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Статті в журналах з теми "Uraemic toxins"
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Bowry, Sudhir K., Peter Kotanko, Rainer Himmele, Xia Tao, and Michael Anger. "The membrane perspective of uraemic toxins: which ones should, or can, be removed?" Clinical Kidney Journal 14, Supplement_4 (December 2021): i17—i31. http://dx.doi.org/10.1093/ckj/sfab202.
Повний текст джерелаАнотація:
ABSTRACT Informed decision-making is paramount to the improvement of dialysis therapies and patient outcomes. A cornerstone of delivery of optimal dialysis therapy is to delineate which substances (uraemic retention solutes or ‘uraemic toxins’) contribute to the condition of uraemia in terms of deleterious biochemical effects they may exert. Thereafter, decisions can be made as to which of the accumulated compounds need to be targeted for removal and by which strategies. For haemodialysis (HD), the non-selectivity of membranes is sometimes considered a limitation. Yet, considering that dozens of substances with potential toxicity need to be eliminated, and targeting removal of individual toxins explicitly is not recommended, current dialysis membranes enable elimination of several molecules of a broad size range within a single therapy session. However, because HD solute removal is based on size-exclusion principles, i.e. the size of the substances to be removed relative to the mean size of the ‘pores’ of the membrane, only a limited degree of selectivity of removal is possible. Removal of unwanted substances during HD needs to be weighed against the unavoidable loss of substances that are recognized to be necessary for bodily functions and physiology. In striving to improve the efficiency of HD by increasing the porosity of membranes, there is a greater potential for the loss of substances that are of benefit. Based on this elementary trade-off and availability of recent guidance on the relative toxicity of substances retained in uraemia, we propose a new evidence-linked uraemic toxin elimination (ELUTE) approach whereby only those clusters of substances for which there is a sufficient body of evidence linking them to deleterious biological effects need to be targeted for removal. Our approach involves correlating the physical properties of retention solutes (deemed to express toxicity) with key determinants of membranes and separation processes. Our analysis revealed that in attempting to remove the relatively small number of ‘larger’ substances graded as having only moderate toxicity, uncontrolled (and efficient) removal of several useful compounds would take place simultaneously and may compromise the well-being or outcomes of patients. The bulk of the uraemic toxin load comprises uraemic toxins below <30 000 Da and are adequately removed by standard membranes. Further, removal of a few difficult-to-remove-by-dialysis (protein-bound) compounds that express toxicity cannot be achieved by manipulation of pore size alone. The trade-off between the benefits of effective removal of the bulk of the uraemic toxin load and risks (increased loss of useful substances) associated with targeting the removal of a few larger substances in ‘high-efficiency’ HD treatment strategies needs to be recognized and better understood. The removability during HD of substances, be they toxic, inert or beneficial, needs be revised to establish the pros and cons of current dialytic elimination strategies.
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Wang, Xifan, Songtao Yang, Shenghui Li, Liang Zhao, Yanling Hao, Junjie Qin, Lian Zhang, et al. "Aberrant gut microbiota alters host metabolome and impacts renal failure in humans and rodents." Gut 69, no. 12 (April 2, 2020): 2131–42. http://dx.doi.org/10.1136/gutjnl-2019-319766.
Повний текст джерелаАнотація:
ObjectivePatients with renal failure suffer from symptoms caused by uraemic toxins, possibly of gut microbial origin, as deduced from studies in animals. The aim of the study is to characterise relationships between the intestinal microbiome composition, uraemic toxins and renal failure symptoms in human end-stage renal disease (ESRD).DesignCharacterisation of gut microbiome, serum and faecal metabolome and human phenotypes in a cohort of 223 patients with ESRD and 69 healthy controls. Multidimensional data integration to reveal links between these datasets and the use of chronic kidney disease (CKD) rodent models to test the effects of intestinal microbiome on toxin accumulation and disease severity.ResultsA group of microbial species enriched in ESRD correlates tightly to patient clinical variables and encode functions involved in toxin and secondary bile acids synthesis; the relative abundance of the microbial functions correlates with the serum or faecal concentrations of these metabolites. Microbiota from patients transplanted to renal injured germ-free mice or antibiotic-treated rats induce higher production of serum uraemic toxins and aggravated renal fibrosis and oxidative stress more than microbiota from controls. Two of the species, Eggerthella lenta and Fusobacterium nucleatum, increase uraemic toxins production and promote renal disease development in a CKD rat model. A probiotic Bifidobacterium animalis decreases abundance of these species, reduces levels of toxins and the severity of the disease in rats.ConclusionAberrant gut microbiota in patients with ESRD sculpts a detrimental metabolome aggravating clinical outcomes, suggesting that the gut microbiota will be a promising target for diminishing uraemic toxicity in those patients.Trial registration numberThis study was registered at ClinicalTrials.gov (NCT03010696).
