How Soon After Taking Naproxen Can I Drink Alcohol?

Frequently asked questions – What should I do if I have already mixed naproxen and alcohol? As naproxen is usually safe to take alongside alcohol, mixing both these substances in safe quantities should not be a cause for concern. However, if you are experiencing any of the side effects listed above or are finding it difficult to control your intake of alcohol or naproxen, we would strongly recommend contacting a health professional or local addiction treatment service to discuss your concerns.

Can I drink alcohol 4 hours after taking naproxen?

Can I drink alcohol while taking naproxen? Yes, you can drink alcohol while taking naproxen. But drinking too much alcohol may irritate your stomach.

How long does 1 naproxen stay in your system?

How long does naproxen stay in your system? Medically reviewed by, Last updated on Oct 17, 2022. After taking your last dose of naproxen it should be out of your system within 93.5 hours. Naproxen has an elimination half life of 12 to 17 hours. This is the time it takes for your body to reduce plasma drug levels by half.

How much naproxen can I drink?

Safe dose for adults For adults using OTC naproxen, the recommended dose is 220 mg (1 tablet) every 8 to 12 hours as needed. Don’t take more than 660 mg (3 tablets) per day.

How long after taking naproxen can I take something else?

Can You Double Up on Pain Killers? My brother-in-law recently asked me if he could take Aleve (naproxen) and Motrin (ibuprofen, Advil) together. Apparently, he pulled a muscle while trying to relive the glory days of his college football playing. When talking about painkillers, it’s important to understand the difference among products.

• There are four main types of oral analgesics that are available without a prescription: naproxen (brand name Aleve), ibuprofen (brand names Advil and Motrin), aspirin, and acetaminophen (brand name Tylenol).
• Naproxen and ibuprofen work in the body the same and have the same side effects.
• Ibuprofen is typically taken every 6-8 hours; naproxen is taken every 12 hours.

Aspirin works a little differently than ibuprofen and naproxen but has very similar side effects. The usual dose of aspirin is 500-1,000 mg every 4-6 hours. Acetaminophen works a little differently than naproxen and ibuprofen, has different side effects, and can be taken every 6-8 hours.

So, to answer my brother-in-law’s question He could take his naproxen (Aleve) eight hours after taking ibuprofen (Motrin, Advil) or he could take ibuprofen 12 hours after taking naproxen. However, if he was not getting adequate pain relief from ibuprofen within the eight-hour period, he could take acetaminophen (Tylenol).

I advised him to stay within the recommended dosage for both medicines. The bottom line for weekend warriors is that you cannot combine ibuprofen and naproxen unless it is time for another dose of either medication. If you need additional pain relief, you can combine aspirin, naproxen, or ibuprofen with acetaminophen.

However, do not take aspirin, naproxen, or ibuprofen within 8-12 hours of each other. Also, watch out for pain medications that might be included in combination products such as those used for cough and cold. It is important to note that my brother-in-law is healthy and has no other medical problems. If you have other medical conditions, please consult your pharmacist to find out which pain medications are safe for you.

: Can You Double Up on Pain Killers?

Can I take naproxen 2 hours after drinking?

There are 4 alcohol/food/lifestyle interactions with naproxen. Ask your doctor before using naproxen together with ethanol. Do not drink alcohol while taking naproxen. Alcohol can increase your risk of stomach bleeding caused by naproxen. Call your doctor at once if you have symptoms of bleeding in your stomach or intestines.

Why avoid caffeine with naproxen?

Table 1 – List of CYP1A2 substrates, inducers and inhibitors.

