Academic literature on the topic 'Glomerular Damage'
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Journal articles on the topic "Glomerular Damage"
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Bertani, T., and G. Remuzzi. "Proteinuria and glomerular damage." Journal of Diabetes and its Complications 6, no. 4 (October 1992): 265. http://dx.doi.org/10.1016/1056-8727(92)90064-r.
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Kakimoto, Tetsuhiro, Kinya Okada, Yoshihiro Hirohashi, Raissa Relator, Mizue Kawai, Taku Iguchi, Keisuke Fujitaka, 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 (April 29, 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. Therefore, we have evaluated early stages of glomerular podocyte damage and the beneficial effect of early treatment with losartan in SDT rats using desmin as a sensitive podocyte injury marker. Moreover, we have developed an automated, computational glomerulus recognition method and illustrated its specific application for quantitatively studying glomerular desmin immunoreactivity. This state-of-the-art method enabled automatic recognition and quantification of glomerular desmin-positive areas, eliminating the need to laboriously trace glomerulus borders by hand. The image analysis method not only enabled assessment of a large number of glomeruli, but also clearly demonstrated that glomerular injury was more severe in the juxtamedullary region than in the superficial cortex region. This applied not only in SDT rat diabetic nephropathy but also in puromycin aminonucleoside-induced nephropathy, which was also studied. The proposed glomerulus image analysis method combined with desmin immunohistochemistry should facilitate evaluations in preclinical drug efficacy studies as well as elucidation of the pathophysiology of diabetic nephropathy.
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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 (February 1, 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 [35S]sulphate content (owing to oxygen-radical damage) exhibited a lower anion charge, of 7.5 +/- 1.6 p-equiv. per glomerulus (n = 5). Glomerular basement membranes prepared from rat glomeruli by a sonication-centrifugation procedure in the presence of enzyme inhibitors had a charge concentration of 6.3 +/- 0.7 mu-equiv./g wet wt. of tissue (n = 4), whereas membranes prepared by sonication, centrifugation, DNAse and detergent treatment had a charge concentration of 7.1 +/- 1.6 mu-equiv./g wet wt. (n = 4). Isotope-dilution experiments with 3H2O on these detergent-prepared glomerular basement membranes demonstrated that they had a water content of approx. 93%, which would then give a net anion charge concentration of 7.6 +/- 1.7 m-equiv./l (n = 4). These values are in good agreement with those obtained by others using titration techniques [Bray and Robinson (1984) Kidney Int. 25, 527-533]. The relatively low magnitude of glomerular anion charge in normal kidneys is consistent with other recent findings that glomerular anion charge is too low to affect the glomerular transport of charged molecules in a direct, passive, biophysical manner through electrostatic interactions.
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Lambert, Robert, Mark Henry, Brian Howden, Paula Jablonski, Derek Rae, Gloria Tavanlis, Vernon Marshall, and John Tange. "GLOMERULAR DAMAGE AFTER KIDNEY PRESERVATION." Transplantation 42, no. 2 (August 1986): 125–29. http://dx.doi.org/10.1097/00007890-198608000-00004.
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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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Ofstad, Jarle, and Bjarne M. Iversen. "Glomerular and tubular damage in normotensive and hypertensive rats." American Journal of Physiology-Renal Physiology 288, no. 4 (April 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 used to demonstrate the relationship between tubular pressure and appearance of vimentin-positive cells. Tubular and glomerular damage was most pronounced in JMC and greater in SHR than in WKY. It was absent in 10-wk-old WKY and significantly higher in JMC of SHR compared with WKY at 70 wk of age. Numbers of vimentin-positive segments were 18 ± 9 vs. 38 ± 7% in JMC of 70-wk-old WKY and SHR ( P < 0.02), and glomerulosclerosis was seen in 8 ± 3 vs. 19 ± 5% of glomeruli in JMC of 70-wk-old WKY and SHR, respectively ( P < 0.01). PGCwas 45 ± 3 mmHg in JMC of WKY and 57 ± 3 mmHg in JMC of 70-wk-old SHR ( P < 0.001). Tubular diameter variation was greatest in SHR ( P < 0.05) during pressure variation. Proteinuria was present only in 40- and 70-wk-old SHR and did not correlate with tissue damage. Tubular and glomerular damage in both strains develops in parallel and may be caused by a common mechanism, which may be glomerular capillary and tubular wall stretch during acute blood pressure variation which is greatest in JMC in SHR.
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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 (April 1, 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 glomerular eicosanoid production. Administration of OX42 16 h before disease induction led to a more substantial decrease in proteinuria (80%) and, in contrast to 30 min pretreatment, decreased the number of neutrophils found in the glomerulus and the accompanying increase in glomerular eicosanoid production (both by 50%). OX42 pretreatment had no effect on the number of macrophages found in glomeruli. Circulating leukocytes from animals treated with OX42 in vivo showed saturating surface levels of antibody by fluorescence-activated cell sorting (FACS) analysis and normal upregulation of CD11b by pharmacological activation. Sixteen hours after in vivo injection of OX42, 50% more peripheral leukocytes were labeled relative to control leukocytes labeled with OX42 ex vivo. Glomerular leukocytes in NTN exhibited upregulated expression of CD11b relative to peripheral leukocytes. These data show that CD11b/CD18 may participate in the acute expression of glomerular damage in NTN in a fashion not wholly dependent on blocking neutrophil migration into glomeruli. Blockade of surface receptors (as opposed to inhibition of upregulation) is sufficient to obtain this effect.