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Liabeuf, Sophie, Cédric Villain, and Ziad A. Massy. "Protein-bound toxins: has the Cinderella of uraemic toxins turned into a princess?" Clinical Science 130, no. 23 (October 31, 2016): 2209–16. http://dx.doi.org/10.1042/cs20160393.
Повний текст джерелаАнотація:
Chronic kidney disease (CKD) has emerged as a global public health problem. Although the incidence and prevalence of CKD vary from one country to another, the estimated worldwide prevalence is 8–16%. The complications associated with CKD include progression to end-stage renal disease (ESRD), mineral and bone disorders, anaemia, cognitive decline and elevated all-cause and cardiovascular (CV) mortality. As a result of progressive nephron loss, patients with late-stage CKD are permanently exposed to uraemic toxins. These toxins have been classified into three groups as a function of the molecular mass: small water-soluble molecules, middle molecules and protein-bound uraemic toxins. The compounds can also be classified according to their origin (i.e. microbial or not) or their protein-binding ability. The present review will focus on the best-characterized protein-bound uraemic toxins, namely indoxylsulfate (IS), indole acetic acid (IAA) and p-cresylsulfate (PCS, a cresol metabolite). Recent research suggests that these toxins accelerate the progression of CV disease, kidney disease, bone disorders and neurological complications. Lastly, we review therapeutic approaches that can be used to decrease toxin levels.
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Massy, Ziad A., and Sophie Liabeuf. "From old uraemic toxins to new uraemic toxins: place of ‘omics’." Nephrology Dialysis Transplantation 33, suppl_3 (October 1, 2018): iii2—iii5. http://dx.doi.org/10.1093/ndt/gfy212.
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Vanholder, R. "Uraemic toxins and cardiovascular disease." Nephrology Dialysis Transplantation 18, no. 3 (March 1, 2003): 463–66. http://dx.doi.org/10.1093/ndt/18.3.463.
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Capeillère-Blandin, Chantal, Valérie Gausson, Anh Thu Nguyen, Béatrice Descamps-Latscha, Tilman Drüeke, and Véronique Witko-Sarsat. "Respective role of uraemic toxins and myeloperoxidase in the uraemic state." Nephrology Dialysis Transplantation 21, no. 6 (February 13, 2006): 1555–63. http://dx.doi.org/10.1093/ndt/gfl007.
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Masereeuw, Rosalinde, and Marianne C. Verhaar. "Innovations in approaches to remove uraemic toxins." Nature Reviews Nephrology 16, no. 10 (May 7, 2020): 552–53. http://dx.doi.org/10.1038/s41581-020-0299-0.
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YE, C., Q. GONG, F. LU, and J. LIANG. "Adsorption of uraemic toxins on carbon nanotubes." Separation and Purification Technology 58, no. 1 (December 1, 2007): 2–6. http://dx.doi.org/10.1016/j.seppur.2007.07.003.
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Bowry, Sudhir K., Fatih Kircelli, Mooppil Nandakumar, and Tushar J. Vachharajani. "Clinical relevance of abstruse transport phenomena in haemodialysis." Clinical Kidney Journal 14, Supplement_4 (December 2021): i85—i97. http://dx.doi.org/10.1093/ckj/sfab183.
