Patients taking angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), beta-blockers, thiazide diuretics, or loop diuretics may have impaired response to these therapies when taking NSAIDs [see Drug Interactions (7)]. This information is generalized and not intended as specific medical advice.
doctor or pharmacist) may already be aware of this drug interaction and may be monitoring you for it. doctor or pharmacist) for more information.The effects of your blood pressure medicine may decrease.
Afferent blood flow to the glomerulus is aided by vasodilation mediated through prostaglandins. There is also evidence of acute kidney injury in both NSAID and ACE inhibitor.
These acute effects were especially prominent in CHF and the elderly.While there is evidence suggesting NSAID’s potential to increase blood pressures of both hypertensive and normotensive patients, pain is also implicated in this issue. Wynckel et al. These medicines may cause some risk when taken together. Monitor blood pressure in patients treated with Sumatriptan and Naproxen sodium tablets.
DDAVP - Clinical Pharmacology. Of the 15, only one patient had pre-existing renal diseases. 2004;59:239-243. From the AKI, the patients experienced one of more of the following: proteinuria, hematuria, elevations in serum creatinine (mean 4.09 ± 4.24 mg/dL), and a mean eGFR 8.2 ± 20.5 mL/min.However, this drug-drug interaction is not entirely one-sided. 2000;172:184-185. The use of NSAIDs, including cyclooxygenase (COX)-2 selective inhibitors, can inhibit this vasodilation, resulting in compromised blood supply to the glomerulus. 2006;72;54. COX-2 produces PG, which help regulate homeostasis within the kidneys. Contact your healthcare professional (e.g. Patients who rely on NSAIDs to treat chronic diseases should not stop taking them without talking to their provider.
For patients taking ACEI mono-therapy, lumiracoxib resulted in a fall of MSABP by 4.6 mmHg and ibuprofen showed an increase 3.7 mmHg. These effects are typically not seen in normotensive patients or those with normal renal function, but occur more in patients with kidney or blood pressure pathologies.Traditional NSAIDs target COX-1 and COX-2 for inhibition, while newer, more selective NSAIDs target just COX-2. The presumed mechanism of these effects on the kidneys and blood pressure stem from NSAIDs affect on prostaglandins (PG). Wynckel et al.
It may be necessary to change the dosage of your blood pressure medicine or change your pain medicine.Your healthcare professionals (e.g. ACEIs/ARBs/RAAS Antagonists .
This copyrighted material has been downloaded from a licensed data provider and is not for distribution, except as may be authorized by the applicable terms of use.Things to remember when you fill your prescription.WebMD does not provide medical advice, diagnosis or treatment. If combination therapy is needed in patients with impaired renal function and/or in those with less-controlled hypertension, therapy can still be recommended, however, regular monitoring of serum creatinine, GFR, and blood pressure will be warranted under those circumstances. If negative changes in renal or BP parameters are seen after administration of NSAID therapy, discontinuation of the NSAIDs should be considered to see if the values normalize, then alternative therapies to NSAIDs should be considered.
ACE inhibitors/ARBs and NSAIDs can act synergistically to compromise renal function.
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