1,721,035 research outputs found
Acute kidney injury.
No full textAcute kidney injury is a frequent and serious complication in hospitalized patients. Mortality rates have not substantially been decreased during the last 20 years. In most patients AKI results from transient renal hypoperfusion or ischemia. The consequences include tubular cell dysfunction/damage, inflammation of the organ, and post-ischemic microvasculopathy. The two latter events perpetuate kidney damage in AKI. Clinical manifestations result from diminished excretion of water, electrolytes, and endogenous / exogenous waste products. Patients are endangered by cardiovascular complications such as hypertension, heart failure, and arrhythmia. In addition, the whole organism may be affected by systemic toxification (uremia). The diagnostic approach in AKI involves several steps with renal biopsy inevitable in some patients. The current therapy focuses on preventing further kidney damage and on treatment of complications. Different pharmacological strategies have failed to significantly improve prognosis in AKI. If dialysis treatment becomes mandatory, intermittent and continuous renal replacement therapies are equally effective. Thus, new therapies are urgently needed in order to reduce short- and long-term outcome in AKI. In this respect, stem cell-based regimens may offer promising perspectives
Akute Nierenschädigung (ANS) – Aktuelles zu (Früh)diagnostik und konservativer Therapie
No full textWas ist neu?
Epidemiologie Die Häufigkeit der akuten Nierenschädigung (ANS) nimmt auf gesamteuropäischer Ebene zu. Dabei lässt sich weltweit keine signifikante Verbesserung der Prognose feststellen.
ANS-Diagnosekriterien und neue Indikatoren der ANS Trotz intensiver Bemühungen konnte bislang kein Marker identifiziert werden, welcher die Serumkreatininkonzentration als ANS-Indikator ersetzen könnte. Mutmaßlich ist eher mit der Etablierung eines diagnostisch-prognostischen Marker-Panels bei ANS zu rechnen.
Konservative Maßnahmen mit gesichertem Nutzen Die derzeit verfügbaren konservativen Therapieempfehlungen sind in den letzten Jahren kaum durch neue Maßnahmen ergänzt worden. Kristalloide Volumenpräparate sind kolloidalen Lösungen meist vorzuziehen. Zudem sind balancierte Elektrolytlösungen Chlorid-reichen Präparationen bei drohender/manifester ANS wahrscheinlich überlegen. Im Rahmen einer jeden Volumentherapie ist eine Hyperhydratation betroffener Patienten jedoch zu vermeiden.</jats:p
Patients with limited and systemic Course of systemic Sclerosis (SS) present a perturbed Regeneration of Endothelial Progenitor Cell System
No full textInflammation and Microvasculopathy in Renal Ischemia Reperfusion Injury
Full text linkAcute renal failure (ARF) severely worsens prognosis of hospitalized patients. The most frequent cause of intrarenal ARF is transient or prolonged renal hypoperfusion (ischemia). Ischemia primarily affects the function and structure of tubular epithelial cells, which, in severe cases, is characterized by epithelial cell necrosis. Nevertheless, ischemia does not exclusively lead to alterations of epithelial cells but also causes interstitial inflammation and interstitial microvasculopathy. Both inflammation and microvasculopathy are particularly important in terms of postischemic kidney repair. Postischemic microvasculopathy is characterized by endothelial cell swelling with subsequent microvascular occlusion. Thus, reperfusion is inhibited (no-reflow phenomenon). Such endothelial cell dysfunction offers new therapeutic perspectives in ischemic ARF. Newer observations point towards the role of the so-called endothelial progenitor cells (EPCs) in the treatment of ARF. Systemic administration of EPCs to mice with bilateral renal ischemia mitigates postischemic endothelial cell dysfunction and protects animals from acute renal failure
Postischemic microvasculopathy and endothelial progenitor cell-based therapy in ischemic AKI: update and perspectives
No full textAcute kidney injury (AKI) dramatically increases mortality of hospitalized patients. Incidences have been increased in recent years. The most frequent cause is transient renal hypoperfusion or ischemia which induces significant tubular cell dysfunction/damage. In addition, two further events take place: interstitial inflammation and microvasculopathy (MV). The latter evolves within minutes to hours postischemia and may result in permanent deterioration of the peritubular capillary network, ultimately increasing the risk for chronic kidney disease (CKD) in the long term. In recent years, our understanding of the molecular/cellular processes responsible for acute and sustained microvasculopathy has increasingly been expanded. The methodical approaches for visualizing impaired peritubular blood flow and increased vascular permeability have been optimized, even allowing the depiction of tissue abnormalities in a three-dimensional manner. In addition, endothelial dysfunction, a hallmark of MV, has increasingly been recognized as an inductor of both vascular malfunction and interstitial inflammation. In this