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Valdivielso, José M., Carlos Crespo, José R. Alonso, Carlos Martı́nez-Salgado, Nelida Eleno, Miguel Arévalo, Fernando Pérez-Barriocanal, and José M. López-Novoa. "Renal ischemia in the rat stimulates glomerular nitric oxide synthesis." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 280, no. 3 (March 1, 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 NO-synthesis activity. Furthermore, we determined the isoform of NO synthase (NOS) implicated in NO synthesis by Western blot and immunohistochemistry. Glomeruli from rats with bilateral ischemia showed elevated glomerular nitrite and cGMP production. Besides, glomeruli from this group of rats showed an increased ND activity, whereas glomeruli from the ischemic and nonischemic rats with unilateral ischemia did not show this increase in nitrite, cGMP, and ND activity. In addition, glomeruli from ischemic kidneys showed an increased expression of endothelial NOS without changes in the inducible isoform. Addition ofl-NAME in the drinking water induced a higher increase in the severity of the functional and structural damage in rats with bilateral ischemia than in rats with unilateral ischemia and in sham-operated animals. We can conclude that after renal ischemia, there is an increased glomerular NO synthesis subsequent to an activation of endothelial NOS that plays a protective role in the renal damage induced by ischemia and reperfusion.
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Saraf, Santosh L., Justin R. Sysol, Alexandru Susma, Suman Setty, Xu Zhang, Krishnamurthy P. Gudehithlu, Jose A. L. Arruda, Ashok K. Singh, Roberto F. Machado, and Victor R. Gordeuk. "Progressive Glomerular Damage in Sickle Cell Trait and Sickle Cell Anemia Mouse Models." Blood 128, no. 22 (December 2, 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 sickle mice >6 months old (Townes model, Jackson Laboratory). Using Masson trichrome stained sections of the kidney, patterns of mesangial expansion were determined in age- and sex-matched mice by a renal pathologist blinded to the hemoglobin genotype of each specimen. Hb AS mice had diffuse (>50% of the glomeruli per slide being involved) mesangial expansion while Hb SS mice had diffuse and global (>50% of the individual glomerulus being involved) mesangial expansion. Glomerular perimeters were measured using NanoZoomer Whole Slide Imaging in 26 randomly selected glomeruli from 2 mice per genotype. Using >300µm in circumference as the definition for an enlarged glomerulus, the proportion of enlarged glomeruli progressively increased from Hb AA to Hb AS to Hb SS mice (Cochran's test of linear trend, P=0.002)(Figure 1A). Progressively higher urine protein-to-creatinine ratios were also observed from Hb AA to Hb AS to Hb SS mice (Figure 1B; test for linear trend, P=0.03) as were progressively higher kidney weights: Hb AA (429±28mg, n=8), Hb AS (446±27mg, n=18), Hb SS (567±19mg, n=5) (Test for linear trend, P=0.047). We then compared the mRNA expression profiles in the kidney cortices, which predominantly include glomerular and proximal tubular cells, of 15 age- and sex-matched mice (5 per Hb genotype) using the Affymetrix Mouse Gene 2.0ST Array. Using an additive model with an FDR<0.01, 6 of the 10 most differentially expressed genes were involved in heme or iron metabolism (HMOX1: β 0.93, P=0.0004; SLC25A37: β 0.75, P=3.9x10-6), kidney function (SLC4A1: β 0.87, P=1.0x10-5; AQP6: β 0.79, P=2.0x10-5), or inflammation (RSAD2: β 0.76, P=5.2x10-6; C3: β 0.76, P=0.0005). Other genes that have been implicated in kidney disease and were differentially expressed at an FDR<0.01 included PODXL and EFNB2 (encode glomerular proteins integral for maintaining the filtration barrier) as well as FRMD3 and ELMO1 (implicated in diabetic nephropathy). KEGG physiologic pathways among the differentially expressed genes included focal adhesion (3.4-fold, P=6.0x10-7), extracellular matrix-receptor interaction (5.0-fold, P=3.2x10-6), and phosphatidylinositol signaling systems (3.5-fold, P=0.003). In conclusion, we observed progressive glomerular injury, determined by mesangial expansion, proportion of enlarged glomeruli, and urine protein concentrations, in Hb AS and Hb SS mice compared to Hb AA mice. Renal cortex-expressed genes involved in heme and iron homeostasis, kidney function, and inflammation were differentially expressed with inheritance of the Hb S mutation and may play important roles in the pathophysiology of kidney disease in individuals with sickle cell trait or sickle cell disease and will require further investigation. Figure Figure. Disclosures No relevant conflicts of interest to declare.