Substrates	Inducers	Inhibitors
agomelatine alosetron amitriptyline asenapine caffeine chlorpromazine clomipramine clopidogrel clozapine cyclobenzaprine dacarbazine domperidone duloxetine ergotamine estradiol flutamide fluvoxamine frovatriptan guanabenz haloperidol imipramine lidocaine melatonin mirtazapine nabumetone	nacetamoline nacetamoline naproxen ondansetron olanzapine oxytamine paracetamol phenacetin pirfenidone pomalidomide propafenone propranolol ramelteon ramosetron riluzole ropivacaine ropirinole R-warfarin tacrine tasimelteon theophylline tizanidine triamterene verapamil zolmitriptan	antipyrine carbamazepine coffee insulin lansoprazole nafcillin nelfinavir omeprazole phenobarbital phenytoin pentobarbital polycyclic hydrocarbons (tobacco smoke) primaquine rifampin ritonavir secobarbital sulfinpyrazone teriflunomide	acyclovir allopurinol amiodarone cimetidine clarithromycin disulfiram duloxetine efavirenz enoxacin erythromycin famotidine fluoroquinolones fluvoxamine grapefruit juice isoniazid ketoconazole methoxsalen mexiletine oral contraceptives peginterferon-alfa-2a piperine propafenone rhytomycin ticlopidine tolfenamic acid	troleandomycin rofecoxib verapamil zafirlukast zileuton

CYP1A2 inducers may decrease caffeine concentrations while inhibitors can increase them, leading to adverse effects. In addition, caffeine interacts with legal and illegal drugs including tobacco, alcohol, and cannabis. Tobacco smoke accelerates the metabolism of caffeine through CYP1A2 induction produced in liver microsomes by polycyclic hydrocarbons of tobacco,

Furthermore, an induction of CYP1A2 through cannabis smoking has also been reported, and therefore a reduction in caffeine concentrations is expected in both cases, Additionally, acute alcohol ingestion inhibits caffeine metabolism through CYP1A2, Likewise, caffeine increases clozapine concentrations due to competitive inhibition of CYP1A2,

It has also been reported that caffeine appears to raise the rate of absorption of paracetamol and levodopa with no clear changes in bioavailability, Caffeine augments lithium excretion. A reduction in its consumption can therefore increase lithium concentrations and adverse effects,

Coadministration with caffeine may raise the serum concentrations of theophylline. The proposed mechanism involves competitive inhibition of theophylline metabolism via CYP450 1A2, as well as metabolic conversion of caffeine to theophylline in vivo, and saturation of theophylline metabolism at higher serum concentrations,

The PD interactions of caffeine can be classified as synergistic, additive, and antagonistic in nature. When the overall effect caused by a drug combination is the sum of the pharmacological effects of each individual drug an additive interaction occurs.

• Synergy is produced when the overall effect of the drug combination is greater than additive, and antagonism takes place when the drug combination effect is less than additive,
• Synergic or additive effects of caffeine with other psychostimulants such as cocaine, amphetamines, 3,4-methylenedioxymethamphetamine (MDMA), and cathinones are expected.

Tachycardic and hypertensive effects of sympathomimetics may be enhanced by caffeine, and myocardial ischemia can appear with concurrent use, Caffeine increases postprandial hyperglycaemia and reduces insulin sensitivity, and may decrease the effectiveness of diabetes medication (insulin and oral hypoglycaemic agents),

• Caffeine also reduces methotrexate efficacy possibly due to its antagonistic effects on adenosine receptors.
• Adenosine accumulation results in anti-inflammatory effects,
• Furthermore, caffeine might decrease blood clotting.
• The ingestion of caffeine jointly with medication that reduces clotting might increase the chances of bruising and bleeding.

Some of these include aspirin, clopidogrel, diclofenac, ibuprofen, naproxen, dalteparin, enoxaparin, heparin, and warfarin. In addition, caffeine modestly raises the bioavailability, rate of absorption, and plasma levels of aspirin, On the other hand, caffeine partially antagonizes the effects of sedative drugs such as benzodiazepines, Z-drugs, and alcohol,

During alcohol intoxication, caffeine antagonizes the somnogenic effects of alcohol by blocking the adenosine A1 receptors, while the anxiolytic effects of alcohol could compensate for the anxiogenic effects of caffeine, Additionally, caffeine blocks peripheral pro-nociceptive adenosine signalling, improves analgesic absorption through lower gastric pH and changes perception of pain.

It has been shown to enhance analgesic effects of paracetamol/acetaminophen, acetylsalicylic acid/aspirin, and ibuprofen,

Why was naproxen taken off the market?

The decision to discontinue production of Naprosyn (naproxen) suspension on a global basis was made because of the discontinuation of one of the flavouring agents. This meant extensive reformulation work, stability testing and then registering the new formulation on a worldwide basis.

