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Gotowe bibliografie tematyczne / Kidney inflammation

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Gotowa bibliografia na temat „Kidney inflammation”

Autor: Grafiati

Data publikacji: 2 czerwca 2025

Data aktualizacji: 31 lipca 2025

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Artykuły w czasopismach na temat "Kidney inflammation"

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Tian, Zhi-Kai, Yu-Jia Zhang, Zhao-Jun Feng, et al. "Nephroprotective effect of gastrodin against lead-induced oxidative stress and inflammation in mice by the GSH, Trx, Nrf2 antioxidant system, and the HMGB1 pathway." Toxicology Research 10, no. 2 (2021): 249–63. http://dx.doi.org/10.1093/toxres/tfab003.

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Abstract Gastrodin (GAS), the main phenolic glycoside derivative from Gastrodiaelata Blume, has several bio-activities. However, the molecular mechanisms of these protective actions currently remain unclear. This study aimed to investigate the mechanisms of GAS on lead (Pb)-induced oxidative stress and inflammation in the kidneys and primary kidney mesangial cells. Results indicated that GAS improved Pb-induced renal dysfunction and morphological changes in mice. GAS ameliorated Pb-induced inflammation in kidneys by reducing the TNF-α and IL-6 levels. GAS inhibited Pb-induced oxidative stress

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Jung, Su Woong, Su-Mi Kim, Yang Gyun Kim, Sang-Ho Lee, and Ju-Young Moon. "Uric acid and inflammation in kidney disease." American Journal of Physiology-Renal Physiology 318, no. 6 (2020): F1327—F1340. http://dx.doi.org/10.1152/ajprenal.00272.2019.

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Asymptomatic hyperuricemia is frequently observed in patients with kidney disease. Although a substantial number of epidemiologic studies have suggested that an elevated uric acid level plays a causative role in the development and progression of kidney disease, whether hyperuricemia is simply a result of decreased renal excretion of uric acid or is a contributor to kidney disease remains a matter of debate. Over the last two decades, multiple experimental studies have expanded the knowledge of the biological effects of uric acid beyond its role in gout. In particular, uric acid induces immune

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Kimura, Tomonori, Yoshitaka Isaka, and Tamotsu Yoshimori. "Autophagy and kidney inflammation." Autophagy 13, no. 6 (2017): 997–1003. http://dx.doi.org/10.1080/15548627.2017.1309485.

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Bachurin, G. V., A. V. Bachurin, and Yu S. Kolomoets. "Enzyme test – early diagnosis of kidney inflammation." Urologiya 28, no. 1-4 (2024): 38–48. https://doi.org/10.26641/2307-5279.28.1-4.2024.322090.

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The aim of the work is to improve the results of early diagnosis of acute infectious kidney diseases at the molecular level in urolithiasis (urinary stone disease) through the study of enzymatic test indicators. Enzymatic tests (NGAL, IL-1β, β2-microglobulin) were investigated at the molecular level using the IFA method in the urine of patients with urolithiasis. Comparative and prognostic significance of the conducted treatment was established between the groups of patients, and an algorithm was developed based on the results of kidney damage predictors. It was found that the indicators of ge

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Goesch, Torsten R., Nancy A. Wilson, Weifeng Zeng, et al. "Suppression of Inflammation-Associated Kidney Damage Post-Transplant Using the New PrC-210 Free Radical Scavenger in Rats." Biomolecules 11, no. 7 (2021): 1054. http://dx.doi.org/10.3390/biom11071054.

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Allograft kidney transplantation, which triggers host cellular- and antibody-mediated rejection of the kidney, is a major contributor to kidney damage during transplant. Here, we asked whether PrC-210 would suppress damage seen in allograft kidney transplant. Brown Norway (BN) rat kidneys were perfused in situ (UW Solution) with or without added 30 mM PrC-210, and then immediately transplanted into Lewis (LEW) rats. 20 h later, the transplanted BN kidneys and LEW rat plasma were analyzed. Kidney histology, and kidney/serum levels of several inflammation-associated cytokines, were measured to a

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Akcay, Ali, Quocan Nguyen, and Charles L. Edelstein. "Mediators of Inflammation in Acute Kidney Injury." Mediators of Inflammation 2009 (2009): 1–12. http://dx.doi.org/10.1155/2009/137072.