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WAGNER, JÜRGEN, CLAUDIUS DECHOW, CHRISTIAN MORATH, INGO LEHRKE, KERSTIN AMANN, RÜDIGER WALDHERR, JÜRGEN FLOEGE, and EBERHARD RITZ. "Retinoic Acid Reduces Glomerular Injury in a Rat Model of Glomerular Damage." Journal of the American Society of Nephrology 11, no. 8 (August 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 daily subcutaneous injections of 10 mg/kg body wt all-trans-RA or 40 mg/kg body wt isotretinoin (n= 9 to 11 per group), using either a pretreatment (days -2 through 8) or posttreatment (days +3 through +8) protocol,i.e., starting before or after the induction of anti-Thy1.1 nephritis, respectively. All-trans-RA prevented the BP increase evoked by anti-Thy1.1 (anti-Thy1.1/vehicle, 112.2 ± 4.8 mmHg; anti-Thy1.1/RA, 87.5 ± 2.5 mmHg;P< 0.001). Treatment with all-trans-RA or isotretinoin produced a 70% decrease in the urinary albumin excretion rate (P< 0.02). Periodic acid-Schiff staining of saline-perfused kidneys (day 8) revealed significantly fewer glomerular cells in RA-treated nephritic rats (anti-Thy1.1/vehicle, 97 ± 3.1 cells/glomerulus; anti-Thy1.1/RA, 80 ± 4.4;P< 0.02; control/vehicle, 69 ± 1.2). No difference was observed between all-trans-RA and isotretinoin treatment. The capillary occlusion scores were significantly lower for the anti-Thy1.1/RA-treated group (1.9 ± 0.1) than for the anti-Thy1.1/vehicle-treated group (2.9 ± 0.5,P< 0.001). In the anti-Thy1.1/vehicle-treated group, 11.9 ± 1.1 glomerular cells were proliferating cell nuclear antigen-positive; however, in the anti-Thy1.1/RA-treated group, only 5.3 ± 0.8 cells were proliferating cell nuclear antigen-positive (P< 0.002; control, 2.2 ± 0.2). Glomerular mitoses were reduced by 67% in the anti-Thy1.1/RA-treated group, compared with the anti-Thy1.1/control group (P< 0.002). Glomerular staining for platelet-derived growth factor B-chain was significantly reduced in anti-Thy1.1-treated nephritic rats in the presence of isotretinoin or all-trans-RA, compared with the vehicle-treated group (P< 0.001). It is concluded that all-trans-RA limits glomerular proliferation, glomerular lesions, and albuminuria in an established model of renal damage. The findings point to retinoids as potential novel modulators of glomerular injury.
Dissertations / Theses on the topic "Glomerular Damage"
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Kuwabara, Takashige. "Urinary neutrophil gelatinase-associated lipocalin levels reflect damage to glomeruli, proximal and distal nephrons." Kyoto University, 2009. http://hdl.handle.net/2433/124312.
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Sun, Guang Hui, and 孫光蕙. "The study on the molecular mechanism of anti-dsDNA antibodies-induced glomerular mesangial cell damage." Thesis, 1995. http://ndltd.ncl.edu.tw/handle/07819673301937536123.
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Dias, João Pedro Faria. "Biomarcadores precoces na Nefropatia Diabética - Do presente para o futuro." Master's thesis, 2019. http://hdl.handle.net/10316/89611.
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Trabalho Final do Mestrado Integrado em Medicina apresentado à Faculdade de MedicinaA nefropatia diabética (ND) é uma das principais causas de doença renal crónica, e representa a complicação microvascular mais frequente e séria da Diabetes mellitus. Atualmente, a albuminúria tem sido considerada como o marcador tradicional na deteção precoce do surgimento e progressão da ND. No entanto, alguns doentes com DM apresentam-se com alterações renais avançadas e declínio progressivo da função renal mesmo com níveis de albumina urinários normais, indicando que a albuminúria não corresponde à potencial chave de diagnóstico em estadios iniciais da ND. A patogénese exata desta patologia é complexa e não muito elucidativa. Inúmeros fatores e mecanismos contribuem para o desenvolvimento e consequente aparecimento da ND. Um diagnóstico e tratamento precoces podem retardar a progressão da doença, favorecendo assim o prognóstico. Na presente revisão científica é exposta uma visão geral da literatura, descrevendo alguns biomarcadores que foram associados à ND com potencial para a sua aplicação clínica, no intuito de prever o início e/ou monitorizar a progressão da ND. Em particular, biomarcadores de lesão renal, inflamação e stresse oxidativo podem vir a ser ferramentas úteis na previsão desta patologia. A descoberta e a investigação centrada na proteómica, metabolómica e nos micro-RNAs representam uma nova estratégia para melhorar o diagnóstico, prognóstico e tratamento da ND. No entanto, a abordagem baseada nestas áreas ainda não está disponível na maioria dos laboratórios de química clínica. O uso de um painel multimarcadores ao invés da albuminúria e TFGe, parece integrar uma apreciação clínica interessante na deteção precoce da ND, incluindo marcadores de lesão glomerular, lesão tubular e marcadores associados à patogénese da doença, nomeadamente de inflamação e stresse oxidativo.
Diabetic Nephropathy is one of the main causes of chronic kidney disease and represents the most common and severe microvascular obstruction of Diabetes Mellitus. Currently, albuminuria has been considered the traditional marker in ND premature detection and progress. However, some patients with DM have shown advanced renal alterations and declined renal function, despite having ordinary urinary albumin levels, meaning that albuminuria does not correspond to the potential key to an early stage diagnosis of ND. The exact pathogenesis of this pathology is complex and not very clear. Various factors and mechanism contribute to the development and emergence of ND. An early diagnosis and treatment may slow down the progression of the illness, favouring the prognostic. In this review it is aimed to expose an overall view of the literature, describing some biomarkers that have been associated to ND with potential for clinical applications, with the purpose to predict the beginning and/or moniter ND progression.In particular, biomarkers for kidney damage, inflammation and oxidative stress may be useful tools to this pathology’s prediction. The discovery and investigation centered in proteomics, metabolomics and in micro-RNAs represents a new strategy to improve the diagnosis, prognosis and treatment of ND. However, the approach based on these fields is not yet available in most clinical chemistry labs.The use of a multimarker panel instead of albuminuria and TFGe, seems to integrate an interesting clinical appraisal in the early detection of ND, including glomerular and tubular lesion markers and markers linked to the pathogenesis of the illness, mainly the inflammation and oxidative stress.
