The Effect of Nonsteroidal Antiinflammatory Drugs on Electrolyte Homeostasis and Blood Pressure in Young and Elderly Persons With and Without Renal Insufficiency

Murray, Michael D.; Lazaridis, Emmanuel N.; Brizendine, Edward J.; Haag, Kathy; Becker, Paula; Brater, D.Craig

doi:10.1016/s0002-9629(15)40173-9

Cited by 4 publications

(6 citation statements)

References 29 publications

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“…In one study, ibuprofen, piroxicam, and sulindac all reduced urinary sodium in both young and elderly patients independent of their renal function. 37 However, ibuprofen use was associated with elevation of blood pressure in patients with renal insufficiency.…”

Section: Nsaid-induced Prerenal Acute Renal Failurementioning

confidence: 99%

How to prevent, recognize, and treat drug-induced nephrotoxicity.

Guo

Nzerue

2002

Cleveland Clinic Journal of Medicine

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Many drugs can injure the kidneys, but they cause renal injury via only a few common mechanisms. Many patients who develop renal injury after drug exposure have identifiable risk factors that could be modified or that should preclude the use of these drugs in the first place. s KEY POINTS Pretreatment hydration can reduce the nephrotoxic potential of many drugs. Renal injury can present as acute renal failure, nephrotic syndrome, renal tubular dysfunction, or chronic renal failure. Early diagnosis is critical; therefore, physicians must be aware of the nephrotoxic potential of the medications they prescribe and the risk status of their patients. One must anticipate the problem and exclude drugs as possible causes of renal disease when no other obvious cause can be found. DRUG-INDUCED NEPHROTOXICITY GUO AND NZERUE Prophylaxis of druginduced renal failure Amphotericin B Adjust dosage Hydrate with normal saline infusion Use liposomal formulation Aminoglycosides Follow levels Correct potassium levels Give once-daily doses Adjust dosage for renal function Avoid use if possible in high-risk patients Possibly give calcium channel blockers Intravenous contrast Hydrate with normal saline infusion Possibly give acetylcysteine Cisplatin Hydrate with normal saline Possibly give thiosulfate ACE inhibitors Avoid in bilateral renal artery stenosis Use with caution in hypovolemia Acyclovir Avoid bolus doses Give intravenous fluids Adjust dose for renal function Lithium Monitor levels Amiloride may prevent nephrogenic diabetes insipidus Interleukin-2 Intravenous saline, albumin infusion Cyclosporine Follow levels Avoid drugs that raise levels (erythromycin, verapamil, ketoconazole) Indinavir Hydrate Establish high urine flow * ACE-angiotensin-converting enzyme COX-cyclo-oxygenase NSAID-nonsteroidal anti-inflammatory drug TTP-HUS-thrombotic thrombocytopenic purpura-hemolytic uremic syndrome

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Section: Nsaid-induced Prerenal Acute Renal Failurementioning

confidence: 99%

How to prevent, recognize, and treat drug-induced nephrotoxicity.

Guo

Nzerue

2002

Cleveland Clinic Journal of Medicine

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“…In the present study, we confirmed our previous finding 7 that, among the tested COX‐2‐selective inhibitors, rofecoxib and celecoxib, but not meloxicam, significantly decreased sodium and potassium excretion. A reduction in urinary electrolyte excretion following treatment with NSAIDs has been shown in several other studies 21–23 …”

Section: Discussionmentioning

confidence: 65%

Extent of Renal Effect of Cyclo‐oxygenase‐2‐selective Inhibitors Is Pharmacokinetic Dependent

Harirforoosh

Aghazadeh‐Habashi

Jamali

2006

Clin Exp Pharma Physio

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Non-steroidal anti-inflammatory drugs (NSAIDs) cause renal side-effects. In the present study, we tested the hypothesis that the extent of the renal effects of cyclo-oxygenase (COX)-2-selective NSAIDs is linked to their pharmacokinetics. A single oral dose of rofecoxib (10 mg/kg), celecoxib (40 mg/kg), meloxicam (3 mg/kg) or placebo was administered to rats. Urinary excretion of electrolytes, a marker of renal effects, and plasma and kidney concentrations of NSAIDs were measured. Rofecoxib and celecoxib, but not meloxicam, significantly decreased urinary sodium and potassium excretion. There was a significant correlation between the area under the 24 h plasma concentration-time curve (AUC0-24) of rofecoxib and the change in sodium (r = -0.65; P < 0.02) and potassium (r = -0.82; P < 0.0006) excretion. The AUC0-24 of celecoxib was correlated with sodium (r = -0.80; P < 0.05) but not potassium excretion. The ratios of kidney to plasma drug concentrations were 1.72, 3.16 and 0.17 for rofecoxib, celecoxib and meloxicam, respectively. The renal effect of the COX-2-selective NSAIDs examined, marked by their ability to reduce the excretion of electrolytes, is influenced by systemic exposure to the drugs. The relatively higher distribution into the kidneys of rofecoxib and celecoxib compared with meloxicam suggests involvement of direct drug exposure in the kidneys in the adverse renal effect.

