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      Association of Individual Non-Steroidal Anti-Inflammatory Drugs and Chronic Kidney Disease: A Population-Based Case Control Study

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          Abstract

          Background

          Non-steroidal anti-inflammatory agents (NSAIDs) are known to be associated with renal damage. No clear evidence exists regarding differential risk of chronic kidney disease (CKD), specifically, across various NSAIDs.

          Aim

          The aim of this population-based case-control study was to evaluate the association between use of individual NSAIDs and risk of CKD in a general population of Southern Italy.

          Methods

          A nested case-control study was carried out using the general practice Arianna database, identifying incident CKD patients as cases and matched controls from 2006 to 2011. The date of first CKD diagnosis was defined as the index date (ID). Conditional logistic regressions were performed to estimate the risk of CKD associated with NSAIDs by class and individual drugs as compared to non-use during different time windows (within one year, six or three months prior to ID), with the latter being defined as current users. Among current users, the effect of cumulative exposure to these drugs was evaluated.

          Results

          Overall, 1,989 CKD cases and 7,906 matched controls were identified. A statistically significant increase in the risk of CKD was found for current users of oxicams (adjusted OR: 1.68; 95% CI: 1.15-2.44) and concerning individual compounds, for ketorolac (adj. OR: 2.54; 95% CI: 1.45-4.44), meloxicam (adj. OR: 1.98; 95% CI: 1.01-3.87) and piroxicam (adj. OR: 1.95; 95% CI: 1.19-3.21).

          Conclusions

          The risk of CKD varies across individual NSAIDs. Increased risk has been found for ketorolac, which may precipitate subclinical CKD through acute renal damage, and long-term exposure to oxicams, especially meloxicam and piroxicam.

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          Most cited references32

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          Drug-induced nephrotoxicity.

          Drugs are a common source of acute kidney injury. Compared with 30 years ago, the average patient today is older, has more comorbidities, and is exposed to more diagnostic and therapeutic procedures with the potential to harm kidney function. Drugs shown to cause nephrotoxicity exert their toxic effects by one or more common pathogenic mechanisms. Drug-induced nephrotoxicity tends to be more common among certain patients and in specific clinical situations. Therefore, successful prevention requires knowledge of pathogenic mechanisms of renal injury, patient-related risk factors, drug-related risk factors, and preemptive measures, coupled with vigilance and early intervention. Some patient-related risk factors for drug-induced nephrotoxicity are age older than 60 years, underlying renal insufficiency (e.g., glomerular filtration rate of less than 60 mL per minute per 1.73 m2), volume depletion, diabetes, heart failure, and sepsis. General preventive measures include using alternative non-nephrotoxic drugs whenever possible; correcting risk factors, if possible; assessing baseline renal function before initiation of therapy, followed by adjusting the dosage; monitoring renal function and vital signs during therapy; and avoiding nephrotoxic drug combinations.
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            NSAID use and progression of chronic kidney disease.

            The effects of nonselective and selective cyclooxygenase-2 specific (COX-2) nonsteroidal anti-inflammatory drug (NSAID) use on the progression of chronic kidney disease (CKD) is uncertain. Due to the high prevalence of both CKD and NSAID use in older adults, we sought to determine the association between NSAID use and the progression of CKD in an elderly community-based cohort. All subjects > or =66 years of age who had at least one serum creatinine measurement in 2 time periods (July-December, 2001 and July-December, 2003) were included. Multiple logistic regression analyses, including covariates for age, sex, baseline estimated glomerular filtration rate (eGFR), diabetes, and comorbidity were used to explore the associations of NSAID use on the primary (decrease in eGFR of > or =15 mL/min/1.73) and secondary (mean change in eGFR) outcomes. A total of 10,184 subjects (mean age 76 years; 57% female) were followed for a median of 2.75 years. High-dose NSAID users (upper decile of cumulative NSAID exposure) experienced a 26% increased risk for the primary outcome (odds ratio [OR] 1.26, 95% confidence interval [CI], 1.04-1.53). A linear association between cumulative NSAID dose and change in mean GFR also was seen. No risk differential was identified between selective and nonselective NSAID users. High cumulative NSAID exposure is associated with an increased risk for rapid CKD progression in the setting of a community-based elderly population. For older adult patients with CKD, these results suggest that nonselective NSAIDs and selective COX-2 inhibitors should be used cautiously and chronic exposure to any NSAID should be avoided.
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              Risk of kidney failure associated with the use of acetaminophen, aspirin, and nonsteroidal antiinflammatory drugs.