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Wakefield, Andrew. "A high protein diet at the upper end of the Acceptable Macronutrient Distribution Range (AMDR) leads to kidney glomerular damage in normal female Sprague-Dawley rats." 2007. http://hdl.handle.net/1993/2834.
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In setting the AMDR for protein at 10-35% of daily energy, the Institute of Medicine acknowledged a lack of data regarding the safety of long-term intakes. The current study assessed the impact of chronic (17 months) protein consumption at the upper end of the AMDR on renal function, histology, and inflammation.
Using plant and animal whole protein sources, female Sprague-Dawley rats (70 days old; n=8-11 at 4, 8, 12, or 17 mo.) were randomized to either a normal (NP; 15% of energy) or high protein (HP; 35% of energy) diet. Egg albumen and skim milk replaced carbohydrates in the HP diet. Diets were balanced for energy, fat, vitamins and minerals, and offered ad libitum. Renal function was analyzed by creatinine clearance and urinary protein levels. Glomerular hypertrophy, glomerulosclerosis and tubulointerstitial fibrosis were assessed on kidney sections. Kidney disease progression was determined by the measurement of transforming growth factor beta-1 (TGF-β1) and renal inflammation by the measurement of chemokines monocyte chemoattractant protein-1 (MCP-1) and regulated upon activation normal T-cell expressed and secreted (RANTES).
Rats consuming the HP compared to NP diet had ~17% higher kidney weights (P<0.0001) and ~4.8 times higher proteinuria (P<0.0001). There was a trend towards higher creatinine clearance with HP (P=0.055). Consistent with this, HP compared to NP rats had ~22% larger glomeruli (P<0.0001) and ~33% more glomerulosclerosis (P=0.0003). The HP diet had no significant effect on tubulointerstitial fibrosis and renal TGF-β1 levels and did not result in higher renal levels of MCP-1 and RANTES. In fact, per mg renal protein, HP rats had ~16% lower MCP-1 (P<0.0001) and ~34% lower levels of RANTES (P<0.0001) than NP. The absence of an increase in cytokine levels may be a reflection of the moderate changes in renal pathology observed in rats offered HP diets.
These data in normal female rats suggest that protein intakes at the upper end of the AMDR are detrimental to kidney health in the long-term. While modest, this may have implications for individuals whose kidney function is compromised, especially given the prevalence of those unaware of their kidney disease within North America.October 2007
Books on the topic "Glomerular Damage"
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Kriz, Wilhelm. Podocyte loss as a common pathway to chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0139.
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Experimental studies show that podocyte death first causes focal scars, but beyond approximately 40% loss is lethal to a glomerulus. Podocytes have limited ability to regenerate, although some degree of replacement may occur from stem cells located near the urinary pole of Bowman’s capsule. It is not yet known whether this plays a significant part in ameliorating damage in disease processes. In one interpretation, foot process effacement may be seen as an adaptation by the podocyte to remain attached to the glomerular basement membrane after injury, at the expense of proteinuria. Podocyte dysfunction is closely associated with proteinuria, which in turn is strongly associated with progressive loss of glomerular filtration rate. Continuing podocyte damage and loss could therefore account for progressive renal disease. In this hypothesis, drugs that protect against progression of renal disease may have their primary protective effects on podocytes themselves, rather than or as well as on haemodynamic factors or on fibrotic processes.
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Hughes, Jeremy. Proteinuria as a direct cause of progression. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0137.
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Proximal tubular cells reabsorb any filtered proteins during health via cell surface receptors such as megalin and cubulin so that very low levels of protein are present in the excreted urine. Significant proteinuria is a common finding in patients with many renal diseases. Proteinuria is a marker of glomerular damage and podocyte loss and injury in particular. The degree of proteinuria at presentation or during the course of the disease correlates with long-term outcome in many renal diseases. Proteinuria per se may be nephrotoxic and thus directly relevant to the progression of renal disease rather than simply acting as a marker of the severity of glomerular injury and podocytes loss. Seminal studies used the atypical renal anatomy of the axolotl to instill proteins directly into the tubular lumen without requiring passage through the glomerulus. This indicated that tubular protein could be cytotoxic and induce interstitial inflammation and fibrosis in the peritubular region. Cell culture studies demonstrate that exposure to proteins results in proximal tubular cell activation and the production of pro-inflammatory and pro-fibrotic mediators. Proximal tubular cell death occurred in some studies reinforcing the potential of protein to exert cytotoxic effects via oxidative stress or endoplasmic reticulum stress. Analysis of renal biopsy material from both experimental studies using models of proteinuric disease or patients with various proteinuric diseases provided evidence of activation of transcription factors and production of chemokines and pro-inflammatory mediators by proximal tubular cells. These data strongly suggest that although proteinuria is the result of glomerular disease it also represents an important cause of progression in patients with chronic kidney disease associated with proteinuria.
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Herrington, William G., Aron Chakera, and Christopher A. O’Callaghan. Diabetic renal disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0164.
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Diabetic nephropathy is kidney damage occurring as a result of diabetes mellitus. Overt diabetic nephropathy is defined as proteinuria greater than 0.5 g/day. Diabetic nephropathy has a complicated pathogenesis including glomerular hypertension with hyperfiltration and advanced glycation end products. Poor glycaemic control is associated with progression to microalbuminuria and overt diabetic nephropathy. The lifetime risk is fairly equivalent for type 1 and type 2 diabetes mellitus. Early disease is usually asymptomatic. Hyperglycaemia causes an osmotic diuresis and, thus, diabetes can present with polyuria. Hypertension develops with microalbuminuria; oedema indicates abnormal sodium and water retention and, occasionally, the development of nephrotic syndrome. Patients with diabetes, perhaps due to accompanying cardiac disease, are particularly susceptible to fluid overload and uraemic symptoms. End-stage renal disease can occur as early as when the estimated glomerular filtration rate is 15 ml/min 1.73 m−2.