How long is 500 mg naproxen good for?

Maximum recommended daily dose – People should only use OTC naproxen for a short-term period of between 3–5 days for pain and no more than 3 days for fever. If they need ongoing treatment, people should consult their doctor first. For children between 2–12 years old, the maximum daily dose by weight is 20 mg/kg.

Is naproxen 500 mg a strong painkiller?

Naproxen Use and Chemistry – Is naproxen a strong painkiller ? While naproxen is not a narcotic pain medication, it can still be used for minor pains, body aches, and headaches. Many people find this to be one of the best over-the-counter medications for treating mild to moderate aches and pains.

• Naproxen helps to relieve the discomfort associated with inflammatory conditions as well.
• These conditions might include arthritis and other types of disorders involving the bones or muscles.
• Naproxen works very similar to opioid pain medications such as those that contain hydrocodone, tramadol, or oxycodone.

The stronger pain killers work by binding to the body’s opioid receptors. They are well-known to lead to reactions of the central nervous system. These reactions often include dissociation and euphoria. That is why narcotic pain medications often make someone feel high.

However, naproxen works a bit differently. The chemical reactions occurring in one’s body after using naproxen aren’t the same as when taking narcotics. Since naproxen is an NSAID it inhibits prostaglandin synthesis. When it goes into your bloodstream, COX or cyclo-oxygenase enzymes producing prostaglandin get blocked.

This can take away your pain for anywhere from around 30 minutes to many hours. Naproxen and other NSAIDs don’t bind to the body’s opioid receptors either, so you won’t get the euphoria you would get with the narcotic pain medications.

What should I avoid when taking naproxen?

Taking naproxen with other painkillers – Do not take naproxen with ibuprofen or other non-steroidal anti-inflammatory drugs ( NSAIDs ). But it’s OK to take naproxen with paracetamol or co-codamol that you buy over the counter. This should just be for short periods of time.

• If you often need to take extra painkillers with naproxen or for more than a few days, talk to your doctor.
• Sometimes, taking different painkillers together is a good way to relieve pain, but there may be other treatments you can try.
• It’s OK to take other painkillers with naproxen for longer if your doctor has given them to you on prescription and told you to take them together.

If you’re unsure, talk to your doctor.

How long after taking NSAID can I drink?

In short, you should wait at least 10 hours after your last dose of ibuprofen before drinking alcohol. That’s about how long it takes the average person’s body to clear ibuprofen after a dose. But if you have liver problems, it might take about 17 hours.

Which is stronger ibuprofen or naproxen?

When pain hits, whether from arthritis, menstrual cramps or muscle strains, you want fast and effective pain relief. Nonsteroidal anti-inflammatory drugs, or NSAIDs, are the most common tools for over-the-counter pain relief. Naproxen (Aleve) and Ibuprofen (Advil or Motrin) are two common NSAIDs that are both effective for relieving pain.

Can I go to bed after taking naproxen?

Do not lie down for at least 10 minutes after taking this drug. The dosage is based on your medical condition and response to treatment. To reduce your risk of stomach bleeding and other side effects, take this medication at the lowest effective dose for the shortest possible time.

Can you take naproxen and go to bed?

Precautions – It is very important that your doctor check your progress at regular visits. This will allow your doctor to see if the medicine is working properly and to decide if you should continue to take it. Blood and urine tests may be needed to check for unwanted effects.

This medicine may raise your risk of having a heart attack or stroke. This is more likely in people who already have heart disease or in people who use this medicine for a longer time. This medicine may cause bleeding in your stomach or intestines. This problem can happen without warning signs. This is more likely if you have had a stomach ulcer in the past, if you smoke or drink alcohol regularly, if you are over 60 years of age, are in poor health, or are using certain other medicines (eg, steroid medicine, blood thinner).

Check with your doctor right away if you have pain or tenderness in the upper stomach, pale stools, dark urine, loss of appetite, nausea, vomiting, or yellow eyes or skin. These could be symptoms of a serious liver problem. Serious skin reactions, including exfoliative dermatitis, Stevens-Johnson syndrome, toxic epidermal necrolysis, and drug reaction with eosinophilia and systemic symptoms (DRESS)can occur during treatment with this medicine.