regard, so-called regulated necrosis of the endothelium could potentially play a role in postischemic inflammation. Endothelial progenitor cells (EPCs), represented by at least two major subpopulations, have been shown to promote vascular repair in experimental AKI, not only in the short but also in the long term. The discussion about the true biology of the cells continues. It has been proposed that early EPCs are most likely myelomonocytic in nature, and thus they may simply be termed proangiogenic cells (PACs). Nevertheless, they reliably protect certain types of tissues/organs from ischemia-induced damage, mostly by modulating the perivascular microenvironment in an indirect manner. The aim of the present review is to summarize the current knowledge on postischemic MV and EPC-mediated renal repair
Gelenkbeteiligung bei Akromegalie
No full textZusammenfassungDie Akromegalie ist eine seltene Erkrankung, welche in den meisten Fällen aus einer hypophysären Überproduktion von Wachstumshormon (GH – Growth Hormone) resultiert. Der in der Folge anhaltende IGF-1(Insulin like Growth Factor-1)-Exzess bewirkt zahlreiche morphologische und metabolische Veränderungen des Organismus inklusive Organomegalie, arterieller Hypertonie und Diabetes mellitus. Insbesondere die kardiovaskuläre Morbidität nimmt zu, diese ist auch hauptverantwortlich für vermehrte Sterblichkeit der Betroffenen. Wiewohl nicht prognoseentscheidend, manifestiert sich die Erkrankung gleichfalls am Bewegungsapparat. Drei Komplikationen sind relevant: eine Arthropathie größerer Gelenke, lumbale Wirbelsäulenveränderungen sowie das Karpaltunnelsyndrom. Die Behandlung dieser Komplikationen unterscheidet sich nicht von der Therapie anderer Krankheitsmanifestationen: entscheidend ist die Beseitigung des GH-/IGF-1-Exzesses. Je früher die Diagnose gestellt und die Behandlung eingeleitet wird, desto besser ist die Prognose, sind doch ossäre/artikuläre Veränderungen in vielen Fällen irreversibel.</jats:p
Weibel–Palade bodies—sentinels of acute stress
No full textWeibel-Palade bodies are uniquely present in endothelial cells and harbor a range of bioactive substances that participate in hemostasis, vasomotion, inflammation and fibrinolysis, in addition to modulating vascular permeability, angiogenic sprouting, and stem cell mobilization. this perspectives article examines the latest insights into the biogenesis of these organelles and the cellular and molecular mechanisms of their exocytosis. in addition, we advance two hypotheses on the pathogenic role of these organelles: first, in the development of endothelial dysfunction associated with the reduction of nitric oxide bioavailability and accumulation of peroxynitrite and second, as a first-line response to acute stress that determines the balance between regenerative and proinflammatory signals.NIDDK NIH HHS [DK54602, R01 DK084394, DK45462, DK052783
LDL Lipid Apheresis Rapidly Increases Peripheral Endothelial Progenitor Cell Competence
No full textBackground and Aim: Endothelial progenitor cells (EPCs) have been shown to promote neovascularization under physiologic and pathologic conditions. Statins have been documented to increase the total number of circulating EPCs in long-term treated patients. Lipid apheresis is used to treat patient with refractory hyperlipidemia. The aim of our study was to evaluate whether lipid apheresis is associated with EPC mobilization. Methods: Thirteen patients with refractory hyperlipidemia (analysis at the beginning and at the end of a single lipid apheresis treatment) and 10 healthy controls were included into the study. For quantifying total peripheral EPCs, CD133+/Flk-1+ myelo-monocytic blood cells were enumerated by flow cytometry. The proliferative potential of EPCs was evaluated by a "colony-forming unit" assay. In some patients, EPC eNOS expression was evaluated before and after treatment. Results: Circulating EPCs and the cells' proliferative activity were lower in hyperlipidemia patients as compared to controls (0.14 +/- 0.07 vs. 0.6 +/- 0.14, P = 0.01, and 13.9 +/- 4.9 vs. 45.6 +/- + 8.1. P = 0.0007). Lipid apheresis treatment was not associated with an increase in total EPCs. The cells' proliferative activity was strongly stimulated by lipid apheresis as reflected by an increase in the number of EPC colonies (13.9 +/- 4.9 to 34.1 +/- 7.1 P = 0.035). Analysis of EPC eNOS expression revealed a threefold increase in the cellular expression intensity after lipid apheresis. Conclusions: Patients with refractory hyperlipidemia exhibit lower peripheral EPC numbers and a lower proliferative activity of circulating EPCs than healthy controls. A single lipid apheresis treatment significantly stimulates EPC proliferation. it furthermore increases cellular eNOS. In summary, these results show that lipid apheresis mediates beneficial effects on the EPC system as an essential element in the process of vascular repair in the human organism. J. Clin. Apheresis 24:180-185. 2009. (C) 2009 Wiley-Liss, Inc.Deutsche Forschungsgemeinschaft [PA1530/2-1, PA1530/3-1
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