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Herrington, William G., Aron Chakera, and Christopher A. O’Callaghan. Chronic kidney disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0163.
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Chronic kidney disease (CKD) is defined as abnormalities of kidney structure or function, where the abnormalities have been present for >3 months and have implications for health. It is characterized by a reduced estimated glomerular filtration rate (eGFR) or other renal abnormalities. CKD is staged according to the eGFR or the degree of albuminuria. The KDIGO (Kidney Disease: Improving Global Outcomes) criteria for CKD is either an eGFR that is <60 ml/min 1.73 m−2 and has been present for >3 months, or one or more markers of kidney damage, when these have been present for >3 months.
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Schreuder, Michiel F. Congenital solitary functioning kidney. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0351.
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The main cause for unilateral non-formation or non-functioning of a kidney can be found in renal agenesis/aplasia and multicystic dysplastic kidney. Even though kidney donation at adult age is considered safe, studies in recent years have shown that this may be different in congenital solitary functioning kidneys. Whether this is based on dysplasia in the remaining kidney or based on glomerular hyperfiltration damage, follow-up has shown renal injury, defined as hypertension and/or proteinuria, in up to 32% of children with a congenital solitary functioning kidney. Therefore, long-term infrequent follow-up of all patients with a congenital solitary functioning kidney seems to be indicated.
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Lopez, Berenice, and Patrick J. Twomey. Biochemical investigation of rheumatic diseases. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0062.
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It is important for rheumatologists to have an understanding of biochemical tests including an awareness of their limitations. The biological variability of an analyte both within and between individuals, the limitations of the measurement technology, the sensitivity of laboratory internal quality control and external quality assurance procedures, as well as interlaboratory variations in practices including sample collection procedures, may all impact on the interpretation of a result. Biochemical tests are often requested to monitor organ-specific dysfunction arising as an adverse consequence of pharmacotherapy or as a component of a systemic rheumatic disease, although dysfunction may also reflect infection or coincidental pathology. Patients with rheumatic diseases are at high risk of renal and hepatic disease. Serum creatinine and its derivative estimated glomerular filtration rate (eGFR) are the most readily available surrogate markers of GFR and are used to assess renal impairment and monitor its course. However, the use of creatinine alone lacks sensitivity and a substantial loss of function must occur before creatinine levels are increased. Additional biochemical screening for kidney damage can be performed by assessment of glomerular integrity, including proteinuria or albuminuria and haematuria. A wide spectrum of rheumatic diseases can affect the liver with various degrees of involvement and hepatic pathology. These often present with cholestatic or hepatitic biochemical profiles. The medical management of rheumatic diseases also involves medications that are hepatotoxic, and routine monitoring of liver function is recommended. This approach is not problem-free and may be improved by quantitative determinations of non-invasive markers of liver fibrosis in the future. Together with imaging techniques, biochemical tests play an important role in the assessment and differential diagnosis of metabolic bone disease.
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Turner, Neil. Mechanisms of progression of chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0136.
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Three major hypotheses attempt to explain progressive kidney disease following diverse diseases and injuries. To varying degrees they can explain the observed risk factors for progression and the ability of interventions to lower risk. The hyperfiltration hypothesis argues that progression is due to stress on residual nephrons leading to injury and damage to remaining glomeruli. The toxicity of proteinuria hypothesis proposes that serum proteins or bound substances are toxic to tubular or tubulointerstitial cells. This sets up cycles of damage which lead to tubulointerstitial scarring. The podocyte loss hypothesis contends that proteinuria is simply a biomarker for damaged or dying podocytes, and that it is further podocyte loss that leads to progressive glomerulosclerosis. Renoprotective strategies might have direct effects on podocytes. Importantly these different hypotheses suggest different therapeutic approaches to protecting the function of damaged kidneys. Differences between repair mechanisms may explain why some injuries lead to recovery and others to progressive disease, and may suggest new targets for protective therapy.
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Muche, Marion, and Seema Baid-Agrawal. Hepatitis B. Edited by Vivekanand Jha. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0185_update_001.
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Hepatitis B virus (HBV) has been causally linked to a variety of renal diseases, the most common being glomerular diseases and systemic autoimmune disease. Membranous nephropathy (MN) is the commonest HBV-associated glomerulonephritis (HBV-GN), followed by membranoproliferative glomerulonephritis (MPGN), mesangial proliferative glomerulonephritis, immunoglobulin (Ig)-A nephropathy, and focal segmental glomerulosclerosis (FSGS). Polyarteritis nodosa is a rare manifestation. The incidence of HBV-associated renal diseases seems to be decreasing with the introduction of vaccination programmes.HBV-MN is the most frequent cause of nephrotic syndrome in children in countries with high endemicity of HBV infection. The clinical course is usually benign in children with high rates of spontaneous remission rates and low risk of progression to renal failure. The prognosis is worse in adults. Of the systemic autoimmune disorders associated with HBV infection that involve the kidneys, the strongest link has been found with polyarteritis nodosa (PAN), a lesion that causes arteritis of medium-sized renal vessels. HBV-associated PAN (HBV-PAN) usually manifests in the first year after infection, and is clinically indistinguishable from classic PAN.Diagnosis of HBV-GN or -PAN is based on the clinical picture, histological findings, evidence of viral replication in serum and/or liver and detection of HBV antigens or DNA in the tissue. Besides deposition of immune complexes, other mechanisms such as virus-induced cytopathic damage have been proposed to explain the pathogenesis.HBV-GN and HBV-PAN appear to respond to antiviral treatment. Both show remission after HBeAg seroconversion. The available studies predominantly employed first-generation agents like interferon alpha and lamivudine, which showed suppression of viral replication and clinical remission of HBV-associated renal disease. Immunosuppressive therapy appears to be inevitable for the control of severe HBV-PAN and could be helpful in addition to antiviral treatment for cases of HBV-GN not responding clinically to antiviral treatment.
