Why do nsaids cause edema

One option is to take separate drugs that reduce acid production in the stomach. Using a different type of pain reliever is another option.

Nonsteroidal anti-inflammatory drugs are non-opioid analgesic medications that people primarily use to treat mild symptoms of pain throughout the body.

People can get OTC versions or get a prescription from a doctor for stronger pain relievers. Many people take NSAIDs on an as-needed basis to treat mild conditions, such as headaches, fever from cold or flu, or period cramps. However, people may wish to take certain precautions to reduce the risk of side effects.

People with risk factors for some health conditions and those who need to take other medications should speak with a doctor before taking NSAIDs. There are many types of headache. Some are mild and pass quickly, while others can indicate a more serious condition. Here, learn about some common…. Bone and muscle pain tend to feel very similar, so it is difficult to differentiate.

Learn more about the causes and types of pain here. Period pain, or dysmenorrhea, is a common condition that causes pain and cramping around menstruation. Learn the causes and treatments. Nonsteroidal anti-inflammatory drugs: prostaglandins, indications, and side effects.

Most of the side effects are related to COX-1 inhibition, due to its action in several systems associated with cell cleansing. In the kidneys, they are in greater quantities acting in glomerular filtration maintenance.

Therefore, studies indicate that individuals with previously compromised renal function are the most affected by the time-dependent use of non-selective NSAIDs. The action of COX-2 is associated with water and electrolytic maintenance in the renal environment, which worsens its effects under dehydration, low renal perfusion or previously existing renal damage. In order to adequately perform their filtration function, these organs have regulatory mechanisms, such as prostaglandin synthesis, which will maintain glomerular filtration rate GFR and renal homeostasis.

NSAIDs and kidney. J Assoc Physicians India ; NSAIDs inhibit the cascade of arachidonic acid, selectively or not, causing a nonpermissive effect on the formation of prostaglandins. Effects of nonsteroidal anti-inflammatory meloxicam on stomach, kidney, and liver of rats. Toxicol Ind Health ; In the kidneys, prostaglandins - mainly prostacyclins, PGE2, PGD2 - will act as vasodilators in the afferent arteriole, increasing renal perfusion, with distribution of the cortex flow to the nephrons in the renal medullary region.

This vasodilatation acts as a negative feedback on the mechanisms, such as the performance of the renin-angiotensin-aldosterone system and the sympathetic nervous system, culminating with compensation to ensure adequate flow to the organ. NSAIDs inhibit this mechanism and may result in acute vasoconstriction and spinal cord ischemia, which can lead to acute renal injury.

In addition to the vasodilatation action, through the stimulation of tubular receptors PGE2 will inhibit the transport of sodium and chloride in the ascending loop of Henle and in the collecting ducts, by means of stimulating of the EP1 receptor, leading to natriuresis.

Eur Rev Med Pharmacol Sci ; Nonsteroidal Anti-Inflammatory Drugs and the Kidney. Pharmaceuticals Basel ; NSAIDs may also cause higher sodium and water retention by inhibiting PGE2 production, leading to the formation of edema, which is often subclinical. Clinical trials comparing different NSAIDs show the development of hypertension, especially when using high doses and for a prolonged time, with ibuprofen being more involved.

Cardiovascular safety of nonsteroidal anti-inflammatory drugs revisited. Postgrad Med ; In addition to its actions in the kidneys, prostaglandins perform several functions related to homeostasis, such as protection of the gastrointestinal mucosa, platelet activation, inflammation, bronchodilation, and others. Kidney damage caused by the use of NSAIDs is not common, especially when it comes to individuals who are previously healthy and who do not use abusive or high doses of these drugs.

Some factors, such as advanced age and comorbidities, which in themselves already lead to a decrease in GFR, increase the risk of NSAID-related nephrotoxicity, contributing to the development of side effects. One of the risk factors is systemic arterial hypertension, which causes an even higher activation of the renin-angiotensin-aldosterone system RAAS and the sympathetic nervous system, leading to vasoconstriction; and the inhibition of prostaglandin synthesis causes the loss of the compensatory mechanism of renal vasodilation.

The same applies to comorbidities that lead to a decrease in effective arterial volume, such as nephrotic syndrome with a high level of proteinuria, liver cirrhosis, especially in those with ascites, heart failure and lupus nephritis.