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Acute kidney injury (AKI) remains to be an independent risk factor for mortality and morbidity. Inflammation is now believed to play a major role in the pathopathophysiology of AKI. It is hypothesized that in ischemia, sepsis and nephrotoxic models that the initial insult results in morphological and/or functional changes in vascular endothelial cells and/or in tubular epithelium. Then, leukocytes including neutrophils, macrophages, natural killer cells, and lymphocytes infiltrate into the injured kidneys. The injury induces the generation of inflammatory mediators like cytokines and chemokine

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Perry, Heather M., Nicole Görldt, Sun-sang J. Sung, et al. "Perivascular CD73+ cells attenuate inflammation and interstitial fibrosis in the kidney microenvironment." American Journal of Physiology-Renal Physiology 317, no. 3 (2019): F658—F669. http://dx.doi.org/10.1152/ajprenal.00243.2019.

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Progressive tubulointerstitial fibrosis may occur after acute kidney injury due to persistent inflammation. Purinergic signaling by 5′-ectonucleotidase, CD73, an enzyme that converts AMP to adenosine on the extracellular surface, can suppress inflammation. The role of CD73 in progressive kidney fibrosis has not been elucidated. We evaluated the effect of deletion of CD73 from kidney perivascular cells (including pericytes and/or fibroblasts of the Foxd1+ lineage) on fibrosis. Perivascular cell expression of CD73 was necessary to suppress inflammation and prevent kidney fibrosis in Foxd1CreCD73

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Huang, Liang-Ti, and Chung-Ming Chen. "Kidney Injuries and Evolution of Chronic Kidney Diseases Due to Neonatal Hyperoxia Exposure Based on Animal Studies." International Journal of Molecular Sciences 23, no. 15 (2022): 8492. http://dx.doi.org/10.3390/ijms23158492.

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Preterm birth interrupts the development and maturation of the kidneys during the critical growth period. The kidneys can also exhibit structural defects and functional impairment due to hyperoxia, as demonstrated by various animal studies. Furthermore, hyperoxia during nephrogenesis impairs renal tubular development and induces glomerular and tubular injuries, which manifest as renal corpuscle enlargement, renal tubular necrosis, interstitial inflammation, and kidney fibrosis. Preterm birth along with hyperoxia exposure induces a pathological predisposition to chronic kidney disease. Hyperoxi

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Baer, Brandon, Jason Lin, Kaitlyn R. Schaaf, Lorraine B. Ware, Ciara M. Shaver, and Julie A. Bastarache. "Matrix metalloproteinase-7 is dispensable in a mouse model of sepsis-induced acute lung injury." PLOS One 20, no. 5 (2025): e0321349. https://doi.org/10.1371/journal.pone.0321349.

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Acute respiratory distress syndrome (ARDS) is a life-threatening form of acute lung injury whose pathogenesis is characterized by excessive lung inflammation and alveolar-capillary barrier permeability. Matrix metalloproteinase 7 (MMP7) can regulate leukocyte recruitment and the production of pro-inflammatory cytokines, but whether it plays a role in acute lung injury (ALI) is an unanswered question. We hypothesized that global loss of MMP7 would attenuate sepsis-induced ALI and systemic inflammation. To test this, male and female MMP7 knockout (MMP7KO) mice and wild-type (WT) littermates were

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García-García, Patricia M. "Inflammation in diabetic kidney disease." World Journal of Diabetes 5, no. 4 (2014): 431. http://dx.doi.org/10.4239/wjd.v5.i4.431.