Повний текст джерелаАнотація:
ABSTRACT Haemodialysis (HD) utilizes the bidirectional properties of semipermeable membranes to remove uraemic toxins from blood while simultaneously replenishing electrolytes and buffers to correct metabolic acidosis. However, the nonspecific size-dependent transport across membranes also means that certain useful plasma constituents may be removed from the patient (together with uraemic toxins), or toxic compounds, e.g. endotoxin fragments, may accompany electrolytes and buffers of the dialysis fluids into blood and elicit severe biological reactions. We describe the mechanisms and implications of these undesirable transport processes that are inherent to all HD therapies and propose approaches to mitigate the effects of such transport. We focus particularly on two undesirable events that are considered to adversely affect HD therapy and possibly impact patient outcomes. Firstly, we describe how loss of albumin (and other essential substances) can occur while striving to eliminate larger uraemic toxins during HD and why hypoalbuminemia is a clinical condition to contend with. Secondly, we describe the origins and mode of transport of biologically active substances (from dialysis fluids with bacterial contamination) into the blood compartment and biological reactions they elicit. Endotoxin fragments activate various proinflammatory pathways to increase the underlying inflammation associated with chronic kidney disease. Both phenomena involve the physical as well as chemical properties of membranes that must be selected judiciously to balance the benefits with potential risks patients may encounter, in both the short and long term.
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Xiong, Siyu, Yaxuan Lyu, Andrew Davenport, and Kwang Leong Choy. "Sponge-like Chitosan Based Porous Monolith for Uraemic Toxins Sorption." Nanomaterials 11, no. 9 (August 30, 2021): 2247. http://dx.doi.org/10.3390/nano11092247.
Повний текст джерелаАнотація:
More than three million patients are treated for kidney failure world-wide. Haemodialysis, the most commonly used treatment, requires large amounts of water and generates mountains of non-recyclable plastic waste. To improve the environmental footprint, dialysis treatments need to develop absorbents to regenerate the waste dialysate. Whereas conventional dialysis clears water-soluble toxins, it is not so effective in clearing protein-bound uraemic toxins (PBUTs), such as indoxyl sulfate (IS). Thus, developing absorption devices to remove both water-soluble toxins and PBUTs would be advantageous. Vapour induced phase separation (VIPS) has been used in this work to produce polycaprolactone/chitosan (PCL/CS) composite symmetric porous monoliths with extra porous carbon additives to increase creatinine and albumin-bound IS absorption. Moreover, these easy-to-fabricate porous monoliths can be formed into the required geometry. The PCL/CS porous monoliths absorbed 436 μg/g of albumin-bound IS and 2865 μg/g of creatinine in a single-pass perfusion model within 1 h. This porous PCL/CS monolith could potentially be used to absorb uraemic toxins, including PBUTs, and thus allow the regeneration of waste dialysate and the development of a new generation of environmentally sustainable dialysis treatments, including wearable devices.
Дисертації з теми "Uraemic toxins"
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Sen, Shaundeep. "Endothelial progenitor cells, uraemic toxins, and the development of endothelial dysfunction in chronic kidney disease." Thesis, 2012. http://hdl.handle.net/2440/83511.
