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Ibuprofen Side Effects on Kidneys. When taken at the recommended dose of no more than 1,200 mg per day for a short duration, the risk of kidney harm from ibuprofen is minimal for most people. In certain situations, however, ibuprofen may damage the kidneys, leading to sudden failure or long-term kidney disease.
While NSAIDs rarely affect the liver, they have important adverse effects on the kidney that you should know about. Here is the science behind the problem. Ibuprofen and other NSAIDs block prostaglandins, natural body chemicals that normally dilate blood vessels leading to the kidneys.
Kidney Effects Rxlist lists several kidney, or renal, effects due to the long-term use of NSAIDs such as ibuprofen. These include renal papillary necrosis, or cell death, renal toxicity and other renal injuries.
Kidney damage -- Ibuprofen: Introduction. Kidney damage -- Ibuprofen: Damage or injury to kidneys caused by a type of analgesic called Ibuprofen. Mild kidney damage may cause few if any symptoms whereas severe damage can ultimately result in kidney failure. Symptoms may be acute, subacute or chronic depending on the severity of the toxicity.
Ibuprofen is a painkiller or NSAIDs that has adverse effects on the organs of the human body. There are countless people in the world who take counter- pain relievers. Excessive intake of ibuprofen directly impacts the kidney function.
The most common side effects are nausea, vomiting, and headache. Other possible adverse effects include rash, heartburn, dermatitis, decreased white blood cells, red blood cells, and platelets, and acute renal failure. While ibuprofen does not itself affect the liver, it can have very significant effects on the kidney.
Analgesic nephropathy is injury to the kidneys caused by analgesic medications such as aspirin, phenacetin, and paracetamol. The term usually refers to damage induced by excessive use of combinations of these medications, especially combinations that include phenacetin. It may also be used to describe kidney injury from any single analgesic medication. The specific kidney injuries induced by analgesics are renal papillary necrosis and chronic interstitial nephritis. They appear to result from decreased blood flow to the kidney, rapid consumption of antioxidants, and subsequent oxidative damage to the kidney. This kidney damage may lead to progressive chronic kidney failure, abnormal urinalysis results, high blood pressure, and anemia. A small proportion of individuals with analgesic nephropathy may develop end-stage kidney disease. Analgesic nephropathy was once a common cause of kidney injury and end-stage kidney disease in parts of Europe, Australia, and the United States. In most areas, its incidence has declined sharply since the use of phenacetin fell in the 1970s and 1980s.
Acute kidney injury (AKI), previously called acute renal failure (ARF), is an abrupt loss of kidney function that develops within 7 days. Its causes are numerous. Generally it occurs because of damage to the kidney tissue caused by decreased kidney blood flow (kidney ischemia) from any cause (e.g., low blood pressure), exposure to substances harmful to the kidney, an inflammatory process in the kidney, or an obstruction of the urinary tract that impedes the flow of urine. AKI is diagnosed on the basis of characteristic laboratory findings, such as elevated blood urea nitrogen and creatinine, or inability of the kidneys to produce sufficient amounts of urine. AKI may lead to a number of complications, including metabolic acidosis, high potassium levels, uremia, changes in body fluid balance, and effects on other organ systems, including death. People who have experienced AKI may have an increased risk of chronic kidney disease in the future. Management includes treatment of the underlying cause and supportive care, such as renal replacement therapy.
Nonsteroidal anti-inflammatory drugs (NSAIDs) are a drug class that reduce pain, decrease fever, prevent blood clots and, in higher doses, decrease inflammation. Side effects depend on the specific drug, but largely include an increased risk of gastrointestinal ulcers and bleeds, heart attack and kidney disease. The term nonsteroidal distinguishes these drugs from steroids, which while having a similar eicosanoid-depressing, anti-inflammatory action, have a broad range of other effects. First used in 1960, the term served to distance these medications from steroids. NSAIDs work by inhibiting the activity of cyclooxygenase enzymes (COX-1 and/or COX-2). In cells, these enzymes are involved in the synthesis of key biological mediators, namely prostaglandins which are involved in inflammation, and thromboxanes which are involved in blood clotting. There are two types of NSAID available: non-selective and COX-2 selective. Most NSAIDs are non-selective, and inhibit the activity of both COX-1 and COX-2. These NSAIDs, while reducing inflammation, also thin the blood (especially aspirin) and increase the risk of gastrointestinal ulcers/bleeds.