Pathophysiological aspects of nephropathy caused by non-steroidal anti-inflammatory drugs

Abstract 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 N...

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Main Authors: Guillherme Nobre Cavalcanti Lucas, Ana Carla Carneiro Leitão, Renan Lima Alencar, Rosa Malena Fagundes Xavier, Elizabeth De Francesco Daher, Geraldo Bezerra da Silva Junior
Format: Article
Language:English
Published: Sociedade Brasileira de Nefrologia 2018-09-01
Series:Brazilian Journal of Nephrology
Subjects:
Online Access:http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0101-28002018005033103&lng=en&tlng=en
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author Guillherme Nobre Cavalcanti Lucas
Ana Carla Carneiro Leitão
Renan Lima Alencar
Rosa Malena Fagundes Xavier
Elizabeth De Francesco Daher
Geraldo Bezerra da Silva Junior
author_facet Guillherme Nobre Cavalcanti Lucas
Ana Carla Carneiro Leitão
Renan Lima Alencar
Rosa Malena Fagundes Xavier
Elizabeth De Francesco Daher
Geraldo Bezerra da Silva Junior
author_sort Guillherme Nobre Cavalcanti Lucas
collection DOAJ
description Abstract 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.
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spelling doaj.art-e179ff00c8204368b5ce04fdeb9383b72022-12-22T03:38:06ZengSociedade Brasileira de NefrologiaBrazilian Journal of Nephrology2175-82392018-09-01010.1590/2175-8239-jbn-2018-0107S0101-28002018005033103Pathophysiological aspects of nephropathy caused by non-steroidal anti-inflammatory drugsGuillherme Nobre Cavalcanti LucasAna Carla Carneiro LeitãoRenan Lima AlencarRosa Malena Fagundes XavierElizabeth De Francesco DaherGeraldo Bezerra da Silva JuniorAbstract 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.http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0101-28002018005033103&lng=en&tlng=enAnti-Inflammatory AgentsDrug-Related Side Effects and Adverse ReactionsToxicityPhysiopathologyReview
spellingShingle Guillherme Nobre Cavalcanti Lucas
Ana Carla Carneiro Leitão
Renan Lima Alencar
Rosa Malena Fagundes Xavier
Elizabeth De Francesco Daher
Geraldo Bezerra da Silva Junior
Pathophysiological aspects of nephropathy caused by non-steroidal anti-inflammatory drugs
Brazilian Journal of Nephrology
Anti-Inflammatory Agents
Drug-Related Side Effects and Adverse Reactions
Toxicity
Physiopathology
Review
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 Anti-Inflammatory Agents
Drug-Related Side Effects and Adverse Reactions
Toxicity
Physiopathology
Review
url http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0101-28002018005033103&lng=en&tlng=en
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