science Signaling 12, no. 611 (2019): eaax9760. http://dx.doi.org/10.1126/scisignal.aax9760.

Full text

Abstract:

Hypertension is a persistent epidemic across the developed world that is closely associated with kidney disease. Here, we applied a metabolomic, phosphoproteomic, and proteomic strategy to analyze the effect of hypertensive insults on kidneys. Our data revealed the metabolic aspects of hypertension-induced glomerular sclerosis, including lipid breakdown at early disease stages and activation of anaplerotic pathways to regenerate energy equivalents to counter stress. For example, branched-chain amino acids and proline, required for collagen synthesis, were depleted in glomeruli at early time po

APA, Harvard, Vancouver, ISO, and other styles

32

Abed, Ahmed, Aurélie S. Leroyer, Panagiotis Kavvadas, et al. "Endothelial-Specific Deletion of CD146 Protects Against Experimental Glomerulonephritis in Mice." Hypertension 77, no. 4 (2021): 1260–72. http://dx.doi.org/10.1161/hypertensionaha.119.14176.

Full text

Abstract:

CD146 is an endothelial junctional adhesion molecule, which expression is increased in human glomerular diseases. However, the pathological significance of this overexpression remains unknown. Induction of glomerulonephritis in mice, by using nephrotoxic serum, showed that CD146 expression was highly induced within damaged glomeruli and was associated with renal inflammation and fibrosis. Interestingly, 2 weeks after glomerulonephritis induction, CD146 knockout mice showed preserved renal function as proteinuria and blood urea nitrogen levels were significantly lower compared with wild-type li

APA, Harvard, Vancouver, ISO, and other styles

33

IJpelaar, Daphne H. T., Angela Schulz, Joris Aben, et al. "Genetic predisposition for glomerulonephritis-induced glomerulosclerosis in rats is linked to chromosome 1." Physiological Genomics 35, no. 2 (2008): 173–81. http://dx.doi.org/10.1152/physiolgenomics.00268.2007.

Full text

Abstract:

Genetic factors influence renal disease progression, and several loci have been linked to the spontaneous development of proteinuria and glomerulosclerosis in animal models. However, the role of genetic susceptibility in glomerulonephritis-induced progressive glomerulosclerosis is unknown. In a rat model of mesangial proliferative glomerulonephritis, anti-Thy-1 glomerulonephritis (antiThy1GN), Lewis/Maastricht (Lew/Maa) rats exhibit progression to glomerulosclerosis, whereas in genetically related Lewis/Møllegard (Lew/Moll) rats, glomerular lesions are repaired within 3 wk. The genetic factors

APA, Harvard, Vancouver, ISO, and other styles

34

Saraf, SL, JR Sysol, JA Arruda, et al. "ID: 139: PROGRESSIVE GLOMERULAR DAMAGE IN SICKLE CELL TRAIT AND SICKLE CELL ANEMIA MOUSE MODELS." Journal of Investigative Medicine 64, no. 4 (2016): 957.2–958. http://dx.doi.org/10.1136/jim-2016-000120.95.

Full text

Abstract:

The hemoglobin S mutation, a glutamic acid to valine substitution in the β-globin chain, results in hemoglobin polymerization under hypoxic conditions and leads to vaso-occlusion and hemolysis. Homozygous inheritance (Hb SS; sickle cell anemia) affects 1 in 500 African Americans and is consistently associated with an increased risk for kidney disease which may be due to cell-free hemoglobin toxicity, ischemic injury, or hyperfiltration-mediated damage to the kidney. Heterozygous inheritance (Hb AS; sickle cell trait) affects 1 in 8 African Americans and has also been associated with an increas

APA, Harvard, Vancouver, ISO, and other styles

35

Palygin, Oleg, Denisha Spires, Vladislav Levchenko, et al. "Progression of diabetic kidney disease in T2DN rats." American Journal of Physiology-Renal Physiology 317, no. 6 (2019): F1450—F1461. http://dx.doi.org/10.1152/ajprenal.00246.2019.

Full text

Abstract:

Diabetic kidney disease (DKD) is one of the leading pathological causes of decreased renal function and progression to end-stage kidney failure. To explore and characterize age-related changes in DKD and associated glomerular damage, we used a rat model of type 2 diabetic nephropathy (T2DN) at 12 wk and older than 48 wk. We compared their disease progression with control nondiabetic Wistar and diabetic Goto-Kakizaki (GK) rats. During the early stages of DKD, T2DN and GK animals revealed significant increases in blood glucose and kidney-to-body weight ratio. Both diabetic groups had significant

APA, Harvard, Vancouver, ISO, and other styles

36

Dwiyana, Yosepha, and Dalima AW Astrawinata. "PERUBAHAN BENTUK ERITROSIT DI GLOMERULONEFRITIS." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 20, no. 3 (2016): 242. http://dx.doi.org/10.24293/ijcpml.v20i3.479.

