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What is the most common cause of acute kidney injury?

What is the most common cause of acute kidney injury?/Acute kidney injury (AKI) is where your kidneys suddenly stop working properly. It can range from minor loss of kidney function to complete kidney failure. AKI normally happens as a complication of another serious illness.

Acute kidney injury, previously known as acute renal failure, denotes a sudden and often reversible reduction in kidney function, as measured by increased creatinine or decreased urine volume. This activity reviews the evaluation and management of acute kidney injury and highlights the role of the interprofessional team in managing patients affected by this condition.

Acute kidney injury (AKI), previously called acute renal failure (ARF), denotes a sudden and often reversible reduction in kidney function, as measured by glomerular filtration rate (GFR).[rx][rx][rx] Although, immediately after a renal insult, blood urea nitrogen (BUN) or creatinine levels may be within the normal range. The only sign of acute kidney injury may be a decline in urine output. AKI can lead to the accumulation of water, sodium, and other metabolic products. It can also result in several electrolyte disturbances. It is a very common condition, especially among hospitalized patients. It can be seen in up to 7% of hospital admissions and 30% of ICU admissions. There is no clear definition of AKI; however, several different criteria have been used in research studies such as RIFLE, AKIN (Acute Kidney Injury Network), and KDIGO (Kidney Disease: Improving Global Outcomes) criteria. Among these, KDIGO is the most recent and most commonly used tool. According to KDIGO, AKI is the presence of any of the following:

Increase in serum creatinine by 0.3 mg/dL or more (26.5 micromoles/L or more) within 48 hours
Increase in serum creatinine to 1.5 times or more baseline within the prior seven days
Urine volume less than 0.5 mL/kg/h for at least 6 hours

Causes of Acute Kidney Injury

The impetus for glomerular filtration is the difference in the pressures between the glomerulus and the Bowman space. This pressure gradient is affected by the renal blood flow and is under the direct control of the combined resistances of afferent and efferent vascular pathways. Nevertheless, whatever the cause of AKI, renal blood flow reduction is a common pathologic pathway for declining glomerular filtration rate. Pathophysiology of AKI has always been traditionally divided into three categories: prerenal, renal, and post-renal. Each of these categories has several different causes associated with it.[rx][rx]

The prerenal form of AKI is because of any cause of reduced blood flow to the kidney. This may be part of systemic hypoperfusion resulting from hypovolemia or hypotension, or maybe due to selective hypoperfusion to the kidneys, such as those resulting from renal artery stenosis and aortic dissection. However, tubular and glomerular function tends to stay normal. Few examples with the mechanism of prerenal AKI are listed below:

Hypovolemia: hemorrhage, severe burns, and gastrointestinal fluid losses such as diarrhea, vomiting, high ostomy output.
Hypotension from the decreased cardiac output: cardiogenic shock, massive pulmonary embolism, acute coronary syndrome
Hypotension from systemic vasodilation: septic shock, anaphylaxis, anesthesia administration, hepatorenal syndrome
Renal vasoconstriction: NSAIDs, iodinated contrast, amphotericin B, calcineurin inhibitors, hepatorenal syndrome
Glomerular efferent arteriolar vasodilation: ACE inhibitors, angiotensin receptor blockers
Renal calculi
Sickle cell anemia
Chronic renal failure
Dehydration
Gastrointestinal bleeding
Heart failure
Urinary tract infection
Protein overloading
Diabetic ketoacidosis
Urinary obstruction

Intrinsic renal causes include conditions that affect the glomerulus or tubule, such as acute tubular necrosis and acute interstitial nephritis. This underlying glomerular or tubular injury is associated with the release of vasoconstrictors from the renal afferent pathways. Prolonged renal ischemia, sepsis, and nephrotoxins being the most common ones. It is worth mentioning that prerenal injury can convert into a renal injury if the offending factor’s exposure is prolonged enough to cause cellular damage. Few examples of this mechanism are listed below:

Acute tubular necrosis: ischemia from prolonged prerenal injury, drugs such as aminoglycosides, vancomycin, amphotericin B, pentamidine; rhabdomyolysis, intravascular hemolysis
Acute interstitial nephritis: Drugs such as beta-lactam antibiotics, penicillins, NSAIDs, proton pump inhibitors (PPIs), 5-ASA; infections, autoimmune conditions (SLE, IgG related disease)
Glomerulonephritis: anti-glomerular basement membrane disease, immune complex-mediated diseases such as SLE, post-infectious glomerulonephritis, cryoglobulinemia, IgA nephropathy, Henoch-Schonlein purpura.
Intratubular obstruction: monoclonal gammopathy seen in multiple myeloma, tumor lysis syndrome, toxins such as ethylene glycol.

