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

Brazilian Journal of Nephrology, 2019-03, Vol.41 (1), p.124-130 [Peer Reviewed Journal]

This work is licensed under a Creative Commons Attribution 4.0 International License. ;ISSN: 0101-2800 ;ISSN: 2175-8239 ;EISSN: 2175-8239 ;DOI: 10.1590/2175-8239-JBN-2018-0107 ;PMID: 30281062

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Title:
Pathophysiological aspects of nephropathy caused by non-steroidal anti-inflammatory drugs
Author: Lucas, Guillherme Nobre Cavalcanti ; Leitão, Ana Carla Carneiro ; Alencar, Renan Lima ; Xavier, Rosa Malena Fagundes ; Daher, Elizabeth De Francesco ; Silva Junior, Geraldo Bezerra da
Subjects: Acute Kidney Injury - chemically induced ; Acute Kidney Injury - physiopathology ; Aged ; Aged, 80 and over ; Anti-Inflammatory Agents ; Anti-Inflammatory Agents, Non-Steroidal - adverse effects ; Anti-Inflammatory Agents, Non-Steroidal - metabolism ; Cyclooxygenase Inhibitors - adverse effects ; Cyclooxygenase Inhibitors - metabolism ; Drug-Related Side Effects and Adverse Reactions ; Humans ; Infant, Newborn ; Nephritis, Interstitial - chemically induced ; Nephritis, Interstitial - physiopathology ; Physiopathology ; Prostaglandins E - metabolism ; Proteinuria - chemically induced ; Renal Insufficiency, Chronic - chemically induced ; Renal Insufficiency, Chronic - physiopathology ; Review ; Risk Factors ; Toxicity ; Update ; UROLOGY & NEPHROLOGY
Is Part Of: Brazilian Journal of Nephrology, 2019-03, Vol.41 (1), p.124-130
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.
Publisher: Brazil: Sociedade Brasileira de Nefrologia
Language: English;Portuguese
Identifier: ISSN: 0101-2800
ISSN: 2175-8239
EISSN: 2175-8239
DOI: 10.1590/2175-8239-JBN-2018-0107
PMID: 30281062
Source: SciELO
GFMER Free Medical Journals
MEDLINE
PubMed Central
Alma/SFX Local Collection
DOAJ Directory of Open Access Journals

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

This work is licensed under a Creative Commons Attribution 4.0 International License. ;ISSN: 0101-2800 ;ISSN: 2175-8239 ;EISSN: 2175-8239 ;DOI: 10.1590/2175-8239-JBN-2018-0107 ;PMID: 30281062

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