<?xml version="1.0"?><rdf:RDF xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:edm="http://www.europeana.eu/schemas/edm/" xmlns:wgs84_pos="http://www.w3.org/2003/01/geo/wgs84_pos" xmlns:foaf="http://xmlns.com/foaf/0.1/" xmlns:rdaGr2="http://rdvocab.info/ElementsGr2" xmlns:oai="http://www.openarchives.org/OAI/2.0/" xmlns:owl="http://www.w3.org/2002/07/owl#" xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:ore="http://www.openarchives.org/ore/terms/" xmlns:skos="http://www.w3.org/2004/02/skos/core#" xmlns:dcterms="http://purl.org/dc/terms/"><edm:WebResource rdf:about="http://www.dlib.si/stream/URN:NBN:SI:doc-PL7ZKRVH/0f12197d-d6da-4d96-acd0-aff582e65dc2/PDF"><dcterms:extent>131 KB</dcterms:extent></edm:WebResource><edm:WebResource rdf:about="http://www.dlib.si/stream/URN:NBN:SI:doc-PL7ZKRVH/93b9d59e-4122-4331-9de1-2a62ce43716a/TEXT"><dcterms:extent>28 KB</dcterms:extent></edm:WebResource><edm:TimeSpan rdf:about="1994-2025"><edm:begin xml:lang="en">1994</edm:begin><edm:end xml:lang="en">2025</edm:end></edm:TimeSpan><edm:ProvidedCHO rdf:about="URN:NBN:SI:doc-PL7ZKRVH"><dcterms:isPartOf rdf:resource="https://www.dlib.si/details/URN:NBN:SI:spr-46R7GGHL" /><dcterms:issued>2007</dcterms:issued><dc:creator>Lindič, Jelka</dc:creator><dc:creator>Ravnikar, Andrea</dc:creator><dc:format xml:lang="sl">številka:4</dc:format><dc:format xml:lang="sl">letnik:46</dc:format><dc:format xml:lang="sl">str. 337-345</dc:format><dc:identifier>ISSN:0025-8121</dc:identifier><dc:identifier>COBISSID:24513497</dc:identifier><dc:identifier>URN:URN:NBN:SI:doc-PL7ZKRVH</dc:identifier><dc:language>sl</dc:language><dc:publisher xml:lang="sl">Medicinski razgledi</dc:publisher><dcterms:isPartOf xml:lang="sl">Medicinski razgledi</dcterms:isPartOf><dc:subject xml:lang="en">Diclofenac</dc:subject><dc:subject xml:lang="sl">Diklofenak</dc:subject><dc:subject xml:lang="en">drug</dc:subject><dc:subject xml:lang="en">Kidney Failure</dc:subject><dc:subject xml:lang="sl">ledvice</dc:subject><dc:subject xml:lang="sl">Ledvična odpoved</dc:subject><dc:subject xml:lang="sl">nefritis</dc:subject><dc:subject xml:lang="sl">Nefritis intersticijski</dc:subject><dc:subject xml:lang="sl">Nefrotični sindrom</dc:subject><dc:subject xml:lang="en">Nephritis, Interstitial</dc:subject><dc:subject xml:lang="en">Nephrotic Syndrome</dc:subject><dc:subject xml:lang="sl">nesterioidni antirevmatiki</dc:subject><dc:subject xml:lang="en">Toxicity</dc:subject><dc:subject xml:lang="sl">zdravila</dc:subject><dc:subject rdf:resource="http://www.wikidata.org/entity/Q9377" /><dcterms:temporal rdf:resource="1994-2025" /><dc:title xml:lang="sl">Nesteroidni antirevmatiki (NSAR) in ledvice| Non-steroidal antiinflamatory drugs (NSAIDs) and the kidney|</dc:title><dc:description xml:lang="sl">Non-steroidal antiinflammatory drugs (NSAIDs) are among the most widely utilized therapeutic agents today. The main mechanism of their action is via inhibition of cyclooxygenase, the enzyme involved in prostaglandin synthesis. Prostaglandins play a crucial role in the renal circulation when systemic circulation is destabilized or when the blood volume and tive arterial blood volume are compromised. They enable vasodilatation of the renal circulation, renin secretion, and sodium and water excretion. There are two isoforms of cyclooxygenase (COX) (COX-1 or the ĆconstitutiveĆ isoform and COX-2 or the inducible isoform). The inhibition of COX-2, which is normally expressed in activated macrophages and induced by proinflammatory substances, accounts for antiinflammatory, analgesic and antipyretic effects whereas COX-1 suppression causes most side effects, for example gastrointestinal bleeding and ulceration, and platelet dysfunction. It was assumed that selective inhibitionof COX-2 would diminish the wide range of toxic organ effects of nonselective NSAIDs. In the kidney, constitutive expression has been demonstrated for both isoforms. Renal toxicity is therefore similar in nonselective and selective COX-2 inhibitors. Moreover, a number of analyses have suggested that prolonged exposure to selective COX-2 inhibitors increasesthe risk of cardiovascular disease. Renal toxicity associated with the use of NSAIDs can be classified in several distinct clinical syndromesČ acute hemodynamic renal failure, acute tubulointerstitial nephritis with nephrotic syndrome and chronic kidney disease. They differ in the time of druguse that is required for its development, pathogenesis and treatment</dc:description><edm:type>TEXT</edm:type><dc:type xml:lang="sl">znanstveno časopisje</dc:type><dc:type xml:lang="en">journals</dc:type><dc:type rdf:resource="http://www.wikidata.org/entity/Q361785" /></edm:ProvidedCHO><ore:Aggregation rdf:about="http://www.dlib.si/?URN=URN:NBN:SI:doc-PL7ZKRVH"><edm:aggregatedCHO rdf:resource="URN:NBN:SI:doc-PL7ZKRVH" /><edm:isShownBy rdf:resource="http://www.dlib.si/stream/URN:NBN:SI:doc-PL7ZKRVH/0f12197d-d6da-4d96-acd0-aff582e65dc2/PDF" /><edm:rights rdf:resource="http://rightsstatements.org/vocab/InC/1.0/" /><edm:provider>Slovenian National E-content Aggregator</edm:provider><edm:intermediateProvider xml:lang="en">National and University Library of Slovenia</edm:intermediateProvider><edm:dataProvider xml:lang="sl">Društvo Medicinski razgledi</edm:dataProvider><edm:object rdf:resource="http://www.dlib.si/streamdb/URN:NBN:SI:doc-PL7ZKRVH/maxi/edm" /><edm:isShownAt rdf:resource="http://www.dlib.si/details/URN:NBN:SI:doc-PL7ZKRVH" /></ore:Aggregation></rdf:RDF>