              People who take analgesic drugs frequently may be at increased risk of end-stage renal disease (ESRD), but the extent of this risk remains unclear. We studied 716 patients treated for ESRD and 361 control subjects of similar age from Maryland, Virginia, West Virginia, and Washington, D.C. The study participants were interviewed by telephone about their past use of medications containing acetaminophen, aspirin, and other nonsteroidal antiinflammatory drugs (NSAIDs). For each analgesic drug, the average use (in pills per year) and the cumulative intake (in pills) were examined for any association with ESRD. Heavier acetaminophen use was associated with an increased risk of ESRD in a dose-dependent fashion. When persons who took an average of 0 to 104 pills per year were used for reference, the odds ratio of ESRD was 1.4 (95 percent confidence interval, 0.8 to 2.4) for those who took 105 to 365 pills per year and 2.1 (95 percent confidence interval, 1.1 to 3.7) for those who took 366 or more pills per year, after adjustment for race, sex, age, and intake of other analgesic drugs. When persons who had taken fewer than 1000 pills containing acetaminophen in their lifetime were used for reference, the odds ratio was 2.0 (95 percent confidence interval, 1.3 to 3.2) for those who had taken 1000 to 4999 pills and 2.4 (95 percent confidence interval, 1.2 to 4.8) for those who had taken 5000 or more pills. Approximately 8 to 10 percent of the overall incidence of ESRD was attributable to acetaminophen use. A cumulative dose of 5000 or more pills containing NSAIDs was also associated with an increased odds of ESRD (odds ratio, 8.8), but the use of aspirin was not. People who often take acetaminophen or NSAIDs have an increased risk of ESRD, but not those who often take aspirin.
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                Author and article information

                Contributors
                Role: Academic Editor
                Journal
                PLoS One
                PLoS ONE
                plos
                plosone
                PLoS ONE
                Public Library of Science (San Francisco, CA USA )
                1932-6203
                16 April 2015
                2015
                : 10
                : 4
                : e0122899
                Affiliations
                [1 ]Department of Clinical and Experimental Medicine, University of Messina, Messina, Italy
                [2 ]Unit of Biostatistics, IRCCS "Casa Sollievo della Sofferenza", San Giovanni Rotondo (FG), Italy
                [3 ]Caserta Local Health Service, Caserta, Italy
                [4 ]Fundació Institut Català de Farmacologia, WHO Collaborating Centre for Research and Training in Pharmacoepidemiology, Department of Pharmacology, Therapeutics and Toxicology, Institut Català de la Salut, Universitat Autònoma de Barcelona, Barcelona, Spain
                University of São Paulo School of Medicine, BRAZIL
                Author notes

                Competing Interests: The authors have declared that no competing interests exist.

                Conceived and designed the experiments: GT DS. Performed the experiments: GT YI FG AF. Analyzed the data: FG YI AF GT. Contributed reagents/materials/analysis tools: GT VA. Wrote the paper: YI JS FG AF DS VA DUT LI MP AS GT.

                ‡ These authors also contributed equally to this work.

                Article
                PONE-D-14-53280
                10.1371/journal.pone.0122899
                4399982
                25880729
                89ea79e1-c801-4718-8cfc-7fdc76ac2d98
                Copyright @ 2015

                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 author and source are credited

                History
                : 11 December 2014
                : 24 February 2015
                Page count
                Figures: 4, Tables: 2, Pages: 14
                Funding
                The authors have no support or funding to report.
                Categories
                Research Article
                Custom metadata
                Fully anonymised dataset is available only upon request to the corresponding author (G. Trifirò) as there is an agreement between corresponding author and data provider (Caserta LHU) not to share the data publicly. The corresponding author may be contacted at: trifirog@ 123456unime.it .

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