Academic literature on the topic 'Diabetic nephropathies Pathophysiology'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Contents
Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Diabetic nephropathies Pathophysiology.'
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.
Journal articles on the topic "Diabetic nephropathies Pathophysiology"
1
Wenzel, René R., Eberhard Ritz, and Maximilian Q. Wenzel. "Endothelin Receptor Antagonists in Diabetic Nephropathy." European Endocrinology 8, no. 1 (2010): 32. http://dx.doi.org/10.17925/ee.2012.08.01.32.
Full textAbstract:
Diabetic nephropathy (DN) is the leading cause of end-stage renal disease and affects an estimated 150 million people worldwide. Despite optimal treatment, including glycaemic control and antihypertensive therapy (e.g., renin–angiotensin–aldosterone system [RAS] blockade), the disease progresses. A ‘late escape’ phenomenon has been described, where proteinuria reappears despite continued RAS blockade. The endothelin (ET) system is strongly involved in the pathophysiology of the disease and contributes to vasoconstriction, inflammation and proliferation. ET antagonists are promising drugs that potently slow down disease progression in animal models and have beneficial effects on cardiac structure, mitochondrial damage and microvascular architecture. However, the available ET antagonists, at least in higher doses, may also inhibit tubular endothelin receptors subtype B, which promote sodium and water excretion. The three clinical trials with avosentan and atrasentan published so far show the unique nephroprotective effects of these drugs, with a reduction of up to 45 % in albuminuria. However, fluid retention, oedema and, in higher stages of chronic kidney disease, heart failure limit their use. The reason may be that we have been using too high doses of these ET antagonists so far and they are inhibiting tubular sodium and water excretion. Thus, we will need to learn more about the role of ET and its antagonists in the tubular and collecting duct system, and on how to use these potent drugs in DN. ET antagonists are among the most promising molecules for the treatment of nephropathies. We should definitely not abandon these drugs because of the initial drawbacks in the first clinical trials.
2
Bohlender, Jürgen M., Sybille Franke, Günter Stein, and Gunter Wolf. "Advanced glycation end products and the kidney." American Journal of Physiology-Renal Physiology 289, no. 4 (October 2005): F645—F659. http://dx.doi.org/10.1152/ajprenal.00398.2004.
Full textAbstract:
Advanced glycation end products (AGEs) are a heterogeneous group of protein and lipids to which sugar residues are covalently bound. AGE formation is increased in situations with hyperglycemia (e.g., diabetes mellitus) and is also stimulated by oxidative stress, for example in uremia. It appears that activation of the renin-angiotensin system may contribute to AGE formation through various mechanisms. Although AGEs could nonspecifically bind to basement membranes and modify their properties, they also induce specific cellular responses including the release of profibrogenic and proinflammatory cytokines by interacting with the receptor for AGE (RAGE). However, additional receptors could bind AGEs, adding to the complexity of this system. The kidney is both: culprit and target of AGEs. A decrease in renal function increases circulating AGE concentrations by reduced clearance as well as increased formation. On the other hand, AGEs are involved in the structural changes of progressive nephropathies such as glomerulosclerosis, interstitial fibrosis, and tubular atrophy. These effects are most prominent in diabetic nephropathy, but they also contribute to renal pathophysiology in other nondiabetic renal diseases. Interference with AGE formation has therapeutic potential for preventing the progression of chronic renal diseases, as shown from data of animal experiments and, more recently, the first clinical trials.
3
Lin, Tien-An, Victor Chien-Chia Wu, and Chao-Yung Wang. "Autophagy in Chronic Kidney Diseases." Cells 8, no. 1 (January 16, 2019): 61. http://dx.doi.org/10.3390/cells8010061.