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Rozprawy doktorskie na temat "Kidney inflammation"

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Khalaf, Fatimah. "Regulation of Renal Inflammation in Chronic Kidney Disease." University of Toledo Health Science Campus / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=mco1588943852414778.

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Campos-Pereira-Da-Cruz-Viana, Joao. "Exercise in chronic kidney disease : impact on immunity and inflammation." Thesis, Loughborough University, 2011. https://dspace.lboro.ac.uk/2134/9090.

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Chronic kidney disease (CKD) is associated with a complex state of immune dysfunction characterised by immune depression, which predisposes CKD patients to infections, and by immune activation resulting in inflammation, which is associated with cardiovascular disease among these patients. It has been suggested that regular moderate exercise may enhance immune function and exert anti-inflammatory effects. However, such effects are still unclear in CKD. Therefore, we investigated the effects of acute and regular (1-month and 6-months) moderate intensity aerobic exercise (walking) on measures of

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YANG, JI YEON. "CD40 monocyte differentiation mediates tissue inflammation in chronic kidney disease." Diss., Temple University Libraries, 2015. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/349139.

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Pharmacology<br>Ph.D.<br>Patients with chronic kidney disease (CKD) develop hyperhomocysteinemia (HHcy), have increased inflammatory monocytes (MC) and 10-times higher cardiovascular mortality than the general population. Here, we investigated HHcy-related MC differentiation in CKD. Twenty seven CKD and CVD, and 14 healthy subjects were recruited. CD40 was selected as a CKD-induced MC activation marker by mining for CKD-MC-mRNA screen database. We found that CD14++CD16+ MC, often denoted as inflammatory subset, soluble CD40 ligand (sCD40L), and TNFα/IL-6 levels were augmented in CVD and CKD su

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Dupre, Tess V., Mark A. Doll, Parag P. Shah, et al. "Inhibiting glucosylceramide synthase exacerbates cisplatin-induced acute kidney injury." AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC, 2017. http://hdl.handle.net/10150/624924.

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Acute kidney injury (AKI), resulting from chemotherapeutic agents such as cisplatin, remains an obstacle in the treatment of cancer. Cisplatin-induced AKI involves apoptotic and necrotic cell death, pathways regulated by sphingolipids such as ceramide and glucosylceramide. Results from this study indicate that C57BL/6J mice treated with cisplatin had increased ceramide and hexosylceramide levels in the renal cortex 72 h following cisplatin treatment. Pretreatment of mice with inhibitors of acid sphingomyelinase and de novo ceramide synthesis (amitriptyline and myriocin, respectively) prevented

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Chitalia, Nihil A. "Vitamin D, inflammation and cardiovascular disease in patients with chronic kidney disease." Thesis, St George's, University of London, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.616978.

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Cardiovascular (CV) disease is the commonest cause of mortality in CKD. CV mortality is not entirely explained by traditional CV risk factors and therefore systemic inflammation and vitamin D deficiency are thought to play a major role in CKD. Vitamin D [25 (hydroxy vitamin D; 25(OH)D] modulates adaptive immune responses and 25(OH)D deficiency is associated with CV mortality. Vascular endothelial dysfunction is a surrogate marker of atherosclerotic CV disease and related to systemic inflammation in CKD. However, the role of vitamin D on inflammation and endothelial function in CKD is largely u

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Bogart, Avery M. "STAT5 Knockout Mice Show Increased Susceptibility to Cisplatin-Induced Acute Kidney Injury." Ohio University Honors Tutorial College / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ouhonors1524841830342307.

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Nehus, Edward J. "Correlates of Resistin in Children with Chronic Kidney Disease: The CKiD Cohort." University of Cincinnati / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1318862589.

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Cheung, Katharine Lana. "Chronic Kidney Disease and the Risk of Venous Thromboembolism." ScholarWorks @ UVM, 2018. https://scholarworks.uvm.edu/graddis/879.