Patients with these conditions using NSAIDs have an inhibition of the kidney-compensation mechanism, as it happens in hypertensive patients, which contributes to renal damage. As already explained above, prostaglandins PGs play an important role in maintaining renal activity.

The main hydroelectrolytic and acid-basic changes caused by this class of drugs are sodium retention causing edema and hypertension , hyperkalemia and metabolic acidosis due to the lower activity of COX-1 and COX Electrolyte and Acid-base disturbances associated with non-steroidal anti-inflammatory drugs. Electrolyte Blood Press ; The inhibition of prostaglandin-mediated vasodilatation PGE-2 prevents adequate renal perfusion.

Diuretics have limited benefit. Elevation of the affected limb above the level of the heart and the use of support stockings can alleviate venous hypertension and reduce edema, 26 and support stockings have been found to significantly reduce the incidence of edema and DVT on long-distance flights i.

Many medications have been implicated in pedal edema, especially vasodilators, estrogens, NSAIDs, and calcium channel blockers. Dihydropyridine drugs are more likely than other calcium channel blockers to cause pedal edema. The edema appears to be dose-dependent and increases over time. However, angiotensin-converting enzyme inhibitors and angiotensin-receptor blockers seem to be effective. Lymphedema is the general term for a group of pathologic conditions characterized by excessive regional interstitial accumulation of protein-rich f luid.

Distinguishing lymphedema from other forms of edema may be challenging, especially early in its course. A computed tomography CT or magnetic resonance imaging MRI scan may be necessary to confirm the diagnosis. A characteristic honeycomb pattern in the subcutaneous compartment distinguishes lymphedema from other edemas; MRI is considered superior to CT in diagnosing patients with this finding. Treatment may be initiated if the circumference of the arm increases by 2 cm from the preoperative measurement.

Long-term use of compression garments coupled with meticulous skin care and avoidance of blood-pressure measurements and other constrictions on the affected site are likely helpful. Diuretics may be of benefit early in the course of the disease but rarely are effective on a long-term basis. Surgical treatment is of little benefit, although it may play a debulking role in patients with advanced elephantiasis.

Already a member or subscriber? Log in. Interested in AAFP membership? Learn more. School of Medicine. Cooperative Hospitals. Chennubhotla received her medical degree from Gandhi Medical College, Osmania University, Hyderabad, India, and completed a family medicine residency and geriatric fellowship at the University of Louisville School of Medicine. Francis Hospital, Evanston, Ill. Address correspondence to James G. Broadway, Suite , Louisville, KY e-mail: jgobri01 gwise.

Reprints are not available from the authors. The authors indicate that they do not have any conflicts of interest. Sources of funding: none reported. Eknoyan G. A history of edema and its management. Kidney Int Suppl. Rose BD. Pathophysiology and etiology of edema. In: Rose BD, ed. Wellesley, Mass. Approach to the adult with edema. Ellison DH. Am J Kidney Dis. How do loop diuretics act? Brater DC. Diuretic therapy. N Engl J Med. Response of the kidney to furosemide. Effects of salt intake and renal compensation.

J Lab Clin Med. Diuretic efficacy of high dose furosemide in severe heart failure: bolus injection versus continuous infusion. J Am Coll Cardiol. Furst DE. Clinically important interactions of nonsteroidal antiinflammatory drugs with other medications. J Rheumatol Suppl. Structural adaptation of the distal convoluted tubule to prolonged furosemide treatment.

Am J Physiol. Knauf H, Mutschler E. Sequential nephron blockade breaks resistance to diuretics in edematous states. J Cardiovasc Pharmacol. De Bruyne LK. Mechanisms and management of diuretic resistance in congestive heart failure.

Postgrad Med J. Consensus recommendations for the management of chronic heart failure. On behalf of the membership of the advisory council to improve outcomes nationwide in heart failure.

Am J Cardiol. If your side effects are mild, you may be able to take another drug to lessen the effects. People with heart, kidney, or digestive conditions, and older people in general, are more likely to have a risk for side effects. In general, discuss any diseases and all your medications and supplements with your doctor to rule out any possible adverse reactions with NSAIDs.

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