Full textAbstract:
Autophagy is a cellular recycling process involving self-degradation and reconstruction of damaged organelles and proteins. Current evidence suggests that autophagy is critical in kidney physiology and homeostasis. In clinical studies, autophagy activations and inhibitions are linked to acute kidney injuries, chronic kidney diseases, diabetic nephropathies, and polycystic kidney diseases. Oxidative stress, inflammation, and mitochondrial dysfunction, which are implicated as important mechanisms underlying many kidney diseases, modulate the autophagy activation and inhibition and lead to cellular recycling dysfunction. Abnormal autophagy function can induce loss of podocytes, damage proximal tubular cells, and glomerulosclerosis. After acute kidney injuries, activated autophagy protects tubular cells from apoptosis and enhances cellular regeneration. Patients with chronic kidney diseases have impaired autophagy that cannot be reversed by hemodialysis. Multiple nephrotoxic medications also alter the autophagy signaling, by which the mechanistic insights of the drugs are revealed, thus providing the unique opportunity to manage the nephrotoxicity of these drugs. In this review, we summarize the current concepts of autophagy and its molecular aspects in different kidney cells pathophysiology. We also discuss the current evidence of autophagy in acute kidney injury, chronic kidney disease, toxic effects of drugs, and aging kidneys. In addition, we examine therapeutic possibilities targeting the autophagy system in kidney diseases.
4
Erley, Christiane, and Anett Hotzwik. "Diabetische Nephropathie." Diabetes aktuell 19, no. 07 (November 2021): 304–10. http://dx.doi.org/10.1055/a-1646-0266.
Full textAbstract:
ZUSAMMENFASSUNGDie diabetische Nephropathie stellt in Deutschland nach wie vor eine der Hauptursachen für eine terminale Niereninsuffizienz dar. Ca. 40 % der an Diabetes Erkrankten entwickeln einen Nierenfunktionsverlust. ⅓ der Dialysepatienten sind Diabetiker. Risikofaktoren wie Alter, Geschlecht, Bluthochdruck, Hyperlipidämie, Rauchen und Adipositas begünstigen die Manifestation einer Nephropathie und steigern die Progression der Niereninsuffizienz sowie das Risiko ein kardiovaskuläres Ereignis zu erleiden und frühzeitig zu versterben. Die histopathologische Einteilung der diabetischen Nephropathie ist von prognostischer Bedeutung. Ein besseres Verständnis der Pathophysiologie, der Einfluss genetischer und nichtgenetischer Faktoren auf die Entstehung und Progression der diabetischen Nephropathie lassen neue Therapieansätze entstehen mit dem Ziel, die Progression der diabetischen Nephropathie und die darunter deutlich höhere kardiovaskuläre Mortalität zu beeinflussen.
5
Scurt, Florian Gunnar, Katrin Bose, Ali Canbay, Peter R. Mertens, and Christos Chatzikyrkou. "Ursachen der chronischen Nierenschädigung in Patienten mit Lebererkrankungen – Pathophysiologie und Therapiemöglichkeiten." Zeitschrift für Gastroenterologie 59, no. 06 (March 16, 2021): 560–79. http://dx.doi.org/10.1055/a-1402-1502.
Full textAbstract:
ZusammenfassungEine akute oder chronische Nierenschädigung bei gleichzeitig bestehender Lebererkrankung stellt ein häufiges Problem dar und geht im weiteren klinischen Verlauf mit zahlreichen Komplikationen sowie einer gesteigerten Dialysepflichtigkeit und Mortalität einher.Die Prävalenz einer chronischen Niereninsuffizienz (CNI) bei Patienten mit Lebererkrankungen ist hoch, nicht zuletzt wegen parallel bestehender Komorbiditäten (z. B. metabolisches Syndrom, chronische Entzündungsprozesse, Hyperkoagulabilität, Hyperfibrinolyse, Diabetes mellitus, Dyslipidämie usw.). Doch nicht jede chronische Verschlechterung der Nierenretentionsparameter lässt sich auf ein hepatorenales Syndrom zurückführen. Neben diesem sind die häufigsten Ursachen der CNI bei bestehenden Lebererkrankungen die diabetische Nephropathie, die alkoholassoziierte IgA-Nephropathie, die mit Hepatitis C assoziierte membranoproliferative Glomerulonephritis und die mit Hepatitis B assoziierte membranöse Glomerulonephritis.Koexistente Erkrankungen, ähnlich bzw. parallel ablaufende pathophysiologische Mechanismen und überlappende Erscheinungsbilder stellen hinsichtlich der Ursachenfindung und entsprechenden Behandlung der CNI im Rahmen einer existenten Lebererkrankung eine Herausforderung an den Kliniker dar. Diese Übersichtsarbeit skizziert sowohl häufige als auch seltene Entitäten, die zu einer chronischen Nierenschädigung in diesem speziellen Patientenkollektiv führen, und zeigt einen Überblick zu therapeutischen Möglichkeiten.