Повний текст джерелаАнотація:
Morbidity and mortality rates for cardiovascular disease (CVD) are increased among end stage kidney disease (ESKD) patients receiving dialysis treatment, and not corrected with kidney transplantation (KTx). Classic CVD risk factors do not fully predict the increased risk, with novel factors causing endothelial dysfunction (ED), leading to arteriosclerosis, congestive heart failure (CHF) and sudden death, key to disease pathogenesis. These novel factors include bone marrow (BM) derived endothelial progenitor cells (EPCs), which have key roles in maintenance, repair and growth of the endothelium. There is limited data about the role of EPCs and CVD in the ESKD population. This uraemic milieu includes p-cresol (sulfate, PC/S) and indoxyl sulfate (IS), toxins associated with CVD in ESKD. In this thesis, the relationship between CVD and ESKD, and the potential role of EPCs and uraemic toxins was examined from epidemiological, clinical and laboratory perspectives. Data was obtained for the period between 2002-2007 for all hospital separations in Australia. Analysis was performed based on ICD-9/10 coding. This showed (for the first time in an Australian population): (i) an increase in risk for CVD hospital separations among dialysis and KTx, with higher rates for CHF than acute cardiac events (ACE); (ii) an advantage for KTx recipients in regards to ACE, but not CHF hospital separations, over dialysis recipients, and (iii) for CHF, no increase in in-hospital mortality, or length of stay per separation for any ESKD group compared to controls. At a clinical level, in groups of haemodialysis (HDx), KTx patients and controls, low peripheral blood (PB) EPC numbers were correlated with surrogate markers of CVD and ED. No clear relationship of IS and PC/S with ED was seen (although study power was limited). For in vitro studies, techniques were developed for isolation (Flow sort and AutoMACS), enumeration (FACS) and culture expansion of EPCs from BM and umbilical cord blood samples. The effects of uraemic serum and toxins PC and IS on cultured endothelial cells (ECs) and EPCs in vitro was examined, as a model of vascular pathology in ESKD. Greater HUVEC VCAM-1 expression and reduced tube formation in Matrigel were observed in response to increasing PC concentration than IS. The effect of IS (but not PC) at higher concentration in Matrigel was reduced by the addition of EPCs. Akt/ERK expression by western blot, cell migration to VEGF, and supernatant investigation by FlowCytoMix for soluble cell surface markers, were also performed. Testing of HUVEC function post-exposure to sera from control, transplant and HDx recipients did not replicate the above results on the basis of sera PC and IS levels. In summary, this thesis has explored the increased burden of CVD in ESKD patients in Australia, the relationship of EPCs, both in vivo and in vitro, to vascular disease in this setting, and the role of uraemic toxins as agents for CVD. These results underline why certain therapies may not be effective in the ESKD population for CVD prevention, and suggest novel approaches are needed.Thesis (Ph.D.) -- University of Adelaide, School of Medicine, 2012
Книги з теми "Uraemic toxins"
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Glorieux, Griet, Nathalie Neirynck, Anneleen Pletinck, Eva Schepers, and Raymond Vanholder. Overview of uraemic toxins. Edited by Jonathan Himmelfarb. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0254_update_001.
Повний текст джерелаАнотація:
The uraemic syndrome is a complex mixture of organ dysfunctions attributed to the retention of a multitude of compounds that under normal conditions are excreted by healthy kidneys. Although important progress has been made in the identification and characterization of uraemic retention solutes and in the revealing of their pathophysiological effects, this knowledge remains far from complete. Data are discussed on general characteristics of specific uraemic retention solutes, on in vitro and in vivo biological effects and on available observational and interventional studies with respect to their removal and related patient outcome are discussed.
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Noris, Marina, and Tim Goodship. The patient with haemolytic uraemic syndrome/thrombotic thrombocytopenic purpura. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0174.
Повний текст джерелаАнотація:
The patient who presents with microangiopathic haemolytic anaemia, thrombocytopenia, and evidence of acute kidney injury presents a diagnostic and management challenge. Haemolytic uraemic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP) are two of the conditions that frequently present with this triad. They are characterized by low platelet count with normal or near-normal coagulation tests, anaemia, and signs of intravascular red cell fragmentation on blood films, and high LDH levels.HUS associated with shiga-like toxins produced usually by E.coli (typically O157 strains) may occur in outbreaks or sporadically, with geographical variations in incidence. It is predominantly a disease of young children in which painful blood diarrhoea in a minority of infected patients is succeeded by microangiopathy and acute kidney injury. Management is supportive and recovery is usual, although permanent renal damage may lead to later deterioration. Older patients may be affected and tend to have worse outcomes. Neuraminidase-producing Streptococcus pneumoniae infections (usually pneumonia) very rarely cause a similar HUS.Atypical HUS occurs sporadically and is increasingly associated with defects in the regulation of the complement pathway, either genetic or autoimmune-caused. It may respond to plasma exchange for fresh frozen plasma. Recurrences are common, including after transplantation.TTP is associated with more neurological disease and less renal involvement, but HUS and TTP overlap substantially in their manifestations. The underlying problem is in von Willebrand factor (vWF) cleavage. The plasma metalloprotease ADAMTS13 is responsible for cleaving vWF multimers, a process that is important to prevent thrombosis in the microvasculature. Autoantibodies or rarely genetic deficiency may impair this process. Plasma exchange may remove antibodies and replenish the protease.