Full text

Abstract:

In glomerulonephritis there are intraglomerular inflammation, cell proliferation, and hematuria. Hematuria is characterized by more than 3 (three) erythrocytes per high-power field in the urine, which indicates the pathological processes in kidney or urinary tract. The combination of mechanical damage of erythrocyte membrane through the damaged glomerular basement membrane followed by the osmotic damage when it passes through the tubular system in the hypotonic osmotic solutions causes dysmorphic morphology. Erythrocytes trapped in the Tamm-Horsfall protein will form erythrocyte casts. Dysmorp

APA, Harvard, Vancouver, ISO, and other styles

37

Kira, Vicente Massaji, Djalma José Fagundes, César Orlando Peralta Bandeira, Anna Tereza Negrini Fagundes, and Valdemar Ortiz. "The repeated extracorporeal shock waves and the renal parenchyma injury on normal and diabetic rats." Acta Cirurgica Brasileira 22, no. 4 (2007): 285–90. http://dx.doi.org/10.1590/s0102-86502007000400010.

Full text

Abstract:

PURPOSE: To assess the effect of repeated extracorporeal shock waves (ESW) on renal parenchyma of normal and diabetic rats. METHODS: 40 normal rats (A) and 40 diabetic rats (B) were assigned for ESW (Direx Tripter X1® - 14 KVA) as follow: A1/B1 and A3/B3 no ESW; A2/B2 one ESW (2,000 SW); A4/B4 two ESW (4,000 SW) in an elapsed 14 days. All the animals were sacrificed 3 days after the ESW and samples of renal parenchyma were histological prepared, stained by H&E. For each animal the frequency of hemorrhage focus (HF) in the subcapasular, interstitial and glomerulus area was calculated (porce

APA, Harvard, Vancouver, ISO, and other styles

38

Meyer, Fernando, Juliana Navarro Lizana, Luiz Felipe Dziedricki, and Luiz Fernando Bleggi-Torres. "Histologic alterations of rat kidneys perfused with a Euro-Collins diltiazem solution." Acta Cirurgica Brasileira 25, no. 6 (2010): 496–500. http://dx.doi.org/10.1590/s0102-86502010000600007.

Full text

Abstract:

PURPOSE: Analyse the histologic changes of rat kidneys perfused with isotonic saline solution (ISS), Euro-Collins solution (ECS) and Euro-Collins solution with diltiazem (ECSD). METHODS: Thirty-six Wistar rats were used divided equally, as follow: group A (ISS), group B (ECS) and group C (ECSD). Through a catheter placed into the abdominal aorta, a renal perfusion was performed using a solution according to the group to which the animal belonged. After the complete perfusion, bilateral nephrectomy was performed and the organs were preserved under hypothermia for five distinct periods of time.

APA, Harvard, Vancouver, ISO, and other styles

39

Sakhi, Hamza, Anissa Moktefi, Khedidja Bouachi, et al. "Podocyte Injury in Lupus Nephritis." Journal of Clinical Medicine 8, no. 9 (2019): 1340. http://dx.doi.org/10.3390/jcm8091340.

Full text

Abstract:

Systemic lupus erythematosus (SLE) is characterized by a broad spectrum of renal lesions. In lupus glomerulonephritis, histological classifications are based on immune-complex (IC) deposits and hypercellularity lesions (mesangial and/or endocapillary) in the glomeruli. However, there is compelling evidence to suggest that glomerular epithelial cells, and podocytes in particular, are also involved in glomerular injury in patients with SLE. Podocytes now appear to be not only subject to collateral damage due to glomerular capillary lesions secondary to IC and inflammatory processes, but they are

APA, Harvard, Vancouver, ISO, and other styles

40

Sorace, Rosaria, Rocco Romeo, Leonardo Sorbello, Luigina Linossi Torrisi, and Luciano Motta. "Glomerular hyperfiltration indicates organ damage in essential hypertension." Current Therapeutic Research 54, no. 4 (1993): 400–405. http://dx.doi.org/10.1016/s0011-393x(05)80643-5.

Full text

APA, Harvard, Vancouver, ISO, and other styles

41

Chebotareva, N. V., I. N. Bobkova, and L. V. Lysenko. "The role of podocytes dysfunction in chronic glomerulonephritis progression." Terapevticheskii arkhiv 90, no. 6 (2018): 92–97. http://dx.doi.org/10.26442/terarkh201890692-97.