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Cui, Zhao, Neil Turner, and Ming-hui Zhao. Antiglomerular basement membrane disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0074_update_001.
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Individuals appear to be predisposed to antiglomerular basement membrane (anti-GBM) disease by carrying a predisposing human leucocyte antigen type, DRB1*1501 being identified as the highest risk factor, and there are likely to be other predisposing genes or influences on top of which a relatively rare ‘second hit’ leads to the development of autoimmunity. In anti-GBM disease this appears to have a self-perpetuating, accelerating component, that may be to do with antibodies and altered antigen presentation. Lymphocyte depletion may also predispose to the disease. A number of second hits have been identified and they seem to share a theme of damage to the glomerulus. There may be a prolonged (months to years) and usually subclinical phase in anti-GBM disease in which usually relatively low level antibody titres are associated with variable haematuria, sometimes minor pulmonary haemorrhage, but often no symptoms. Damage to the lung seems to determine whether there is a pulmonary component to the disease. Without pulmonary damage caused typically by smoking, inhalation of other fumes, and potentially infection or oxygen toxicity, the disease remains an isolated kidney disease. Antibodies appear to be an important component of the disease, but cell-mediated immunity is also critical to the clinical picture. In animal models, cell-mediated immunity triggered by the GBM antigen can cause severe renal damage in the absence of pathogenic antibody. The development of specific antibody also requires T-cell sensitization and help, and suppressing the response is likely to require suppressing both antibody and cell-mediated immunity. Antibodies recognize one major and some other epitopes, which are now well described. T-cell epitopes are becoming better understood. Evidence from animal models also suggests that the damage in anti-GBM disease is dependent on complement, macrophages, and neutrophils.
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Haymann, Jean-Philippe, and Francois Lionnet. The patient with sickle cell anaemia. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0167.
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In sickle cell anaemia (SCA) a single mutation in the haemoglobin beta-globin gene is responsible for a pleomorphic phenotype leading to acute and chronic life-threatening complications. Healthcare management programmes, patient and family education, infection prophylaxis (especially in childhood), and long-term treatment for some patients (such as hydroxyurea) have significantly improved survival, giving rise to some new long-term issues.Sickle cell-associated nephropathy (SCAN) leads in some cases to chronic renal failure with a significant impact on survival. SCAN is characterized by an increased effective plasma renal flow and glomerular filtration rate, glomerular hypertrophy, and damaged vasa recta system leading to albuminuria and impaired urinary concentration.Early onset of hyperfiltration occurs in 60% of SCA patients often associated with microalbuminuria. SCAN risk factors are still under investigation, but may be related to chronic haemolysis at an early time point. Other lesions in patients with sickle cell anaemia include papillary necrosis, and recurrent acute kidney injury in association with crises or infections.ACEI are recommended if there is proteinuria. There is no current agreement on whether angiotensin-converting enzyme inhibitors (ACEI) should be introduced earlier, but systematic screening for microalbuminuria and hypertension, and avoidance of nephrotoxic agents are strongly advised.Patients with sickle cell trait (carriers for sickle cell anaemia) are prone to microscopic haematuria and abnormalities of the vasa recta have been described. A very rare tumour, renal medullary carcinoma, is largely restricted to this group (in whom it is still extremely rare). Increased risk of other renal problems is still largely hypothetical rather than proven.The prevalence of nephropathies in other sickle cell diseases (in particular haemoglobin SC disease) is much lower.
Book chapters on the topic "Glomerular Damage"
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Redon, Josep, Gernot Pichler, and Fernando Martinez. "Glomerular Filtration Rate in Renal Damage." In Assessment of Preclinical Organ Damage in Hypertension, 165–70. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-15603-3_15.
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Hardwicke, J., and J. F. Soothill. "Glomerular Damage in Terms of “Pore Size”." In Novartis Foundation Symposia, 32–50. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470719244.ch3.
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Zanetti, G., A. Trinchieri, E. Montanari, A. Guarneri, G. B. Fogazzi, P. Passerini, A. Currò, and E. Austoni. "Urinary Red Blood Cell Microscopic Morphology after ESWL: A Parameter of Glomerular Damage." In Urolithiasis 2, 547. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2556-1_218.
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Mallick, Netar P., and G. Williams. "Glomerular and associated tubular injury by light chains. The spectrum of damage and effect of treatment." In The Kidney in Plasma Cell Dyscrasias, 77–84. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-009-1315-8_7.
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Burova, Larissa A., Vladimir A. Nagornev, Peter V. Pigarevsky, Maria M. Gladilina, Valentina G. Seliverstova, Claes Schalen, and Artem A. Totolian. "Circulating Anti-IgG and Glomerular Damage in Rabbits Immunized with IgG Fc-Receptor Positive Group A Streptococci." In Streptococci and the Host, 531–35. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-1825-3_124.
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Keeling, John, and Guillermo A. Herrera. "The Mesangium as a Target for Glomerulopathic Light and Heavy Chains: Pathogenic Considerations in Light and Heavy Chain-Mediated Glomerular Damage." In Contributions to Nephrology, 116–34. Basel: KARGER, 2006. http://dx.doi.org/10.1159/000096764.