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Sever, Mehmet Şükrü, and Raymond Vanholder. Acute kidney injury in polytrauma and rhabdomyolysis. Edited by Norbert Lameire. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0252_update_001.
Повний текст джерелаАнотація:
The term ‘polytrauma’ refers to blunt (or crush) trauma that involves multiple body regions or cavities, and compromises physiology to potentially cause dysfunction of uninjured organs. Polytrauma frequently affects muscles resulting in rhabdomyolysis. In daily life, it mostly occurs after motor vehicle accidents, influencing a limited number of patients; after mass disasters, however, thousands of polytrauma victims may present at once with only surgical features or with additional medical complications (crush syndrome). Among the medical complications, acute kidney injury (AKI) deserves special mention, since it is frequent and has a substantial impact on the ultimate outcome.Several factors play a role in the pathogenesis of polytrauma (or crush)-induced AKI: (1) hypoperfusion of the kidneys, (2) myoglobin-induced direct nephrotoxicity, and intratubular obstruction, and also (3) several other mechanisms (i.e. iron and free radical-induced damage, disseminated intravascular coagulation, and ischaemia reperfusion injury). Crush-related AKI is prerenal at the beginning; however, acute tubular necrosis may develop eventually. In patients with crush syndrome, apart from findings of trauma, clinical features may include (but are not limited to) hypotension, oliguria, brownish discoloration of urine, and other symptoms and findings, such as sepsis, acute respiratory distress syndrome, disseminated intravascular coagulation, bleeding, cardiac failure, arrhythmias, electrolyte disturbances, and also psychological trauma.In the biochemical evaluation, life-threatening hyperkalaemia, retention of uraemic toxins, high anion gap metabolic acidosis, elevated serum levels of myoglobin, and muscle enzymes are noted; creatine phosphokinase is very useful for diagnosing rhabdomyolysis.Early fluid administration is vital to prevent crush-related AKI; the rate of initial fluid volume should be 1000 mL/hour. Overall, 3–6 L are administered within a 6-hour period considering environmental, demographic and clinical features, and urinary response to fluids. In disaster circumstances, the preferred fluid formulation is isotonic saline because of its ready availability. Alkaline (bicarbonate-added) hypotonic saline may be more useful, especially in isolated cases not related to disaster, as it may prevent intratubular myoglobin, and uric acid plugs, metabolic acidosis, and also life-threatening hyperkalaemia.In the case of established acute tubular necrosis, dialysis support is life-saving. Although all types of dialysis techniques may be used, intermittent haemodialysis is the preferred modality because of medical and logistic advantages. Close follow-up and appropriate treatment improve mortality rates, which may be as low as 15–20% even in disaster circumstances. Polytrauma victims after mass disasters deserve special mention, because crush syndrome is the second most frequent cause of death after trauma. Chaos, overwhelming number of patients, and logistical drawbacks often result in delayed, and sometimes incorrect treatment. Medical and logistical disaster preparedness is useful to improve the ultimate outcome of disaster victims.
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Karmali, Mohamed A., and Jan M. Sargeant. Verocytotoxin-producing Escherichia coli (VTEC) infections. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0008.
