Like other NSAIDs, ibuprofen relieves inflammation, which causes pain, or blocks pain signals going to the brain. Some analgesics contain a combination of painkilling ingredients in one pill——such as aspirin, acetaminophen and caffeine. What analgesics are safe for people who have kidney disease? My doctor recommended that I take an aspirin in low doses every day to prevent heart attacks. Will this hurt my kidneys? I have arthritis and I need pain medicines frequently.
How do I know if analgesics have affected my kidneys? If I need pain medicines, what can I do to keep my kidneys healthy? How you take these medicines makes a difference: Make sure you read the warning label before using any over—the—counter analgesics. Do not use over—the—counter pain relievers more than 10 days for pain or more than three days for fever. If you have pain or fever for a longer time, you should see your doctor. Avoid using pain medicines that contain a combination of ingredients, like aspirin, acetaminophen and caffeine mixed together in one pill.
If you are taking pain medicines, increase the amount of fluid you drink to six to eight glasses a day. If you are taking pain medicines, avoid drinking alcohol. Talking with your doctor about pain medicines can also make a difference: If you have kidney disease, ask your doctor before taking a pain medicine, particularly NSAIDs and higher dose aspirin. This is especially important if you take diuretic medications or are over 65 years of age.
Make sure your doctor knows about all medicines you are taking, even over-the-counter medicines. Other safety tips: If you have pain medicines in your house, make sure children cannot reach them. To avoid serious interactions with prescription medicines, check with your pharmacist or doctor before using analgesics, if you take other drugs on a regular basis. And, throw away any unused pain medicines after the expiration date.
Patients with pre-renal injury may have signs of volume depletion eg, tachycardia, absolute or postural hypotension, low jugular venous pressure, dry mucous membranes. Patients with interstitial nephritis may have features of a systemic hypersensitivity including fever, arthralgia and a pruritic erythematous rash.
Eosinophilia may also be present. Maximal inhibition occurs at steady state plasma concentrations usually 3—7 days. Renal prostaglandins cause dilatation of the renal afferent arteriole. This mechanism is important for maintaining GFR when renal blood flow is reduced ie, not in young, healthy people 1. Patients and Methods Medical records of fifteen inpatients aged 9 to 19 years mean age of Results Table 1 describes the clinical characteristics of the fifteen patients.
Open in a separate window. Nephrotic syndrome Only one out of the fifteen patients had nephrotic range proteinuria. Kidney Biopsy Five out of fifteen patients underwent biopsy including the patient above. Dialysis Therapy Two patients required dialysis for uremic symptoms. Steroid Therapy One patient with biopsy confirmed AIN required steroid therapy for six months for complete recovery of renal function [ 8 ].
Outcome The mean duration of hospitalization was 7. Discussion We describe fifteen inpatients that were previously healthy without a history of previous kidney conditions and developed AKI. Acknowledgements The authors wish to thank Cason Jones for assistance with manuscript preparation.
References and Notes 1. John R. Renal Toxicity of Therapeutic Drugs. J Clin. Onay O. Acute, reversible nonoliguric renal failure in two children associated with analgesic-antipyretic drugs. Kause I. Acute renal failure, associated with non-steroidal anti-inflammatory drugs in healthy children. Moghal N. Care in the use of ibuprofen as antipyretic in children. Whelton A. Nephrotoxicity of nonsteroidal anti-inflammatory drugs: physiological foundations and clinical implications.
Ulinski T. Acute renal failure after treatment with non-steroidal anti-inflammatory drugs. Clarkson M. Acute interstitial nephritis: clinical features and response to corticosteroid therapy. Dixit M. Non-steroidal anti-inflammatory drugs-associated acute interstitial nephritis with granular tubular basement membrane deposits. Schwartz G.
A simple estimate of glomerular filtration rate in children derived from body length and plasma creatinine. John C. Ravnskov U. Glomerular, tubular and interstitial nephritis associated with non-steroidal anti-inflammatory drugs. Evidence of a common mechanism.
You can change your cookie settings at any time. Non-steroidal anti-inflammatory drugs NSAIDs , including COX-2 inhibitors may rarely precipitate renal failure, and vulnerable particularly elderly patients may be at increased risk.
Prescribing information for NSAIDs includes warnings about renal impairment and renal failure, and advises that the risk of renal failure is highest in those with existing renal impairment. In patients with conditions that cause renal hypoperfusion, prostaglandin production may be increased to maintain adequate renal blood flow. The adverse renal effects associated with NSAIDs are mainly mediated via inhibition of prostaglandin-induced vasodilation and can result in reduced renal blood flow.
Patients with conditions such as hypovolaemia, congestive heart failure, liver cirrhosis, or multiple myeloma are at particular risk. Contributing risk factors include the current administration of medicines such as angiotensin converting enzyme ACE inhibitors, angiotensin II receptors antagonists, and diuretics.
NSAIDs may also produce direct toxic effects on the kidney. The main mechanisms for acute renal failure include acute tubular necrosis and acute interstitial nephritis.
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