Check with your doctor right away if you have black, tarry stools, blistering, peeling, or loosening of the skin, chest pain, chills, cough, diarrhea, fever, itching, joint or muscle pain, painful or difficult urination, red irritated eyes, red skin lesions, sore throat, sores, ulcers, or white spots in the mouth or on the lips, swollen glands, unusual bleeding or bruising, or unusual tiredness or weakness.

Some possible warning signs of some serious side effects that can occur during treatment with this medicine may include swelling of the face, fingers, feet, or lower legs, severe stomach pain, black, tarry stools, or vomiting of blood or material that looks like coffee grounds, unusual weight gain, yellow skin or eyes, decreased urination, unusual bleeding or bruising, or skin rash.

• Also, signs of serious heart problems could occur including chest pain or tightness fast or irregular heartbeat, unusual flushing or warmth of the skin, weakness, or slurring of speech.
• Check with your doctor immediately if you notice any of these warning signs.
• Check with your doctor right away if you have bloody urine, a decrease in frequency or amount of urine, an increase in blood pressure, increased thirst, loss of appetite, lower back or side pain, nausea, swelling of the face, fingers, or lower legs, trouble breathing, unusual tiredness or weakness, vomiting, or weight gain.

These could be symptoms of a serious kidney problem. Hyperkalemia (high potassium in the blood) may occur while you are using this medicine. Check with your doctor right away if you have stomach pain, confusion, difficulty with breathing, irregular heartbeat, nausea or vomiting, nervousness, numbness or tingling in the hands, feet, or lips, or weakness or heaviness of the legs.

This medicine may also cause serious allergic reaction called anaphylaxis, which can be life-threatening and requires medical attention. Although this is rare, it may occur more often in patients who are allergic to aspirin or to any of the nonsteroidal anti-inflammatory drugs. Anaphylaxis can be life-threatening and requires immediate medical attention.

Tell your doctor right away if you have a rash, itching, hoarseness, trouble breathing, trouble swallowing, or any swelling of your hands, face, or mouth after using this medicine. Using this medicine during the later part of a pregnancy can harm your unborn baby.

1. If you think you have become pregnant while using the medicine, tell your doctor right away.
2. This medicine may cause a delay in ovulation for women and may affect their ability to have children.
3. If you plan to have children, talk with your doctor before using this medicine.
4. Check with your doctor immediately if blurred vision, difficulty with reading, or any other change in vision occurs during or after your treatment.

Your doctor may want you to have your eyes checked by an ophthalmologist (eye doctor). Before having any kind of surgery or medical tests, tell your doctor that you are taking this medicine. It may be necessary for you to stop treatment for a while, or to change to a different nonsteroidal anti-inflammatory drug before your procedure.

• This medicine may cause some people to become dizzy, lightheaded, drowsy, or less alert than they are normally.
• Even if taken at bedtime, it may cause some people to feel drowsy or less alert on arising.
• Make sure you know how you react to this medicine before you drive, use machines, or do anything else that could be dangerous if you are not alert.

Do not take other medicines unless they have been discussed with your doctor. This includes prescription or nonprescription (over-the-counter ) medicines and herbal or vitamin supplements.

Does naproxen make you sleepy?

Key facts –

Take naproxen with or just after a meal or snack.Take the lowest dose of naproxen for the shortest time to control your symptoms.The most common side effects of naproxen are confusion, headache, ringing in the ears, changes in vision, tiredness, drowsiness, dizziness and rashes.For strains and sprains, some doctors recommend waiting 48 hours before taking naproxen because it may slow down healing. If you’re unsure, speak to a doctor.If you’re taking naproxen for a long time or at risk of getting a stomach ulcer, your doctor may prescribe a medicine, such as omeprazole or lansoprazole, to protect your stomach.

Page last reviewed: 20 January 2022 Next review due: 20 January 2025

Can I take naproxen for headache after drinking alcohol?

After a night of drinking, make sure you don’t take Tylenol, Excedrin, or other pain relievers with acetaminophen. The combination of alcohol and acetaminophen can seriously hurt your liver. If you want some pain relief, take aspirin, ibuprofen (Advil) or naproxen (Aleve).