Повний текст джерелаАнотація:
Verocytotoxin (VT)-producing Escherichia coli (VTEC), also known as Shiga toxin producing E. coli (STEC), are zoonotic agents, which cause a potentially fatal illness whose clinical spectrum includes diarrhoea, haemorrhagic colitis, and the haemolytic uraemic syndrome (HUS). VTEC are of serious public health concern because of their association with large outbreaks and with HUS, which is the leading cause of acute renal failure in children. Although over 200 different OH serotypes of VTEC have been associated with human illness, the vast majority of reported outbreaks and sporadic cases of VTEC-infection in humans have been associated with serotype O157:H7.VTs constitute a family of related protein subunit exotoxins, the major ones implicated in human disease being VT1, VT2, and VT2c. Following their translocation into the circulation, VTs bind to endothelial cells of the renal glomeruli, and of other organs and tissues via a specific receptor globotriosylceramide (Gb 3), are internalized by a process of receptor-mediated endocytosis, and cause subcellular damage that results in the characteristic microangiopathic disease observed in HUS.The incubation period of VTEC-associated illness is about 3–5 days. After ingestion VTEC (especially of serotype O157:H7) multiply in the bowel and colonize the mucosa of probably the large bowel with a characteristic attaching and effacing (AE) cytopathology. Colonization is followed by the translocation of VTs into the circulation and the subsequent manifestation of disease.The majority of patients with uncomplicated VTEC infection recover fully with general supportive measures. Historically, the case-fatality rate was high for HUS. However, improvement in the treatment of renal failure and the attendant biochemical disturbances has substantially improved the outlook, although long-term sequelae may develop.Ruminants, especially cattle, are the main reservoirs of VTEC. Infection is acquired through the ingestion of contaminated food, especially under-cooked hamburger, through direct contact with animals, via contaminated water or environments, or via personto-person transmission.The occurrence of large outbreaks of food-borne VTEC-associated illness has promoted close scrutiny of this zoonoses at all levels in the chain of transmission, including the farm, abattoir, food processing, packaging and distribution plants, the wholesaler, the retailer and the consumer. While eradication of VTEC O157 at the farm may not be an option, interventions to increase animal resistance or to decrease animal exposure are being developed and validated. Hazard Analysis and Critical Control Programmes are being implemented in the processing sector and appear to be associated with temporal decreases in VTEC serotype O157 illness in humans. Education programmes targeting food handling procedures and hygiene practices are being advocated at the retail and consumer level. Continued efforts at all stages from the farm to the consumer will be necessary to reduce the risk of VTEC-associated illness in humans.
Частини книг з теми "Uraemic toxins"
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Barsotti, G., E. Chiellini, E. Dossi, D. Giannasi, S. Giovannetti, G. Mazzanti, and R. Solaro. "New Polymeric Hydrogels for the Removal of Uraemic Toxins." In Advanced Biomaterials in Biomedical Engineering and Drug Delivery Systems, 299–300. Tokyo: Springer Japan, 1996. http://dx.doi.org/10.1007/978-4-431-65883-2_86.
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Glorieux, Griet, Nathalie Neirynck, Anneleen Pletinck, Eva Schepers, and Raymond Vanholder. "Uraemic toxins." In Oxford Textbook of Clinical Nephrology, 2161–72. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0254.
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Curry, Nicola, and Susie Shapiro. "Thrombocytopenia and disorders of platelet function." In Oxford Textbook of Medicine, edited by Chris Hatton and Deborah Hay, 5520–32. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0545.
Повний текст джерелаАнотація:
The platelet is the smallest circulating blood cell. In health, it plays a vital role in haemostasis, and in disease contributes to problems of bleeding and/or thrombosis. The number of platelets produced is under tight homeostatic control, regulated by the cytokine thrombopoietin. A normal platelet count lies within the range 150 to 450 × 109/litre. Thrombocytopenia is defined as a reduction in the number of circulating platelets to fewer than the normal reference range (typically <150 × 109/litre). Spontaneous bleeding is uncommon unless the platelet count falls below 10 to 20 × 109/litre or unless there is abnormal platelet function. Thrombocytopenia can be classified according to three main pathologies: (1) increased platelet destruction, (2) reduced platelet production, and (3) increased platelet sequestration. Disorders of increased platelet destruction may be immune mediated or nonimmune. Primary immune thrombocytopenia (ITP) is an acquired disorder affecting both adults and children, characterized by an isolated thrombocytopenia (platelet count <100 × 109 /litre) for which no precipitant can be found. Primary ITP is a diagnosis of exclusion. Corticosteroids are the main first-line therapy for adult ITP, commonly prednisolone. Nonimmune causes of platelet destruction include microangiopathic haemolytic disorders such as thrombotic thrombocytopenic purpura, haemolytic uraemic syndrome, and disseminated intravascular coagulation. Decreased platelet production—most cases are acquired, with common or important causes being toxins (drugs, alcohol), nutritional deficiencies (folate or vitamin B12), bone marrow infiltration, and myelodysplastic syndrome. Disorders of platelet distribution and platelet sequestration include splenomegaly and hypersplenism, haemodilution, and extracorporeal circulation. Disorders of platelet function are usually acquired. The most common causes are medications and toxins, systemic disorders, and haematological diseases. Congenital disorders are a rare cause of symptomatic bleeding.