Post-renal causes mainly include obstructive causes, which lead to congestion of the filtration system leading to a shift in the filtration driving forces. The most common ones being renal/ureteral calculi, tumors, blood clots, or any urethral obstruction. Another noteworthy fact is that a unilateral obstruction may not always present as AKI, especially if the obstruction is gradual such as a tumor, because a normal working contralateral kidney may compensate for the function of the affected kidney. Therefore, the most common etiology of post-renal AKI is bladder outlet obstruction.

Decreased blood flow

Some diseases and conditions can slow blood flow to your kidneys and cause AKI.

These diseases and conditions include:

Low blood pressure (called “hypotension”) or shock
Blood or fluid loss (such as bleeding, severe diarrhea)
Heart attack, heart failure, and other conditions leading to decreased heart function
Organ failure (e.g., heart, liver)
Overuse of pain medicines called “NSAIDs”, which are used to reduce swelling or relieve pain from headaches, colds, flu, and other ailments. Examples include ibuprofen, ketoprofen, and naproxen.
Severe allergic reactions
Burns
Injury
Major surgery

Direct Damage to the Kidneys

Some diseases and conditions can damage your kidneys and lead to AKI. Some examples include:

A type of severe, life-threatening infection called “sepsis”
A type of cancer called “multiple myeloma”
A rare condition that causes inflammation and scarring to your blood vessels, making them stiff, weak, and narrow (called “vasculitis”)
An allergic reaction to certain types of drugs (called “interstitial nephritis”)
A group of diseases (called “scleroderma”) that affect the connective tissue that supports your internal organs
Conditions that cause inflammation or damage to the kidney tubules, to the small blood vessels in the kidneys, or to the filtering units in the kidneys (such as “tubular necrosis,” “glomerulonephritis, “vasculitis” or “thrombotic microangiopathy”).
Blood clots in or around the kidneys
Diseases that affect the kidneys, such as glomerulonephritis and lupus
Infection
Certain medicines, such as some chemotherapy drugs, some antibiotics, and contrast dyes used during CT scans, MRI scans, and other imaging tests
Alcohol or drug abuse
Some blood or blood vessel disorders

Blockage of the urinary tract

In some people, conditions or diseases can block the passage of urine out of the body and can lead to AKI.

Blockage can be caused by:

Bladder, prostate, or cervical cancer
Enlarged prostate
Problems with the nervous system that affect the bladder and urination
Kidney stones
Blood clots in the urinary tract
Some cancers
Blood clots in or around the kidneys
Bladder problems
Enlarged prostate (in men)

Some examples of problems that can cause you to have too little blood flowing through your kidneys are:

Low blood pressure
Bleeding too much
Having severe diarrhea
Heart disease or heart attack
Infection
Liver failure
Using NSAIDs (non-steroidal anti-inflammatory drugs), such as aspirin, ibuprofen and naproxen
Serious burns
Being very dehydrated (not having enough fluid in your body)
Severe allergic reaction

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Symptoms of Acute Kidney Injury

Too little urine leaving the body
Swelling in legs, ankles, and around the eyes
Fatigue or tiredness
Shortness of breath
Confusion
Nausea
Seizures or coma in severe cases
Chest pain or pressure

In some cases, AKI causes no symptoms and is only found through other tests done by your healthcare provider.