Full text

Abstract:

In the review, the mechanisms of podocytes damage underlying the development of proteinuria and progression of glomerulosclerosis in chronic glomerulonephritis are discussed in detail. The results of experimental and clinical studies are presented. Under the different immune and non-immune factors the podocytes form a stereotyped response to damage consisting in the reorganization of the actin cytoskeleton, foot process effacement, the detachment of podocytes from the glomerular basement membrane, and the appearance of specific podocyte proteins and whole cells (podocyturia) in the urine. Mass

APA, Harvard, Vancouver, ISO, and other styles

42

Chang, Chia-Jung, Pi-Chao Wang, Tzou-Chi Huang, and Akiyoshi Taniguchi. "Change in Renal Glomerular Collagens and Glomerular Filtration Barrier-Related Proteins in a Dextran Sulfate Sodium-Induced Colitis Mouse Model." International Journal of Molecular Sciences 20, no. 6 (2019): 1458. http://dx.doi.org/10.3390/ijms20061458.

Full text

Abstract:

Renal disease is not rare among patients with inflammatory bowel disease (IBD) and is gaining interest as a target of research. However, related changes in glomerular structural have rarely been investigated. This study was aimed at clarifying the changes in collagens and glomerular filtration barrier (GFB)-related proteins of glomeruli in a dextran sulfate sodium (DSS)-induced colitis mouse model. Acute colitis was induced by administering 3.5% DSS in Slc:ICR strain mice for eight days. Histological changes to glomeruli were examined by periodic acid-Schiff (PAS) and Masson’s trichrome staini

APA, Harvard, Vancouver, ISO, and other styles

43

Marinaki, Smaragdi, and John Boletis. "Immune Renal Injury: Similarities and Differences Between Glomerular Diseases and Transplantation." BANTAO Journal 13, no. 2 (2015): 53–58. http://dx.doi.org/10.1515/bj-2015-0013.

Full text

Abstract:

AbstractGlomerular diseases and renal transplantation are the main fields in nephrology in which the immune system plays a prevalent role. They have for long been considered as independent conditions due to the prominent role of autoimmunity in glomerular diseases and of alloimmunity in renal transplantation.Moreover, histologic features differ between glomerular diseases and transplantation: in glomerular diseases, histologic damage involves primarily the glomeruli and secondarily the tubulointerstitium and small vessels, whereas in transplantation, allograft injury comprises primarily the tu

APA, Harvard, Vancouver, ISO, and other styles

44

Stahl, R. A., F. Thaiss, G. Oberle, et al. "The platelet activating factor receptor antagonist WEB 2170 improves glomerular hemodynamics and morphology in a proliferative model of mesangial cell injury." Journal of the American Society of Nephrology 2, no. 1 (1991): 37–44. http://dx.doi.org/10.1681/asn.v2137.

Full text

Abstract:

Rats were treated with the platelet activating factor receptor antagonist WEB 2170 (15 mg/kg/day) in three different protocols to evaluate a possible role of platelet activating factor in an experimental proliferative model of glomerular disease. The glomerular immune injury was initiated by the i.v. administration of a rabbit anti-rat thymocyte antiserum. Anti-rat thymocyte antiserum induces a proliferative glomerulonephritis with reduction of glomerular filtration rate (614 +/- 94) compared with controls (1,120 +/- 192 microL/min/100 g body wt) when studied at day 7. Treatment of rats with W

APA, Harvard, Vancouver, ISO, and other styles

45

Wang, Linlin, and Helen Ka Wai Law. "Immune Complexes Impaired Glomerular Endothelial Cell Functions in Lupus Nephritis." International Journal of Molecular Sciences 20, no. 21 (2019): 5281. http://dx.doi.org/10.3390/ijms20215281.

Full text

Abstract:

Lupus nephritis (LN) is one of the most common and severe complications of lupus. However, the mechanisms for renal damage have not been well elucidated. There are evidences show that glomerular endothelial cells (GECs) are damaged in LN. Immune complexes can deposit in subendothelial area and could affect GEC functions. In the present study, we used heat-aggregated gamma globulin (HAGG) to simulate immune complexes and investigated their effects on GEC functions. Our results revealed that HAGG impaired different aspect of the GEC functions. HAGG changed cell morphology, upregulated the expres

APA, Harvard, Vancouver, ISO, and other styles

46

Garg, Puneet. "A Review of Podocyte Biology." American Journal of Nephrology 47, Suppl. 1 (2018): 3–13. http://dx.doi.org/10.1159/000481633.