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Wong, Edwin K. S., and David Kavanagh. "Haemolytic uraemic syndrome." In Oxford Textbook of Medicine, edited by John D. Firth, 5027–32. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0496.
Повний текст джерелаАнотація:
Haemolytic uraemic syndrome (HUS) is a thrombotic microangiopathy characterized by the triad of thrombocytopenia, microangiopathic haemolytic anaemia, and acute kidney injury. It is most often caused by Shiga toxin-producing Escherichia coli (STEC-HUS), and any HUS not caused by this is often termed atypical HUS (aHUS). aHUS may be caused by an underlying complement system abnormality (primary aHUS) or by a range of precipitating events, such as infections or drugs (secondary aHUS). Management of STEC-HUS is supportive. In aHUS, plasma exchange is the initial treatment of choice until ADAMTS13 activity is available to exclude thrombotic thrombocytopenic purpura as a diagnosis. Once this has been done, eculizumab should be instigated as soon as possible.
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White, William. "Renal Medicine." In Oxford Assess and Progress: Clinical Medicine. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198812968.003.0012.
Повний текст джерелаАнотація:
The kidney causes problems for medical students and junior doctors alike— the convoluted journey from plasma to urine, the conundrum of what is reabsorbed and excreted where, and the tangled web of the glomerulonephritides are traditionally learnt, rather than actually understood. As in all clinical medicine, a good place to start is with the fundamentals of the organ in question. Passage from plasma to urine follows the pathway: ● Blood ● Glomerulus ● Tubules ● Collecting duct ● Ureter ● Bladder ● Urethra. The primary functions of the kidney are: ● Removal of toxins ● Electrolyte homeostasis ● Maintenance of acid– base balance ● Activation of vitamin D ● Stimulation of erythropoiesis ● Maintenance of blood volume. The challenge then is to implement these basics by being sensitive to deviations from normal physiology: recognizing the accumulation of any potential toxins (hyperkalaemia, uraemia, and acidosis) or the lack of any synthetic products (hypocalcaemia and anaemia), suggesting triggers for such deviations, and pinpointing the specific parts of the anatomy that may be malfunctioning in some way so as to cause impairment. Despite its bad reputation, the kidney reveals more about itself than any other organ and, in theory, should be the easiest to monitor. It achieves this through its raison d’être: urine. Its presence, absence, contents, smell, and colour offer a running commentary on the activity of the renal tract at any given point in time— it is the internal, intangible workings of specialized cells made physical, measurable, and dippable. So, far from being those much- feared Objective Structured Clinical Examination (OSCE) stations, the dipstick and the catheter are our friends. Or they should be, for it is our ability to harness the information that they provide, allied to the series of numbers on the oft- requested ‘U&Es’ (urea and electrolytes), against a background of wide- ranging symptoms that will make us sensitive to the running of the kidney. This— not just our ability to regurgitate the three types of renal tubular acidosis— is what is at stake in this chapter.
Тези доповідей конференцій з теми "Uraemic toxins"
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Maurin, N. "PILOT STUDY WITH AN “IN VITRO BLEEDING TIME” (“IN VITRO BT”) TO MONITOR THE USE OF A STABLE PROSTACYCLIN (PGI2 ANALOGUE IN HAEMODI ALYSIS (HD)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644224.
