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Pathophysiological aspects of nephropathy caused by non-steroidal anti-inflammatory drugs
Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly used medications associated with nephrotoxicity, especially when used chronically. Factors such as advanced age and comorbidities, which in themselves already lead to a decrease in glomerular filtration rate, increase the risk of NSAID-rela...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Sociedade Brasileira de Nefrologia
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6534025/ https://www.ncbi.nlm.nih.gov/pubmed/30281062 http://dx.doi.org/10.1590/2175-8239-JBN-2018-0107 |
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author | Lucas, Guillherme Nobre Cavalcanti Leitão, Ana Carla Carneiro Alencar, Renan Lima Xavier, Rosa Malena Fagundes Daher, Elizabeth De Francesco da Silva, Geraldo Bezerra |
author_facet | Lucas, Guillherme Nobre Cavalcanti Leitão, Ana Carla Carneiro Alencar, Renan Lima Xavier, Rosa Malena Fagundes Daher, Elizabeth De Francesco da Silva, Geraldo Bezerra |
author_sort | Lucas, Guillherme Nobre Cavalcanti |
collection | PubMed |
description | Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly used medications associated with nephrotoxicity, especially when used chronically. Factors such as advanced age and comorbidities, which in themselves already lead to a decrease in glomerular filtration rate, increase the risk of NSAID-related nephrotoxicity. The main mechanism of NSAID action is cyclooxygenase (COX) enzyme inhibition, interfering on arachidonic acid conversion into E2 prostaglandins E2, prostacyclins and thromboxanes. Within the kidneys, prostaglandins act as vasodilators, increasing renal perfusion. This vasodilatation is a counter regulation of mechanisms, such as the renin-angiotensin-aldosterone system works and that of the sympathetic nervous system, culminating with compensation to ensure adequate flow to the organ. NSAIDs inhibit this mechanism and can lead to acute kidney injury (AKI). High doses of NSAIDs have been implicated as causes of AKI, especially in the elderly. The main form of AKI by NSAIDs is hemodynamically mediated. The second form of NSAID-induced AKI is acute interstitial nephritis, which may manifest as nephrotic proteinuria. Long-term NSAID use can lead to chronic kidney disease (CKD). In patients without renal diseases, young and without comorbidities, NSAIDs are not greatly harmful. However, because of its dose-dependent effect, caution should be exercised in chronic use, since it increases the risk of developing nephrotoxicity. |
format | Online Article Text |
id | pubmed-6534025 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Sociedade Brasileira de Nefrologia |
record_format | MEDLINE/PubMed |
spelling | pubmed-65340252019-06-17 Pathophysiological aspects of nephropathy caused by non-steroidal anti-inflammatory drugs Lucas, Guillherme Nobre Cavalcanti Leitão, Ana Carla Carneiro Alencar, Renan Lima Xavier, Rosa Malena Fagundes Daher, Elizabeth De Francesco da Silva, Geraldo Bezerra J Bras Nefrol Update Article Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly used medications associated with nephrotoxicity, especially when used chronically. Factors such as advanced age and comorbidities, which in themselves already lead to a decrease in glomerular filtration rate, increase the risk of NSAID-related nephrotoxicity. The main mechanism of NSAID action is cyclooxygenase (COX) enzyme inhibition, interfering on arachidonic acid conversion into E2 prostaglandins E2, prostacyclins and thromboxanes. Within the kidneys, prostaglandins act as vasodilators, increasing renal perfusion. This vasodilatation is a counter regulation of mechanisms, such as the renin-angiotensin-aldosterone system works and that of the sympathetic nervous system, culminating with compensation to ensure adequate flow to the organ. NSAIDs inhibit this mechanism and can lead to acute kidney injury (AKI). High doses of NSAIDs have been implicated as causes of AKI, especially in the elderly. The main form of AKI by NSAIDs is hemodynamically mediated. The second form of NSAID-induced AKI is acute interstitial nephritis, which may manifest as nephrotic proteinuria. Long-term NSAID use can lead to chronic kidney disease (CKD). In patients without renal diseases, young and without comorbidities, NSAIDs are not greatly harmful. However, because of its dose-dependent effect, caution should be exercised in chronic use, since it increases the risk of developing nephrotoxicity. Sociedade Brasileira de Nefrologia 2018-09-21 2019 /pmc/articles/PMC6534025/ /pubmed/30281062 http://dx.doi.org/10.1590/2175-8239-JBN-2018-0107 Text en https://creativecommons.org/licenses/by/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Update Article Lucas, Guillherme Nobre Cavalcanti Leitão, Ana Carla Carneiro Alencar, Renan Lima Xavier, Rosa Malena Fagundes Daher, Elizabeth De Francesco da Silva, Geraldo Bezerra Pathophysiological aspects of nephropathy caused by non-steroidal anti-inflammatory drugs |
title | Pathophysiological aspects of nephropathy caused by non-steroidal anti-inflammatory drugs |
title_full | Pathophysiological aspects of nephropathy caused by non-steroidal anti-inflammatory drugs |
title_fullStr | Pathophysiological aspects of nephropathy caused by non-steroidal anti-inflammatory drugs |
title_full_unstemmed | Pathophysiological aspects of nephropathy caused by non-steroidal anti-inflammatory drugs |
title_short | Pathophysiological aspects of nephropathy caused by non-steroidal anti-inflammatory drugs |
title_sort | pathophysiological aspects of nephropathy caused by non-steroidal anti-inflammatory drugs |
topic | Update Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6534025/ https://www.ncbi.nlm.nih.gov/pubmed/30281062 http://dx.doi.org/10.1590/2175-8239-JBN-2018-0107 |
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