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ROBBINS, M., R. JAENKE, T. BYWATERS, M. REZVANI, and J. HOPEWELL. "ULTRASTRUCTURAL EVALUATION OF RADIATION-INDUCED GLOMERULAR DAMAGE IN THE PIG." In Radiation Research: A Twentieth-century Perspective, 161. Elsevier, 1991. http://dx.doi.org/10.1016/b978-0-12-168561-4.50620-x.
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Ritz, Eberhard, and Tilman B. Drüeke. "Chronic kidney disease." In Oxford Textbook of Medicine, edited by John D. Firth, 3904–29. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199204854.003.2106_update_001.
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Definition—chronic kidney disease (CKD) is defined as kidney damage lasting for more than 3 months characterized by structural or functional abnormalities of the kidney, with or without decreased glomerular filtration rate (GFR). Staging—CKD has been subdivided into five stages depending on the estimated GFR (eGFR), as described in ...
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Singh, Ajay K. "Chronic Kidney Disease." In The Brigham Intensive Review of Internal Medicine, 638–52. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199358274.003.0063.
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Chronic kidney disease (CKD) is defined by the National Kidney Foundation (NKF) as either (1) a glomerular filtration rate (GFR) of 〈60 mL/min with or without kidney damage for 3 or more months or (2) the presence of kidney damage for 3 or more months demonstrated by pathologic abnormalities, markers of kidney damage (e.g., blood or urine composition), or imaging tests. In the United States it is estimated that CKD affects 7–10% of the adult population or 15–20 million individuals, although specific subgroups such as African Americans and Hispanics are at especially high risk. Chapter 60 in this section of the volume reviews the complications of CKD.
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Glassock, Richard J. "Symptomatic therapy." In Treatment of Primary Glomerulonephritis, 1–46. Oxford University Press, 2009. http://dx.doi.org/10.1093/med/9780199552887.003.0001.
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Patients with glomerular diseases develop a wide variety of biochemical disturbances and pathophysiologic alterations leading to overt clinical manifestations (Remuzzi, 1993; Glassock et al., 1995, Remuzzi and Bertani, 1998; Schrier and Fassett, 1998; Vaziri, 2003; Floege and Feehally, 2007; Kim et al., 2007; Haraldsson et al., 2008). These occur as a direct result of injury to the capillary wall and disturbances in normal glomerular function, including loss of filtration capacity and excessive transfer of erythrocytes and/or plasma proteins from blood to tubular lumina eventuating in hematuria and/or proteinuria. Proteinuria—which is believed to be the consequence of disturbed glomerular capillary wall permselectivity (Haraldsson et al., 2008) —when substantial, can lead to hypoproteinemia and thereby to a reduction in plasma oncotic pressure. Changes in the synthesis, turnover, and plasma concentration of various proteins and lipids develop and can lead to an imbalance of pro-thrombotic and anti-thrombotic factors promoting a ‘thrombophilic’ state (Vaziri, 2003; Crew et al., 2004; Glassock, 2007) Disturbances in the renal handling of sodium chloride (NaCl) and water are often associated with edema formation and/or hypertension (Perico and Remuzzi, 1993; Schrier and Fassett, 1998). Finally, the rapid or slow loss of the glomerular filtration capacity (glomerular filtration rate, GFR) due to damage of single nephrons (perhaps mediated by filtered proteins and their reabsorption) as well as by the ‘drop out’ of functioning nephrons from the overall population of nephrons in the two kidneys is responsible for ultimate progression to end-stage renal disease (ESRD) in many, but not all, of the primary glomerular disorders (Drummond et al., 1994; Remuzzi and Bertani, 1998; Squarer, et al., 1998; Floege and Feehally, 2007). Collectively these abnormalities give rise to ‘syndromes’ of glomerular disease. These ‘syndromes’ can be arbitrarily, but usefully, grouped into five categories which may overlap to some degree; namely, the acute nephritic syndrome, rapidly progressive glomerulonephritis, the nephrotic syndrome, ‘symptomless’, haematuria and/or proteinuria, and slowly progressive ‘chronic’ nephritis (Glassock et al., 1995). The cardinal features of these syndromes and the diseases to which they are most closely associated are discussed in this monograph. This monograph will deal largely with those glomerular diseases which primarily affect the kidneys and in which the extra-renal manifestations are the consequence of the impairment or disturbance of kidney function itself (the so-called primary glomerular diseases).
Conference papers on the topic "Glomerular Damage"
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Montani, N., S. B. Solerte, G. Gamba, M. Fioravanti, and E. Ferrari. "RELATIONSHIPS BETWEEN HAEMOSTATIC ENDOTHELIAL FUNCTIONS AND GLOMERULAR FILTRATION RATE IN SHORT-TERM TYPE I DIABETES MELLITUS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643101.
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It is known that the increase of glomerular filtration rate (GFR) represents an early sign of diabetic nephropathy. The changes of endothelial functions observed in diabetes might play a role in this respect. As F VIII vWF and fibronectin are synthetized by endothelial cells, we evaluated these components in 33 diabetic patients with short-term Type I (insulin dependent) diabetes mellitus, without retinopathy and macro-vascular complications. 15 pts. (mean age 29 ± 7 yrs; mean diabetes duration 2.9 ± 0.9 yrs) presented high GFR (154 ± 19 ml/min per 1.73 m2 ; albuminuria 7.2 ± 3.2 μg/min) and 18 pts. (mean age 30 ± 6 yrs; mean diabetes duration 3.0 ± 1 yrs) normal GFR (105 ± 11 ml/min per 1.73 m2 ; albuminuria 5 ± 2.8 μg/min).The following results were obtained:In conclusion the significant increase of FVIIIR:Ag and fibronectin levels in short-time type I diabetic patients with high GFR suggests an early endothelial cell function damage also related to the Door metabolic control.