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Chronic kidney disease (CKD) affects more than 30 million adults in the U.S. and is strongly associated with cardiovascular events and mortality. Venous thromboembolism (VTE) is the third leading vascular disease, affects up to 900,000 Americans each year and contributes to as many as 100,000 deaths annually. The relationship of CKD and VTE has been described in patients receiving dialysis, kidney transplants recipients and in nephrotic syndrome, however, data supporting the association of VTE in mild to moderate CKD is conflicted. The overall goal of this research was to study the association

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Palau, González Vanesa. "Role of ADAM17 in kidney disease: a clinical and experimental approach”." Doctoral thesis, Universitat Autònoma de Barcelona, 2021. http://hdl.handle.net/10803/672003.

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Les desintegrines i metal·loproteases (ADAMs) són una família de proteïnases que alliberen dominis proteics solubles en un procés conegut com a “shedding”. En concret, l’ADAM17 és el membre de la família millor estudiat. Aquest, es troba altament expressat en les cèl·lules dels túbuls distals i augmenta la seva expressió en totes les cèl·lules del ronyó en la malaltia renal crònica (MRC), la nefropatia diabètica (ND) i la malaltia cardiovascular (CV), entre d’altres. Basant-nos en aquests antecedents, es van dissenyar tres estudis per aquesta tesi doctoral. En primer lloc, es va analitzar l’ac

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Satou, Yuuki. "Heterogeneous fibroblasts underlie age-dependent tertiary lymphoid tissues in the kidney." 京都大学 (Kyoto University), 2017. http://hdl.handle.net/2433/225471.

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Książki na temat "Kidney inflammation"

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F, Zipfel Peter, ed. Complement and kidney disease. Birkhäuser, 2005.

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Kidney Inflammation, Injury and Regeneration. MDPI, 2020. http://dx.doi.org/10.3390/books978-3-03928-539-6.

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Kidney Inflammation, Injury and Regeneration 2020. MDPI, 2021. http://dx.doi.org/10.3390/books978-3-0365-2369-9.

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Carrero, Juan Jesús, and Peter Stenvinkel. The role of inflammation in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0110.

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Low-grade persistent inflammation is a common feature of chronic kidney disease. This chapter provides an overview of the pathogenesis and clinical consequences of elevated pro-inflammatory cytokines in the uraemic milieu with an emphasis on dialysis stages. It reviews the multifactorial dialysis- and non-dialysis-related causes of inflammation and its purported role in the development of protein energy wasting, vascular calcification, endocrine disorders, and depression. The chapter also discusses the use and the need of monitoring C-reactive protein levels regularly in the clinical setting a

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Herrington, William G., Aron Chakera, and Christopher A. O’Callaghan. The kidney in systemic disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0170.

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Many systemic diseases can affect the kidney, including autoimmune conditions, malignancies, infections, and vascular diseases. Autoimmune conditions can cause inflammation of the glomeruli or tubules, or deposition of inflammatory proteins (AA amyloidosis). Malignancy can cause infiltration of normal renal tissue, immunoglobulin deposition in the renal vessels, glomeruli or tubules, or paraneoplastic renal dysfunction as occurs in secondary focal segmental glomerulosclerosis. Infections can cause inflammation in glomeruli, in association with immune complex deposition. Vascular disease and va

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Dr. Sebi Cure for Kidney Disease: Through Alkaline Medicinal Herbs and Diets to Remove Kidney Stones, Inflammation; Detox, Cleanse and Revitalize Kidney and Liver of Electric Body. Independently Published, 2020.

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Low Oxalate Diet Cookbook: Healthy, Gluten-Free Recipes to Treat Kidney Stones, Inflammation and More. Independently Published, 2021.

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Malyszko, Jolanta, and Iain C. Macdougall. Iron metabolism in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0125.