6
Bourlier, Virginie, Caroline Conte, Colette Denis, Cédric Dray, Pascale Guillou, Manuela Belliure, Anne Lorsignol, Marion Noël, and Bénédicte Buffin-Meyer. "Collective and experimental research project for master’s students on the pathophysiology of obesity." Advances in Physiology Education 41, no. 4 (December 1, 2017): 505–13. http://dx.doi.org/10.1152/advan.00147.2016.
Full textAbstract:
We describe here a collective and experimental research project-based learning (ERPBL) for master’s students that can be used to illustrate some basic concepts on glucose/lipid homeostasis and renal function around a topical issue. The primary objective of this ERPBL was to strengthen students’ knowledge and understanding of physiology and pathophysiology. The secondary objectives were to help students to develop technical/practical abilities and acquire transversal skills with real-world connections. Obesity is a worldwide public health problem that increases the risk for developing type 2 diabetes and nephropathies. To study the impact of western dietary habits, students evaluated the effects of a diet enriched with fat and cola [high-fat and cola diet (HFCD)] on metabolism and renal function in mice. Students mainly worked in tandem to prepare and perform experiments, but also collectively to compile, analyze, and discuss data. Students showed that HFCD-fed mice 1) developed obesity; 2) exhibited glucose homeostasis impairments associated to ectopic fat storage; and 3) displayed reduced glomerular filtration. The educational benefit of the program was estimated using three evaluation metrics: a conventional multicriteria assessment by teachers, a pre-/posttest, and a self-evaluation questionnaire. They showed that the current approach successfully strengthened scientific student knowledge and understanding of physiology/pathophysiology. In addition, it helped students develop new skills, such as technical and transversal skills. We concluded that this ERPBL dealing with the pathophysiology of obesity was strongly beneficial for master’s students, thereby appearing as an efficient and performing educational tool.
7
Steffes, M. W., and S. M. Mauer. "Diabetic nephropathy: a disease causing and complicated by hypertension." Clinical Chemistry 37, no. 10 (October 1, 1991): 1838–42. http://dx.doi.org/10.1093/clinchem/37.10.1838.
Full textAbstract:
Abstract In examining the pathophysiology underlying the development of hypertension in diabetes mellitus, it is important to draw clear distinctions between Type I and Type II diabetes. In patients with Type I diabetes, with a peak onset of disease early in the second decade of life, hypertension clearly represents the sequelae to the development of substantial renal lesions, especially in the glomerulus. Thus the prevalence of hypertension in those patients without substantial glomerular lesions approximates the incidence of hypertension in the general population (approximately 4%). In patients with Type II diabetes mellitus and onset generally later in adult life, an increase in blood pressure can often be demonstrated early after or even before diagnosis of the disease (most readily demonstrated in the Pima Indians). Furthermore, clear familial tendencies towards the development of nephropathic complications of diabetes can be shown. In patients with Type I disease, the fall in glomerular filtration rate parallels the fall in glomerular capillary surface available for filtration. This reduction in the peripheral glomerular capillary surface correlates well with the expansion of the mesangium, strongly implicating the mesangial expansion in the demise in renal function. For both Type I and Type II diabetes mellitus, the increase in albuminuria may reflect an opening of large pores in the glomerular basement membrane, thereby allowing serum proteins to cross into the filtration space.