Повний текст джерелаАнотація:
Administering PGI2 instead of heparin (H) during HD enables the risk of bleeding to be reduced. A serious disadvantage of this method of inhibiting coagulation by inhibiting thrombocyte function is however that, in contrast to anticoagu1 ation with H alone, there exists no quickly measurable monitoring parameter. Recently Kratzer and Born (Haemostasis 1985; 15: 357-52) presented a new method for measuring the primary haemostatis: the “in vitro BT”. Our pilot study was to determine whether this “in vitro BT” is concentration - d epe nd ent 1 y prolonged by administering a stable PGI2 analogue during HD. In 5 HD’s the stable P G I 2 analogue CG 4203 (dose gradually raised starting 45 rfnn before HD to 25 ng/kg b.w./min during HD; Gruenenthal GmbH, FRG) were given. Before, during and after the HD the “in vitro BT” (Thrombostat 4000, VDG, FRG) was measured under standardised conditions 15 min after taking 1 ml of citrate blood from the arterial branch of the extracorporeal system. The “in vitro BT” was concentration-dependent!y prolonged by CG 4203. The time interval between taking and measuring the blood sample affect the measured value. If the blood sample is taken directly before the dialyser, the “in vitro BT” is greater than if the sample is taken directly after the dialyser; from which it can be assumed that the dialyser activates the platelets. 1 h after ending HD and discontinuing the CG 4203, the “in vitro BT” is shorter than it was before starting HD; perhaps this is due to platelet activation during HD in the extracorporeal system and to removal of uraemic toxins. Furthermore, the “in vitro BT” was measured in a healthy volunteer 20 times consecutively. The coefficient of variability was 9.3 %. Further studies should be performed to see whether adjusting the “in vitro BT” to a given range allows the dosing of PGI2 or a stable PGI2 analogue to be so controlled as to prevent occlusion in the extracorporeal system.
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Gordge, M. P., R. W. Faint, P. B. Rylance, and G. H. Neild. "THE BLEEDING TENDENCY OF PROGRESSIVE RENAL FAILURE IS NOT ASSOCIATED WITH DEFECTIVE PLATELET AGGREGATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644566.
Повний текст джерелаАнотація:
The bleeding tendency of uraemia may be related to reduction by anaemia of erythrocyte/platelet interaction, toxic inhibition of platelet aggregation and abnormal von Willebrand Factor (vWF) mediated platelet adhesion. Our aim in this study was to determine at what stage of renal failure bleeding time becomes prolonged and to investigate the mechanisms involved.We have measured bleeding time (Simplate II), plasma levels of fibrinogen and vWF, and ex-vivo platelet responsiveness in 31 patients with chronic renal failure (CRF) of various degrees of severity and compared them with values obtained in 22 healthy controls. No patient was dialysed, nephrotic or suffering from immunological renal disease. Patients were divided into mild (plasma creatinine <300 umol/1), n=10, moderate (300-600 umol/1), n=14, or severe (>600 umol/1), n=7, CRF.Bleeding time became significantly prolonged only in severe CRF (p<0.005). Haematocrit fell as renal failure advanced, and correlated with bleeding time (r=0.40, p<0.05). Platelet counts were normal. Platelet aggregation in response to ristocetin (mediated by vWF) and ADP increased progressively (p<0.005 in severe CRF), as did spontaneous aggregation (p<0.005 in severe CRF). This was associated with an increase in plasma vWF and fibrinogen (p<0.005 in severe CRF). Collagen induced aggregation was slightly, but not significantly increased. Thromboxane (TxB2) generation in clotting blood was the only measurement that showed a reduced platelet response (p<0.025 in severe CRF).In summary, a bleeding tendency develops late in the course of progressive CRF when plasma creatinine has risen to at least 600 umol/1. Platelet aggregation is enhanced rather than reduced and platelet interaction with vWF is not defective. Anaemia appears more important than abnormal platelet aggregation in mediating uraemic bleeding, although reduced serum TxB2 generation suggests a defect in platelet response to endogenous thrombin which may also contribute. Increased platelet aggregation and fibrinogen concentrations might promote glomerular thrombosis and contribute to the progression of CRF.