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While whole-body (‘absolute’) iron deficiency is common and probably increased in frequency in chronic kidney disease (CKD), functional iron deficiency is a particular problem in CKD. Absolute iron deficiency is likely to be present in advanced CKD when the ferritin falls below 100 ng/mL and the TSAT falls below 20%. Functional iron deficiency is characterized by the presence of adequate iron stores (as defined by conventional criteria), but with an inability to mobilize this iron rapidly enough to adequately support erythropoiesis with the administration of erythropoietin. Among such patients

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Prowle, John, and Rinaldo Bellomo. Acute kidney injury in severe sepsis. Edited by Norbert Lameire. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0244_update_001.

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Septic acute kidney injury (S-AKI) accounts for close to 50% of all cases of AKI in ICU and, in its various forms, affects between 15% and 20% of ICU patients. Patients typically present with clinical evidence of severe sepsis and septic shock, developing oliguria or anuria, and rapidly rising serum creatinine concentration. The pathophysiology of S-AKI is poorly understood. Although haemodynamic factors might play a role in the loss of glomerular filtration rate, this may not be through the induction of renal ischaemia. Inflammation, microvascular shunting, and changes in glomerular arteriola

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Cruz, Dinna N., Anna Giuliani, and Claudio Ronco. Acute kidney injury in heart failure. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0248.

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Acute kidney injury (AKI) occurring during heart failure (HF) has been labelled cardiorenal syndrome (CRS) type 1. CRS is defined as a group of ‘disorders of the heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction of the other’. This consensus definition was proposed by the Acute Dialysis Quality Initiative, with the aim to standardize those disorders where cardiac and renal diseases coexist. Five subtypes have been proposed, according to which organ is affected first (cardiac vs renal) and whether the dysfunction is acute or chronic. Ano

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Części książek na temat "Kidney inflammation"

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Gupta, Ameet, and Krishna Narahari. "Kidney and Ureter Inflammation." In Blandy's Urology. John Wiley & Sons, Ltd, 2019. http://dx.doi.org/10.1002/9781118863343.ch12.

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Pauletto, Paolo, and Marcello Rattazzi. "Inflammation and Hypertension." In Chronic Kidney Disease and Hypertension. Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1982-6_14.

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Liu, Haoxin, Tram N. Diep, and Liang-Jun Yan. "Mitigating Oxidative Stress and Inflammation: The Protective Role of β-lapachone in Kidney Disease." In Inflammation. Springer Nature Switzerland, 2025. https://doi.org/10.1007/978-3-031-55254-0_3-1.

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Schneider, Florian, and Sascha Pahernik. "Kidney and Renal Pelvis: Inflammation." In Abdominal Imaging. Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-13327-5_229.

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Fadem, Stephen Z. "Inflammation in Kidney Disease Glomerulonephritis." In Staying Healthy with Kidney Disease. Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-93528-3_6.

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Santos-Silva, Alice, Elísio Costa, and Rui Alves. "Chronic Kidney Disease." In Biomarkers of Cardiometabolic Risk, Inflammation and Disease. Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-16018-4_5.

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Mårtensson, Johan, and Rinaldo Bellomo. "Acute Kidney Injury." In Inflammation - From Molecular and Cellular Mechanisms to the Clinic. Wiley-VCH Verlag GmbH & Co. KGaA, 2017. http://dx.doi.org/10.1002/9783527692156.ch50.

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Harms, James C., Cheng Jack Song, and Michal Mrug. "The Role of Inflammation and Fibrosis in Cystic Kidney Disease." In Polycystic Kidney Disease. Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7784-0_6.

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Spittle, Margaret, Nicholas A. Hoenich, Garry Handelman, Rohini Adhikarla, Peter Homel, and Nathan W. Levin. "Oxidative Stress and Inflammation in Hemodialysis Patients." In Improving Prognosis for Kidney Disorders. Springer Netherlands, 2002. http://dx.doi.org/10.1007/978-94-017-1848-6_5.

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Trieb, Klemens. "Heat shock protein expression in transplanted kidney." In Heat Shock Proteins and Inflammation. Birkhäuser Basel, 2003. http://dx.doi.org/10.1007/978-3-0348-8028-2_14.