Full text

Abstract:

Background: Podocyte biology is a developing science that promises to help improve understanding of the mechanistic nature of multiple diseases associated with proteinuria. Proteinuria in nephrotic syndrome has been linked to mechanistic dysfunctions in the renal glomerulus involving the function of podocyte epithelial cells, including podocyte foot process effacement. Summary: Developments in imaging technology are improving knowledge of the detailed structure of the human renal glomerulus and cortex. Podocyte foot processes attach themselves to the glomerular capillaries at the glomerular ba

APA, Harvard, Vancouver, ISO, and other styles

47

Bremer, V., A. Tojo, K. Kimura, et al. "Role of nitric oxide in rat nephrotoxic nephritis: comparison between inducible and constitutive nitric oxide synthase." Journal of the American Society of Nephrology 8, no. 11 (1997): 1712–21. http://dx.doi.org/10.1681/asn.v8111712.

Full text

Abstract:

Nitric oxide (NO), generated by inducible NO synthase (iNOS) in migrating macrophages, is increased in glomerulonephritis. This study investigates the effect of NO inhibition on rat nephrotoxic nephritis (NTN) to clarify the role of NO production in glomerular damage. NTN was induced in Sprague Dawley rats by an injection of an anti-glomerular basement membrane (GBM) antibody. Urinary nitrite excretion and nitrite release from kidney slices (5.47 +/- 1.19 versus 2.15 +/- 0.73 nmol/mg protein, NTN versus Control, P < 0.05) were increased in NTN on day 2. Glomerular macrophage infiltration an

APA, Harvard, Vancouver, ISO, and other styles

48

Turner-Stokes, Tabitha, Ana Garcia Diaz, Damilola Pinheiro, et al. "Live Imaging of Monocyte Subsets in Immune Complex-Mediated Glomerulonephritis Reveals Distinct Phenotypes and Effector Functions." Journal of the American Society of Nephrology 31, no. 11 (2020): 2523–42. http://dx.doi.org/10.1681/asn.2019121326.

Full text

Abstract:

BackgroundImmune complexes within glomerular capillary walls cause crescentic GN (CrGN). Monocytes and macrophages are important in mediating CrGN, but little work has been done to phenotype the subpopulations involved and determine their respective contributions to glomerular inflammation.MethodsLive glomerular imaging using confocal microscopy monitored intravascular monocyte subset behavior during nephrotoxic nephritis (NTN) in a novel WKY-hCD68-GFP monocyte/macrophage reporter rat strain. Flow cytometry and qPCR further analyzed ex vivo the glomerular leukocyte infiltrate during NTN.Result

APA, Harvard, Vancouver, ISO, and other styles

49

Huang, Li-Min, and Jian-Hua Mao. "Glomerular podocyte dysfunction in inherited renal tubular disease." World Journal of Pediatrics 17, no. 3 (2021): 227–33. http://dx.doi.org/10.1007/s12519-021-00417-0.

Full text

Abstract:

Abstract Background Hereditary renal tubular disease can cause hypercalciuria, acid-base imbalance, hypokalemia, hypomagnesemia, rickets, kidney stones, etc. If these diseases are not diagnosed or treated in time, they can cause kidney damage and electrolyte disturbances, which can be detrimental to the maturation and development of the child. Glomerular involvement in renal tubular disease patients has only been considered recently. Methods We screened 71 papers (including experimental research, clinical research, etc.) about Dent’s disease, Gitelman syndrome, and cystinosis from PubMed, and

APA, Harvard, Vancouver, ISO, and other styles

50

Stahl, R. A., F. Thaiss, U. Wenzel, and U. Helmchen. "Morphologic and functional consequences of immune-mediated mesangiolysis: development of chronic glomerular sclerosis." Journal of the American Society of Nephrology 2, no. 10 (1992): S144. http://dx.doi.org/10.1681/asn.v210s144.

Full text

Abstract:

The i.v. injection of a rabbit anti-rat thymocyte serum (ATS) induces mesangiolysis in rats, followed by a mesangioproliferative glomerulonephritis (4 to 7 days after antibody). This proliferative lesion disappears 4 to 6 wks after antibody. In order to induce an antibody-mediated sclerotic glomerular disease, uninephrectomized rats received ATS twice at 6-wk interval. At 6 months after the first antibody injection, albuminuria, arterial blood pressure, and inulin clearances were evaluated and renal morphologic studies were performed. At the time of evaluation, mean arterial blood pressure and

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!