8
Scurt, Florian Gunnar, Katrin Bose, Ali Canbay, Peter R. Mertens, and Christos Chatzikyrkou. "Paradigmenwechsel im Verständnis der akuten Nierenschädigung bei chronischer Leberinsuffizienz: Von der Pathophysiologie zur Definition von Krankheitsentitäten." Zeitschrift für Gastroenterologie 58, no. 03 (March 2020): 254–66. http://dx.doi.org/10.1055/a-1088-1582.
Full textAbstract:
ZusammenfassungSeit den ersten Beschreibungen von Patienten mit Aszites und fortgeschrittener Leberzirrhose durch Helvig und Schutz in den 1930er- und weiteren Obduktionsstudien von Hecker und Sherlock in den 1960er-Jahren wird das gleichzeitige Vorliegen einer Nierenfunktionsstörung als hepatorenales Syndrom (HRS) bezeichnet. Forschungsarbeiten der letzten Jahre liefern Hinweise, dass insbesondere systemische Entzündungsreaktionen einen kritischen Punkt in der Pathogenese der dekompensierten Leberzirrhose darstellen und maßgeblich an der Entstehung eines akut-auf-chronischen Leberversagens (ACLF) und einer Nierenfunktionsstörung beteiligt sind.Das HRS ist nur ein Aspekt des Spektrums der Nierenschädigung in Zirrhosepatienten. Die fortgeschrittene chronische Lebererkrankung per se bzw. ihre Ätiologie, aber auch weitere begleitende komorbide systemische Erkrankungen bzw. deren Komplikationen wie Diabetes, Adipositas und Hypertonie können direkt zu parenchymatösen Veränderungen (z. B. Gallensäurenephropathie, ischämische Tubulusepithelzellnekrose, diabetische Nephropathie, Glomerulonephritiden assoziiert mit Hepatitis B und C usw.) führen. Diese Art der Nierenschädigung wird deskriptiv als Non-HRS-AKI bezeichnet.In der vorliegenden Übersicht konzentrieren wir uns auf die neue Definition, Klassifikation und die zugrunde liegenden pathophysiologischen Mechanismen für das HRS, HRS-AKI und Non-HRS-AKI und untersuchen in dieser Hinsicht den diagnostischen und prognostischen Stellenwert neuerer Serum- und Urinmarker.
9
Feng, Ying, Ming-yue Jin, Dong-wei Liu, and Li Wei. "Proteasome subunit-α type-6 protein is post-transcriptionally repressed by the microRNA-4490 in diabetic nephropathy." Bioscience Reports 38, no. 5 (October 31, 2018). http://dx.doi.org/10.1042/bsr20180815.
Full textAbstract:
A common complication of both type I and type II diabetes is nephropathy, characterized by accumulation of extracellular matrix in the glomerular mesangium. This indicates a central role of mesangial cells in the pathophysiology of diabetic nephropathy. Using the proteomic approach, it was earlier elucidated in a rat model that the proteasome subunit-α type-6 protein (PSMA6) is suppressed in the renal cortex in nephropathic kidney. However, the underlying mechanism effecting suppression of PSMA6 protein in the renal cortex is not yet known. Twenty diabetic patients were enrolled and the expression level of PSMA6 in them was detected by immunohistochemistry. The protein and mRNA expression levels of PSMA6 in NRK-52E cells under high glucose condition were determined by Western blot and quantitative real-time PCR, respectively. Dual luciferase assay was used to detect the relationship of PSMA6 and miR-4490. Our results show that PSMA6 protein is down-regulated in patients with diabetic nephropathy compared with healthy control. Using the NRK-52E cell line cultured under high glucose condition as an in vitro model of diabetic nephropathy, we show that loss of PSMA6 protein expression occured independent of changes the in PSMA6 mRNA expression. We next elucidate that PSMA6 mRNA is post-transcriptionally regulated by the microRNA (miRNA)-4490, whose expression is inversely correlated to PSMA6 protein expression. Using reporter assays we show that PSMA6 is a direct target of the miR-4490. Exogenous manipulation of miR-4490 levels modulated expression of PSMA6, indicating that miR-4490 can be tested as a biomarker for nephropathy in diabetic patients.