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Streszczenia konferencji na temat "Kidney inflammation"

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Petrović, Vladimir. "Renal dysfunction in cardiovascular diseases – from molecular to clinical level." In 7 th International Congress of Cardionephrology - KARNEF 2025. Punta Niš, 2025. https://doi.org/10.46793/karnef25.013p.

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The heart and kidneys are vital for maintaining cardiovascular (CV) homeostasis, with the heart supplying blood and oxygen to organs, and the kidneys maintain fluid, electrolyte, and acid-base balance, erythropoetin production, and waste removal. In healthy individuals, renal hemodynamics affect cardiac hemodynamics and vice versa. When cardiovascular and kidney diseases coexist, it may lead to cardiorenal syndromes (CRS), where dysfunction in one organ triggers the dysfunction in the other [4]. Studies have shown that majority of patients affected by cardiovascular disease usually display som

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Dimitrijevic, Zorica M. "Residual Kidney Function and Prevention of Cardiovascular Risk – Have We Said It All?" In 7 th International Congress of Cardionephrology - KARNEF 2025. Punta Niš, 2025. https://doi.org/10.46793/karnef25.095d.

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Chronic kidney disease (CKD) has a strong association with increased cardiovascular (CV) risk, and residual kidney function (RKF) has recently been recognized as a key determinant of this burden. Through the removal of fluids and uremic toxins, modulation of systemic inflammation, and improved metabolic stability, RKF is linked to better cardiovascular outcomes. Despite advances in pharmacological therapies, dialysis innovation, and lifestyle interventions, patients with CKD still generally experience increased CVD mortality. This highlights the necessity of evaluating the multifactorial funct

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Bevc, Sebastjan, Tadej Petreski, Luka Varda, Nejc Piko, Robert Ekart, and Radovan Hojs. "Vitamin D and cardiorenal diseases." In 7 th International Congress of Cardionephrology - KARNEF 2025. Punta Niš, 2025. https://doi.org/10.46793/karnef25.019b.

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Vitamin D is a crucial fat-soluble compound primarily involved in maintaining calcium-phosphate balance and promoting bone health. In recent years, its broader physiological roles, particularly in cardiovascular (CV) and kidney function, have garnered significant interest. Deficiency in vitamin D is a widespread issue, affecting a large portion of the global population, and is associated with various health problems, including CV disease. Research suggests adequate vitamin D levels help preserve vascular function, reduce inflammation and fibrosis, and potentially protect against hypertension,

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Fava, A., M. Atta, J. Monroy-Trujillo, et al. "OP0228 PERSISTENCE OF URINARY BIOMARKERS OF INTRARENAL INFLAMMATION PRECEDES LOSS OF KIDNEY FUNCTION IN LUPUS NEPHRITIS." In EULAR 2024 European Congress of Rheumatology, 12-15 June. Vienna, Austria. BMJ Publishing Group Ltd and European League Against Rheumatism, 2024. http://dx.doi.org/10.1136/annrheumdis-2024-eular.3068.

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Fava, Andrea, Mohammed G. Atta, Jose Monroy Trujillo, et al. "306 Persistence of urinary biomarkers of intrarenal inflammation precedes loss of kidney function in lupus nephritis." In Lupus 21st Century 2023 Abstracts, September 27–30, Naples, Florida. Lupus Foundation of America, 2024. http://dx.doi.org/10.1136/lupus-2023-lupus21century.19.

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Fava, Andrea, Mohammed G. Atta, Jose Monroy Trujillo, et al. "O38 Persistence of urinary biomarkers of intrarenal inflammation precedes loss of kidney function in lupus nephritis." In 14th European Lupus Meeting, Bruges, Belgium, March 19–22, 2024. Lupus Foundation of America, 2024. http://dx.doi.org/10.1136/lupus-2024-el.47.

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Canaud, Bernard. "Mechanisms Supporting the Clinical Benefits of Hemodiafiltration: A Comprehensive Review." In 7th International Congress of Cardionephrology KARNEF 2025. Punta Niš, 2025. https://doi.org/10.46793/karnef25.144c.

