NSAIDs interactions with diuretics

Thiazide diuretics do not stimulate or require prostaglandins to produce their desired effect and they do not directly interact with NSAIDs. The magnitude of increased risk of NSAID-induced AKI with concomitant triamterene cannot be estimated based on sporadic case reports [44]. 

The hypotensive effects of most antihypertensive dru are increased when administered with diuretics and other antihypertensives. Many dnigp can interact with the antihypertensive drugs and decrease their effectiveness (eg, antidepressants, monoamine oxidase inhibitors, antihistamines, and sympathomimetic bronchodilators). When the ACE inhibitors are administered with the NSAIDs, their antihypertensive effect may be decreased. Absorption of the ACE inhibitors may be decreased when administered with the antacids. Administration of potassium-sparing diuretics or potassium supplements concurrently with the ACE inhibitors may cause hyperkalemia. When the angiotensin II receptor agonists are administered with... 

Sulfonylureas In acute poisoning with sulfonylureas, the stomach should be washed and treated with activated charcoal, and hypoglycemia must be treated. Sulfonylureas interact with oral contraceptives, thiazide diuretics, corticosteroids, adrenaline, chlorpromazine, ACE inhibitors, some NSAIDs, antihistamines, anticoagulants, MAOIs, antidepressants, and many other drugs. Care must be exercised when treating with sulfonylureas. 

Drug interactions with lithium have been reviewed (569-573) another review focused on interactions in the elderly (573). A review of drug interactions with lithium considered both pharmacokinetic interactions [for example diuretics, nonsteroidal anti-inflammatory drugs (NSAIDs)] and pharmacodynamic interactions (for example antipsychotic drugs, SSRIs) and summarized the most important ones in tabular form (569). 

Clinically important, potentially hazardous interactions with aspirin, boswellia, ciprofibrate, diuretics, methotrexate, NSAIDs, oxycodone hydrochloride, salicylates, tacrine, tacrolimus, urokinase... 

Much less is known about the interactions of NSAIDs with bumetanide, and even less about piretanide and torasemide, but the evidence suggests that they probably interact in the same way as furosemide and indomet-acin. It would therefore seem prudent to be alert for interactions with any of the NSAIDs with which furosemide interacts. See also Loop diuretics + Aspirin , p.948, for a discussion of the interactions between aspirin and bumetanide or furosemide. 

The most potentially serious drug interactions include the concomitant use of NSAIDs with lithium, warfarin, oral hypoglycemics, high-dose methotrexate, antihypertensives, angiotensin-converting enzyme inhibitors, fi-blockers, and diuretics. 

Lithium intoxication can be precipitated by the use of diuretics, particularly thiazides and metola-zone, and ACE inhibitors. NSAIDs can also precipitate lithium toxicity, mainly due to NSAID inhibition of prostaglandin-dependent renal excretion mechanisms. NSAIDs also impair renal function and cause sodium and water retention, effects which can predispose to interactions. Many case reports describe the antagonistic effects of NSAIDs on diuretics and antihypertensive drugs. The combination of triamterene and indomethacin appears particularly hazardous as it may result in acute renal failure. NSAIDs may also interfere with the beneficial effects of diuretics and ACE inhibitors in heart failure. It is not unusual to see patients whose heart failure has deteriorated in spite of increased doses of frusemide who are also concurrently taking an NSAID. 

Renal prostaglandins are involved in the mechanism of action of diuretics. NSAIDs block the synthesis of prostaglandins and hence can reduce the effects of diuretics. The combination may also increase the risk of NSAID-induced nephrotoxicity [5]. Patients with cirrhosis and ascites are at a greater risk of this interaction. 

The interaction between potassium-sparing diuretics and NSAIDs is well documented (SED-14, 674). The major complications are deterioration of renal function and hjrper-kalemia. The risk associated with the non-selective COX-2 inhibitors is unknown. However, three patients had hyperkalemia (8.5, 5.4, and 5.1 mmol/1) after developing acute renal insufficiency while taking these drugs (8). 

NSAIDs can cause or aggravate hjrpertension and interact negatively with the effects of antihjrpertensive drugs, including diuretics, although contrasting data from experimental and clinical studies have been published (21). 

All NSAIDs interfere with hypertension control in patients taking diuretics, beta-blockers, or vasodilators, although contrasting data have been published on the effects of these drugs on blood pressure (233). Moreover, they interact diversely with different... 

Persons at greatest risk for NSAID hemodynamic nephropathy generally have pre-existing renal insufficiency, medical problems associated with high plasma renin activity (hepatic disease with ascites, decompensated congestive heart failure, or intravascular volume depletion), or systemic lupus erythematosus. Additional risk factors include atherosclerotic cardiovascular disease and diuretic therapy. The elderly are also at higher risk due to interaction of prevalent medical problems, multiple drug therapies, and reduced renal hemodynamics. Advanced age, however, has not been shown to be an independent risk factor for toxicity in limited trials in otherwise healthy elderly subjects. Combined NSAID and ACEl or ARB therapy is also a concern and should be avoided. 

DRUG INTERACTIONS As do other NSAIDs, the propionic acid derivatives may interfere with the action of antihypertensive and diuretic agents, increase the risk of bleeding with warfarin, and increase the risk of bone marrow suppression with methotrexate. Ibuprofen also has been... 

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