How long after taking ibuprofen can you drink alcohol?

How long after taking ibuprofen can you drink alcohol? – Ibuprofen has a half-life of about 1.9 to 2.2 hours and experts generally agree it takes 4 to 5 half-lives for the body to eliminate a medication. This means it would take at least 10 hours for your body to clear ibuprofen.

Why can’t I sleep after taking naproxen?

Abstract – Previous studies have demonstrated that some nonsteroidal anti-inflammatory drugs (NSAIDs), specifically aspirin and indomethacin, have acute negative effects on sleep in humans and animals. Whether this finding can be replicated and extended to other NSAIDs, particularly the widely used over-the-counter drugs ibuprofen and acetaminophen, was the focus of the present investigation.

1. Thirty-seven male and female subjects slept in the sleep laboratory on 2 consecutive nights; sleep was polygraphically recorded on the second night.
2. Three doses of a prostaglandin-inhibiting drug (i.e., aspirin, acetaminophen, or ibuprofen) or placebo were administered, one each at 2300 h on the day prior to sleep recording, and at 0815 h and 2300 h on the day sleep was recorded.

Subjects slept from 2400-0800 h both nights. Aspirin and ibuprofen disrupted sleep in comparison to placebo by increasing the number of awakenings and percentage of time spent in stage wake, and by decreasing sleep efficiency. Ibuprofen also delayed the onset of the deeper stages of sleep.

Is naproxen hard on the liver or kidneys?

Naproxen Induced Acute Interstitial Nephritis with Renal Cortical Necrosis Department of Nephrology, Aster Medcity Hospital, Kochii, Kerala, India Find articles by Department of Nephrology, Aster Medcity Hospital, Kochii, Kerala, India Find articles by Department of Nephrology, Aster Medcity Hospital, Kochii, Kerala, India Find articles by 1 Department of Pathology, Aster Medcity Hospital, Kochii, Kerala, India Find articles by Department of Nephrology, Aster Medcity Hospital, Kochii, Kerala, India Find articles by Department of Nephrology, Aster Medcity Hospital, Kochii, Kerala, India Find articles by Department of Nephrology, Aster Medcity Hospital, Kochii, Kerala, India 1 Department of Pathology, Aster Medcity Hospital, Kochii, Kerala, India Address for correspondence: Dr.V.

1. Narayanan Unni, Lead Senior Consultant, Nephrology, Aster Medcity Hospital, Kuttisahib Road, Near Kothad Bridge, South Chittor P.
2. O, Cheranelloor, Kochi – 682 027, Kerala, India.
3. E-mail: Received 2019 Feb 25; Revised 2019 Aug 2; Accepted 2019 Sep 9.
4. © 2020 Indian Journal of Nephrology This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.

Drug induced acute interstitial nephritis is an idiosyncratic reaction following a drug exposure. The commonest drugs implicated are nonsteroidal anti-inflammatory drugs (NSAIDs), antibiotics and proton pump inhibitors. Renal cortical necrosis is a rare cause of acute kidney injury caused by severe and sustained vasoconstriction of small renal vessels.

1. There is a change in the epidemiology of acute kidney injury especially in developing countries where drug induced acute kidney injury is becoming increasingly common.
2. Naproxen is known to cause renal failure by renal papillary necrosis, tubular damage and acute interstitial nephritis.
3. We present a case of Naproxen induced acute interstitial nephritis with acute cortical necrosis.

To the best of our knowledge this is the first documented case of Naproxen induced renal cortical necrosis. Keywords: Renal cortical necrosis, Naproxen, NSAIDs Significant changes are observed in the epidemiology of acute kidney injury (AKI) in the past decade.

Sepsis and shock is the commonest cause of AKI, especially in developing countries. With better health care and quality of life, now there is a change in epidemiology; more cases of drug induced renal injury are being reported. Incidence of renal cortical necrosis (RCN) is 1.9-2% of all AKI, the commonest cause being obstetric complications.

Drugs especially non-steroidal anti-inflammatory drugs (NSAID’s) are very rarely described in the literature to cause cortical necrosis. A 62-year-old gentleman, presented with fever, nausea, vomiting and bilateral flank pain for 2 days. He had bilateral pedal oedema and was breathless.