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Background: Online hemodiafiltration (OHDF) is an advanced kidney replacement therapy (KRT) that enhances uremic toxin clearance and offers cardiovascular benefits over conventional high-flux hemodialysis (HD), provided that high convective volumes are achieved. Objective: This review examines the mechanisms underlying OHDF’s clinical and benefits and how they contribute to improve patient outcomes. Key Findings: OHDF improves vascular and cardiac health by stabilizing hemodynamics, reducing inflammation and oxidative stress, and enhancing middle- and large-molecular-weight toxin removal. Addi

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Vilacosta, Isidre. "Valvular heart disease in patients with chronic kidney disease – modern aspects of diagnosis and treatment." In 7 th International Congress of Cardionephrology - KARNEF 2025. Punta Niš, 2025. https://doi.org/10.46793/karnef25.045v.

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Valvular heart disease (VHD) is a prevalent and clinically relevant problem in patients with chronic kidney disease (CKD), particularly in those with advanced stages of renal dysfunction or on dialysis. The relationship between CKD and VHD is multifactorial and includes systemic inflammation, endothelial dysfunction, and disturbances in calcium-phosphorus metabolism, which together contribute to accelerated valvular fibrosis and calcification. As a result, patients with CKD are at increased risk of developing aortic stenosis (AS) and mitral regurgitation (MR), the two most common valvular path

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Gupta, A., K. K. Singh, S. Fatima, et al. "Platelet hyperactivation and neutrophil extracellular traps promote thrombo-inflammation and glomerular endothelial dysfunction in diabetic kidney disease." In GTH Congress 2023 – 67th Annual Meeting of the Society of Thrombosis and Haemostasis Research – The patient as a benchmark. Georg Thieme Verlag, 2023. http://dx.doi.org/10.1055/s-0042-1760477.

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Krentz, Andrew J. "Cardio-Renal-Metabolic connection – Do we have possibilities for solving this problem?" In 7th International Congress of Cardionephrology KARNEF 2025. Punta Niš, 2025. https://doi.org/10.46793/karnef25.190k.

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Within the continuum of cardiometabolic diseases, a cardiovascular-kidney-metabolic (CKM) syndrome has been conceptualised. The CKM syndrome is a systemic disorder characterised by pathophysiological interactions between metabolic risk factors, chronic kidney disease (CKD), and the cardiovascular system. CKM syndrome is characterised by multiorgan dysfunction and confers a high risk of adverse cardiovascular outcomes. Relevant haemodynamic and neurohormonal pathologies of the include the metabolic syndrome (central adiposity, insulin resistance, hypertension, hyperglycaemia, atherogenic dyslip

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Raporty organizacyjne na temat "Kidney inflammation"

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Wu, Lihua, Hongmei Lu, Ling Wu, Bo Qu, Yu Liu, and Mingquan Li. Effects of exercise on inflammation and nutrition outcomes in patients with chronic kidney disease: a protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2020. http://dx.doi.org/10.37766/inplasy2020.10.0025.

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Yu, Winifred W., Elise Digga, Courtney Luterbach, et al. Linking Dental Services to Treatment Outcomes for Chronic Kidney Disease: A Rapid Response Review. Agency for Healthcare Research and Quality, 2024. https://doi.org/10.23970/ahrqepcrapid_dental_kidney.

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Summary: Notwithstanding the gaps noted above or the heterogeneity in the studies, the patient population or periodontitis severity, there is consistent evidence showing a reduction in inflammation post-periodontal treatment in patients with CKD. The evidence for mortality and cardiovascular outcomes also offers evidence (although weak) that these outcomes may be favorable to patients with CKD in the medium term. The Centers for Disease Control recommends oral health maintenance for patients with diabetes. CKD is common in people with type 1 and type 2 diabetes. Approximately 1 in 2 adults wit

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