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“…First, through prostacyclin (PGI2) reduction that increases in turn systemic vascular resistance due to unopposed vasoconstriction of angiotensin II and catecholamines, and that also increases renal vascular resistance with reduced natriuresis and sodium and water retention. 4,27 Second, through prostaglandin E2 reduction which may reduce natriuresis by 30%-50%, especially in patients with chronic kidney disease (a potential conditions in individuals taking COX inhibitors chronically). [28][29][30][31] Finally, some authors propose inhibition of aldosterone metabolism with subsequent hyperaldosteronism, as a potential mechanism for increased BP in aspirin users.…”

Section: Discussionmentioning

confidence: 99%

“…The most widely proposed and accepted mechanism is blockage of cyclooxygenase (COX) enzymes. 4,27 COX-1 is related to normal cell function, like protective gastric mucosa secretion in the stomach, salt and water handling in the kidney or platelet and endothelium normal function. COX-2 is more related to inflammatory states, manifested with pain, heat, and swelling.…”

Section: Discussionmentioning

confidence: 99%

“…3 Aspirin and other analgesics like acetaminophen and other non steroidal anti-inflammatory drugs (NSAIDs) are widely used worldwide and could increase the BP levels through prostaglandins inhibition, and through sodium retention in the case of NSAIDs. 4 Results from different prospective studies conducted in the United States assessing the association between use of aspirin, NSAIDs and other analgesics and the risk of hypertension suggest that chronic users of aspirin, NSAIDS, and acetaminophen have a higher risk of hypertension. [5][6][7][8][9] However, some clinical trials conducted in Spain have shown the opposite effect 10,11 and no previous prospective study has assessed this potential relationship in a European cohort, where a different health system probably means different access to medication and a different pattern of drug use.…”

Section: Assessment Of Incident Hypertensionmentioning

confidence: 99%

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Aspirin, Non-Aspirin Analgesics and the Risk of Hypertension in the SUN Cohort

Beunza

Martínez‐González

Bes–Rastrollo

et al. 2010

Revista Española de Cardiología (English Edition)

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Introduction and objectives. The use of aspirin and non-aspirin analgesics have been associated with changes in blood pressure. The aim of this study was to investigate prospectively the association between the regular use of aspirin and non-aspirin analgesics and the incidence of hypertension.Methods. The SUN project is an ongoing, continuously expanding, prospective cohort of Spanish university graduates initially free of hypertension, cardiovascular disease, diabetes, and cancer; 9986 (mean age, 36 years) were recruited during 1999-2005 and followed up for a mean of 51 months. Regular aspirin and non-aspirin analgesic use and the presence of other risk factors for hypertension were assessed by questionnaire at baseline, and the incidence of hypertension was assessed using biennial follow-up questionnaires.Results. In total, 543 new cases of hypertension were identified during follow-up. Regular aspirin use (ie, ≥2 days/ week) was associated with a higher risk of hypertension (hazard ratio = 1.45; 95% confidence interval, 1.02-2.04) after adjustment for various confounding factors. Regular use of non-aspirin analgesic drugs was also associated with a higher risk of hypertension (hazard ratio = 1.69; 95% confidence interval, 1.28-2.23).Conclusions. The regular use of aspirin and non-aspirin analgesics were both associated with an increased risk of developing hypertension, independently of other risk factors. Aspirina, analgésicos y riesgo de hipertensión arterial en la Cohorte SUN Introducción y objetivos. Se ha relacionado el consumo de aspirina y de otros analgésicos con cambios en la presión arterial. El objetivo de nuestro estudio fue valorar prospectivamente la asociación del uso habitual de aspirina y otros analgésicos con la incidencia de hipertensión arterial.Métodos. El proyecto SUN es una cohorte prospectiva y dinámica que incluyó a 9.986 graduados universitarios españoles inicialmente libres de hipertensión, enfermedad cardiovascular, diabetes o cáncer (media de edad, 36 años). Fueron reclutados durante el periodo 1999-2005 y se los siguió prospectivamente durante una media de 51 meses. El uso habitual de aspirina y otros analgési-cos, así como la presencia de otros factores de riesgo de hipertensión arterial, se valoró mediante un cuestionario basal. La incidencia de hipertensión se valoró con cuestionarios de seguimiento bienales.Resultados. Durante el seguimiento se identificaron 543 casos nuevos de hipertensión arterial. El uso habitual de aspirina (2 o más días/semana) se asoció con un mayor riesgo de hipertensión (hazard ratio [HR] = 1,45; intervalo de confianza [IC] del 95%, 1,02-2,04) tras ajustar por diversos factores de confusión. El uso habitual de otros analgésicos diferentes de la aspirina también se asoció a un mayor riesgo de hipertensión arterial (HR = 1,69; IC del 95%, 1,28-2,23).Conclusiones. El uso habitual tanto de aspirina como de otros analgésicos diferentes a la aspirina parece asociarse a mayor riesgo de hipertensión arterial, independientemente de otros factores de riesgo.

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The Effect of Nonsteroidal Antiinflammatory Drugs on Electrolyte Homeostasis and Blood Pressure in Young and Elderly Persons With and Without Renal Insufficiency

Cited by 4 publications

References 29 publications

How to prevent, recognize, and treat drug-induced nephrotoxicity.

How to prevent, recognize, and treat drug-induced nephrotoxicity.

Extent of Renal Effect of Cyclo‐oxygenase‐2‐selective Inhibitors Is Pharmacokinetic Dependent

Aspirin, Non-Aspirin Analgesics and the Risk of Hypertension in the SUN Cohort

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