He is known to have Type 2 diabetes mellitus for 30 years, with poorly controlled blood sugars (HbA1c – 10%), bilateral non-proliferative diabetic retinopathy and sub-nephrotic range proteinuria with normal serum creatinine. He had systemic hypertension for ten years and was on Losartan (50 mg once daily) for control of blood pressure.

He had taken Naproxen 500 mg twice daily (for migraine) for one week prior to admission. He had no myalgia, icterus, skin or mucosal bleeds, rash, or arthritis. He had no dysuria, haematuria, or lower abdominal pain. No history of haemoptysis or blood in stools, chest pain or hypotensive episodes.

1. He did not have productive cough, sore throat, skin lesions or other focus of infections; no abdominal pain radiating to back.
2. On examination, he was febrile, tachypneic with a blood pressure of 170/90 mmHg.
3. He had bilateral pedal oedema and bilateral basal coarse crepitations on auscultation of chest.

Investigations revealed serum creatinine of 3.1 mg/dl, serum Sodium: 127 meq/L, serum potassium: 5.4 meq/L, metabolic acidosis (pH 7.28, HCO3 18.9, pCO2 35.7, Lactate 1.93); random blood sugar was 200 mg/dl. His haemoglobin was 10.1 g/dL, total count 19,800/Cu.

Mm with neutrophils 75%, lymphocytes 2.9%, eosinophils 14.5% and platelet count 1.8 L/cu mm. He had eosinophilic leucocytosis with absolute eosinophil count of 2800/Cu. mm (normal 20-500/Cu mm) and eosinophiluria (urine eosinophils 39%). Liver function test and Creatinine phosphokinase levels (65.6 mg/dl) were normal.

Ultrasonogram of abdomen showed mildly enlarged kidneys (right kidney 12.5 cm and left kidney 12 cm); both kidneys were hyperechoeic in echotexture with normal pelvicalyceal system. X ray chest was normal and echocardiogram did not show any vegetations.

Plain CT abdomen showed mildly enlarged kidneys and normal collecting system. With the above clinical picture, a provisional diagnosis of acute pyelonephritis was considered and broad-spectrum parenteral antibiotics started. However, there were no urinary tract symptoms, ultrasonogram of abdomen ruled out obstructive uropathy or any collection or abscess.

Meanwhile, urine microscopy showed 3 + albumin, RBC 1/hpf, and WBC 24/hpf. There were no cast or crystals; blood and urine cultures were sterile. C reactive protein was only mildly elevated (55.75 mg/dl). Stool routine and microscopy did not show any ova or cysts.

• Peripheral blood smear was negative for haemoparasites, atypical cells or schistocytes.
• There were no features of hemolysis on blood smear.
• Other infective causes like Leptospirosis, Dengue fever and Malarial illness were ruled out with appropriate tests.
• There were no features of Raynaud’s phenomenon, livedo reticularis, rash or Hollerhorst plaque on ophthalmic fundus examination.

History was reviewed and there was no history of ingestion of any other medications (other than Naproxen and Losartan), native medicines, and poisonous substances. There was no history of animal, insect or snake bite, and no recent severe physical exertion either.

There was no evidence of acute pancreatitis on blood tests or on abdominal imaging. Renal failure worsened over a period of two days and he became oligoanuric with severe uremic symptoms and worsening breathlessness. He was initiated on haemodialysis via non-tunneled internal jugular venous catheter. The patient had persistent fever spikes in spite of broad-spectrum antibiotic and his urine culture and blood cultures were sterile, with no other evidence of sepsis.

Serial blood counts showed a progressive increase in eosinophils from 18.7 to 35.7% (AEC 2880 to 6450 cells/cubic mm). In view of eosinophilia, drug induced fever was considered, and antibiotics were stopped. Renal functions did not improve over a period of ten days and a renal biopsy was done, which showed patchy cortical necrosis and dense eosinophilic infiltrate admixed with lymphoplasmacytic inflammatory infiltrates and focal interstitial edema, suggestive of acute interstitial nephritis.