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Delani, F., M. Tagliaferri, D. Macconi, C. Lupini, N. Perico, and G. Rumuzzi. "PLATELET ACTIVATING FACTOR (PAF) AS A MEDIATOR OF PROTEINURIA IN ISOLATED PERFUSED KIDNEY (IPK)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643485.
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PAF amplifies tissue damage in glomerulonephritis and can promote proteinuria stimulating platelet and neutrophil cationic protein release. We used IPK to establish whether PAF directly causes proteinuria. Kidneys were isolated from male Sprague-Dawley rats and perfused at constant pressure (100 mmHg) in a closed circuit with a Krebs-Henseleit buffer containing glucose urea creatinine, BSA (1%), Ficoll 70 (3.5%) and amino acids. After 25 min stabilization period, a basal 10 min clearance period was followed by PAF (1.8 nM f.c. n = 6) or vehicle (n = 5) injection into the renal artery. As seen in the figure PAF but not vehicle significantly (p<0.01) increased urine protein excretion. No significant changes in GFR (as creatinine clearance) were observed after PAF or vehicle injection (Basal: 0.786 ± 0.075 PAF: 0.658 ± 0.070. Basal 0.653 ± 0.081, vehicle 0.639 ± 0.074 ml/min/g kidney). The data indicate that PAF may directly increase glomerular permeability to proteins.
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Nieto-Chaupis, Huber. "Prospects for anticipating kidney damage in type-2 diabetes patients through the sensing of albumin passing through the renal glomerulus." In 2017 IEEE EMBS International Conference on Biomedical & Health Informatics (BHI). IEEE, 2017. http://dx.doi.org/10.1109/bhi.2017.7897254.
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Bini, A., V. D"Agati, C. Pirani, B. Kudryk, and K. L. Kaplan. "MONOCLONAL ANTIBODY IDENTIFICATION OF FIBRIN DEPOSITS IN RENAL DISEASE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643319.
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Glomerular and vascular "fibrin" deposition has frequently been reported in human and experimental renal diseases. The biochemical form of this "fibrin" has not been well defined. We studied 16 renal biopsies (Bouin's fixed paraffin embedded) with the ABC-immunoperoxidase technique using monoclonal antibodies (MAbs); MAb I8C6 (Bβ1-42) to fibrinogen and fibrin I; MAb T2G1 (β15-42) to fibrin II; and MAb GC4 to fragment D or D-D. Polyclonal antisera to fibrinogen, albumin and IgG were used as controls. Renal biopsy specimens included 9 cases of microangiopathy (Group I: 6 hemolytic uremic syndrome (HUS), 1 sclerodero-ma, 2 acute humoral rejection) and 7 miscellaneous cases of other renal disease (Group II: 2 IgA nephropathy, 2 minimal change disease, 2 membranous GN, 1 acute interstitial nephritis). Fibrinogen and fibrin I were present on the glomerular (glom) endothelial cells in 8/9 Group I and 7/7 Group II cases, but was present in glom capillary lumens in Group I only. Staining of the endothelial aspect of interstitial capillaries, arterioles and arteries was also observed in both groups. Fibrin II was present in most glom and interstitial capillaries in both groups. However, intense staining for fibrin II was observed in arterioles and arteries in Group I only. Staining for fragments D and D-D was observed in glom capillaries in 6 Group I cases (6 HUS) and 3 Group II cases (2 IgA nephropathy, 1 membranous GN) but was most diffuse and intense in Group I. Traditional histochemical stains for fibrin (Lendrum and PTAH) were positive in 4 Group I cases only, indicating that the ABC technique is far more sensitive. Controls (14 needle biopsies of non-renal tissue) showed no vascular ractivity for fibrinogen, fibrin I, II and fragments D and D-D, suggesting that the vascular staining observed in renal biopsy tissue is not caused by the biopsy procedure itself. These findings indicate that 1) Fibrin formation and lysis occur in many renal diseases of both vascular and non—vascular origin. 2) Fibrinolytic activity is higher in the glom capillaries than in the larger vessels. 3) Damaged renal endothelium may be an active participant in these processes.
Reports on the topic "Glomerular Damage"
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Viksna, Ludmila, Oksana Kolesova, Aleksandrs Kolesovs, Ieva Vanaga, and Seda Arutjunana. Clinical characteristics of COVID-19 patients (Latvia, Spring 2020). Rīga Stradiņš University, December 2020. http://dx.doi.org/10.25143/fk2/hnmlhh.
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Data include following variables: Demographics, epidemiological history, comorbidities, diagnosis, complications, and symptoms on admission to the hospital. Also, body’s temperature and SpO2. Blood cells: white cells count (WBC), neutrophils (Neu), lymphocytes (Ly), eosinophils (Eo) and monocytes (Mo), percentages of segmented and banded neutrophils, erythrocytes (RBC), platelet count (PLT), hemoglobin (Hb), and hematocrit (HCT); Inflammatory indicators: erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP); Tissue damage indicators: alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and troponin T (TnT); Electrolytes: potassium and sodium concentration; Renal function indicators: creatinine and glomerular filtration rate (GFR); Coagulation tests: D-dimer, prothrombin time, and prothrombin index on admission to the hospital.