10
Singh, Shailendra Pratap, Aayushi Bhatnagar, Sujeet Kumar Singh, Sanjib K. Patra, Navjot Kanwar, Abhinav Kanwal, Salomon Amar, and Ranata Manna. "SARS-CoV-2 Infections, Impaired Tissue, and Metabolic Health: Pathophysiology and Potential Therapeutics." Mini-Reviews in Medicinal Chemistry 22 (February 1, 2022). http://dx.doi.org/10.2174/1389557522666220201154845.
Full textAbstract:
Abstract: The SARS-CoV-2 enters the human airways and comes into contact with the mucous membranes lining the mouth, nose, and eyes. The virus enters the healthy cells and uses cell machinery to make several copies of the virus. Critically ill patients infected with SARS-CoV-2 may have damaged lungs, air sacs, lining, and walls. Since COVID-19 causes cytokine storm, it damages the alveolar cells of the lungs and fills them with fluid, making it harder to exchange oxygen and carbon dioxide. The SARS-CoV-2 infection causes a range of complications, including mild to critical breathing difficulties. It has been observed that older people suffering from health conditions like cardiomyopathies, nephropathies, metabolic syndrome, and diabetes instigate severe symptoms. Many people who died due to COVID-19 had impaired metabolic health [IMH], characterized by hypertension, dyslipidemia, and hyperglycemia, i.e., diabetes, cardiovascular system, and renal diseases making their retrieval challenging. Jeopardy stresses for increased mortality from COVID-19 include older age, COPD, ischemic heart disease, diabetes mellitus, and immunosuppression. However, no targeted therapies are available as of now. Almost two-thirds of diagnosed coronavirus patients had cardiovascular diseases and diabetes, out of which 37% were under 60. The NHS audit revealed that with a higher expression of ACE-2 receptors, viral particles could easily bind their protein spikes and get inside the cells, finally causing COVID-19 infection. Hence, people with IMH are more prone to COVID-19 and, ultimately, comorbidities. This review provides enormous information about tissue [lungs, heart and kidneys] damage, pathophysiological changes, and impaired metabolic health of SARS-CoV-2 infected patients. Moreover, it also designates the possible therapeutic targets of COVID-19 and drugs which can be used against these targets.
Books on the topic "Diabetic nephropathies Pathophysiology"
1
(Editor), Angela D'Angelo, Silvana Favaro (Editor), and Giovanni Gambaro (Editor), eds. Advanced Glycation End Products in Nephrology: Meeting on Advanced Glycosylation End-Products in Nephrology: Much More Than Diabetic Nephropathy, Padua, ... Padua, Italy (Contributions to Nephrology). S. Karger Publishers (USA), 2000.
Find full textConference papers on the topic "Diabetic nephropathies Pathophysiology"
1
Albrecht, M., C. Sticht, C. De La Torre, J. Qiu, S. Hettler, N. Kretz, B. Yard, BK Garvalov, and JP Sleeman. "Der Einfluss von Hyperglykämie- sowie Methylglyoxal- induziertem Stress auf die Genexpression co-kultivierter Podozyten und glomerulärer Endothelzellen in der Pathophysiologie der Diabetischen Nephropathie." In Diabetes Kongress 2021 – 55. Jahrestagung der DDG. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1727476.
Full text