There was no interstitial granuloma seen. There was no endocapillary proliferation or crescents. There was no evidence of capillary thrombi suggestive of hemolytic uremic syndrome or any features of vasculitis. However, afferent and efferent arterioles showed medial hypertrophy and hyaline arteriosclerosis.

Immunofluorescence test was negative for IgG, IgA, IgM, C3, C1q, kappa, lambda light chains and fibrinogen. There were no intra-parenchymal crystals seen. Doppler of renal vessels was normal and did not show any thrombus that could embolise to kidneys.

The patient was started on oral Prednisolone (1 mg/Kg) and he was continued on dialysis. His urine output steadily increased, serum creatinine improved to 2.6 mg/dL and he was off dialysis after 6 weeks. Steroid was tapered and stopped. The incidence of AKI has been increasing recently and significant changes are observed in the past decade.

There is a change in epidemiology of AKI – the shift of etiology from infectious causes, sepsis and obstetric causes to non-infectious causes like drugs. In a study conducted in Eastern India (1996-2008), in an analysis of 2405 cases, there has been significant increase in drug induced renal failure, mostly caused by NSAIDs and Rifampicin.

NSAIDs are one of the most abused drugs in the community and in a hospital setting that can cause significant renal injury. Acute interstitial nephritis (AIN) accounts for 15-27% of patients with acute kidney injury, whereas renal cortical necrosis is much rarer entity accounting for only 1.9%-2% of all patients with AKI.

Acute interstitial nephritis is caused by drugs, infections and toxins. It is more common with antibiotics, NSAIDs and proton pump inhibitors. It was classically described with Methicillin as a triad of fever, eosinophilia and skin rash which is present in less than 10% of cases.

• NSAID induced acute interstitial nephritis can have more prominent renal failure and proteinuria in the absence of skin rash or other systemic symptoms and can have arthralgia and microscopic haematuria.
• Our patient had most features of AIN – fever, eosinophilic leucocytosis, eosinophiluria, and AKI with fever responding to stopping of offending drug.

The presence of concomitant patchy renal cortical necrosis in a case of acute interstitial nephritis due to NSAIDs is an unusual and unexpected finding. Renal cortical necrosis is caused by intense, severe and sustained vasoconstriction of small renal vessels like afferent arteriole, renal artery thrombosis causing embolic showers or endothelial damage or coagulopathy causing thrombosis that results in severe ischaemic necrosis of patches of glomeruli and tubules.

1. It is a rare cause of AKI (1.9%-2%).
2. Obstetric complications were the main causes (60-70%) of RCN in developing countries.
3. The remaining cases of RCN caused by non-obstetric causes were mostly due to sepsis and haemolytic uremic syndrome.
4. It generally has a poor prognosis.
5. However, with improvement in healthcare, the epidemiology is slowly changing.

The non-obstetric conditions leading to acute cortical necrosis include snake bite (sea snake, green pit viper, Russell viper) (14.2% of all cases of acute renal cortical necrosis in the study), Haemolytic Uremic Syndrome (11.5%), hyper acute kidney rejection in transplant recipients, acute gastroenteritis (4.4%), acute pancreatitis (3.5%), septicemia (2.7%) and drugs (0.9%).

Other causes of ACN include shock, extensive burns, diabetic keto-acidosis, multiple fractures, haemorrhage, other infections like Leptospirosis, Plasmodium falciparum, Meningococcal meningitis, Acquired anti protein S deficiency, post Varicella infection, SLE related and primary anti-phospholipid antibody syndrome, wasp sting, dehydration in infancy or childhood, intra-abdominal procedures, sickle cell crisis and cryoglobulinemia.

Drug-induced cortical necrosis is very rare (0.9% of acute cortical necrosis). Many toxins and drugs are implicated in causing cortical necrosis like hypophosphatemia and myoglobinuria in rhabdomyolysis (severe physical exertion), Tranexamic acid, ethanol and contrast dye.

1. NSAID induced cortical necrosis is even rarer.
2. In our case no other cause of acute cortical necrosis could be found except NSAIDs.
3. NSAIDs cause both immune mediated damage and non-immune mediated damage to the kidneys.
4. Immune mediated damage is due to immunological reaction against endogenous nephritogenic antigens or exogenous antigens processed by tubular cells with cell mediated immunity having a pathogenic role.

Mechanism of non-immune mediated damage is by various mechanisms mostly by non-selective Cyclooxygenase inhibition. NSAID is hypothesised to have caused this intense vasoconstriction by release of cytokines like Endothelin 1 and blocking prostaglandins.

• Naproxen is a non-selective Cyclooxygenase inhibitor, known to cause renal failure by renal papillary necrosis, tubular damage and interstitial nephritis.
• To the best of our knowledge, this is the first reported case of Naproxen-induced renal cortical necrosis.
• The presence of renal cortical necrosis and acute interstitial nephritis due to NSAIDs in the same patient is very rare.

A high index of suspicion is essential to detect this condition early as it has prognostic implications. The authors certify that they have obtained all appropriate patient consent forms. In the form the patient has given his consent for his images and other clinical information to be reported in the journal.

The patient understands that his name and initials will not be published and due efforts will be made to conceal his identity, but anonymity cannot be guaranteed. There are no conflicts of interest.1. Hoste EAJ, Kellum JA, Katz NM, Rosner MH, Haase M, Ronco C. Epidemiology of acute kidney injury. Contrib Nephrol.2010; 165 :1–8.2.

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Is naproxen hard on your system?

– Long-term use of Aleve can make your heart work harder. Aleve makes you retain water, which increases the load on your heart. This extra work can cause pressure on your cardiovascular system and can sometimes lead to a heart attack or stroke. These risks are even greater at higher dosages, even if you don’t have any heart conditions or risk of heart disease.

chest painshortness of breathslurred speechweakness in your arms or legs

These are signs of a stroke or heart attack, If you take Aleve and have unexplained weight gain or swelling, especially in your legs and feet, talk to your doctor right away. These may be signs of heart failure. To lower your risk of heart problems, use the lowest dosage for the shortest amount of time.

Can I take paracetamol 4 hours after naproxen?

Taking naproxen with other painkillers – Do not take naproxen with ibuprofen or other non-steroidal anti-inflammatory drugs ( NSAIDs ). But it’s OK to take naproxen with paracetamol or co-codamol that you buy over the counter. This should just be for short periods of time.

If you often need to take extra painkillers with naproxen or for more than a few days, talk to your doctor. Sometimes, taking different painkillers together is a good way to relieve pain, but there may be other treatments you can try. It’s OK to take other painkillers with naproxen for longer if your doctor has given them to you on prescription and told you to take them together.

If you’re unsure, talk to your doctor.

How long after taking NSAID can I drink?

In short, you should wait at least 10 hours after your last dose of ibuprofen before drinking alcohol. That’s about how long it takes the average person’s body to clear ibuprofen after a dose. But if you have liver problems, it might take about 17 hours.

What happens if I take 4 naproxen in 24 hours?

Symptoms of naproxen sodium overdose include: Agitation, confusion, incoherence (the person is not understandable) Blurred vision. Coma.

Is naproxen 500 mg a strong painkiller?

Naproxen Use and Chemistry – Is naproxen a strong painkiller ? While naproxen is not a narcotic pain medication, it can still be used for minor pains, body aches, and headaches. Many people find this to be one of the best over-the-counter medications for treating mild to moderate aches and pains.

1. Naproxen helps to relieve the discomfort associated with inflammatory conditions as well.
2. These conditions might include arthritis and other types of disorders involving the bones or muscles.
3. Naproxen works very similar to opioid pain medications such as those that contain hydrocodone, tramadol, or oxycodone.

The stronger pain killers work by binding to the body’s opioid receptors. They are well-known to lead to reactions of the central nervous system. These reactions often include dissociation and euphoria. That is why narcotic pain medications often make someone feel high.

However, naproxen works a bit differently. The chemical reactions occurring in one’s body after using naproxen aren’t the same as when taking narcotics. Since naproxen is an NSAID it inhibits prostaglandin synthesis. When it goes into your bloodstream, COX or cyclo-oxygenase enzymes producing prostaglandin get blocked.

This can take away your pain for anywhere from around 30 minutes to many hours. Naproxen and other NSAIDs don’t bind to the body’s opioid receptors either, so you won’t get the euphoria you would get with the narcotic pain medications.