Loss of appetite
Fatigue and weakness
Sleep problems
Changes in how much you urinate
Decreased mental sharpness
Muscle twitches and cramps
Swelling of feet and ankles
Persistent itching
Chest pain, if fluid builds up around the lining of the heart
Shortness of breath, if fluid builds up in the lungs
High blood pressure (hypertension) that’s difficult to control

Diagnosis of Acute Kidney Injury

Histopathology can reliably differentiate the intrinsic renal pattern of AKI from others; however, histopathology may not be reliable at narrowing down a specific cause in every situation. Renal biopsy is an invasive procedure and is usually only pursued in cases where a significant impact on management is expected, such as suspected glomerulonephritis. In those cases, immunofluorescence patterns and electron microscopy can help differentiate between various causes.

History and Physical

The history and physical exam should focus on determining the etiology of AKI and the timeline of progression. If the history points towards hypovolemia or hypotension, then the treatment is guided towards volume repletion. The providers need to look for inciting events such as diarrhea, nausea, vomiting, which may have caused volume loss, or any over-the-counter drugs such as NSAIDs or other nephrotoxins. Differentiating between AKI and chronic kidney disease (CKD) is essential as CKD itself is not an uncommon risk factor for AKI. This can be achieved with the help of history in which one may find features suggestive of CKD such as chronic fatigue, anorexia, nocturia, disturbed sleep-wake cycle, polyuria, and pruritis. Moreover, a careful review of past medical history to reveal any co-morbid conditions can also help narrow down the etiology of AKI, for instance, cirrhosis and history of blood clots requiring anticoagulation. History and physical examination are very important in AKI because, more often than not, labs are unable to provide a clear answer as to the etiology of AKI.

The most common causes of AKI in hospitalized patients are in this order:

ATN – 45%
Prerenal disease – 21%
Acute superimposed on CKD – 13%
Urinary tract obstruction – 10% (most often due to Benign prostatic hypertrophy in older men)
Glomerulonephritis or vasculitis – 4%
AIN – 2%
Atheroemboli – 1%

A history of urine output is important, which may give clues to the cause of AKI. Following are some associations:

Oliguria – favors AKI
Sudden anuria – suggests acute urinary tract obstruction, acute glomerulonephritis, or vascular catastrophe
Gradually diminishing urine output – may be secondary to urethral stricture or bladder outlet obstruction due to causes such as prostate enlargement.

Performing a detailed examination is imperative as it provides extremely valuable information in establishing the etiology of AKI. A crucial part of the physical exam should be orthostatic vital signs since they are an important clue for hypovolemia and, in an appropriate clinical context, would guide treatment. Several organ systems need to be examined to find clues regarding the cause of AKI.

Lab Test and Imaging

Skin – livedo reticularis, digital ischemia, butterfly rash, and purpuras to suggest vasculitis. Track marks to suggest endocarditis in an IV drug abuser.
Eyes and ears – jaundice in liver disease, band keratopathy in multiple myeloma, signs of diabetes mellitus, atheroemboli in retinopathy, and signs of hypertension. Keratitis, iritis, and uveitis in autoimmune vasculitis. Hearing loss in Alport disease.
Cardiovascular system – pulse rate, blood pressure, and jugulovenous pulse in establishing volume status. Irregular rhythm may indicate electrolyte imbalance-related arrhythmias. Pericardial friction rub in uremic pericarditis.
Measuring urine output – Your healthcare provider will track how much urine you pass each day to help find the cause of your AKI.
Urine tests – Your healthcare provider will look at your urine (urinalysis) to find signs of kidney failure
Blood tests – Blood tests will help find levels of creatinine, urea nitrogen phosphorus and potassium should be done in addition to blood tests for protein in order to look at kidney function.
Serum creatinine test – This test helps your doctor check whether creatinine is building up in your blood. Creatinine is a waste product that your kidneys should filter out of your body.
Blood urea nitrogen test – This test helps your doctor check how much nitrogen is in your blood.
Estimated glomerular filtration rate – This test allows your doctor to estimate how well your kidneys filter waste.
Imaging tests – such as ultrasound, magnetic resonance imaging or computed tomography (CT) scan, to assess your kidneys’ structure and size and look for abnormalities.
Removing a sample of kidney tissue (biopsy) – to examine under a microscope to learn what type of kidney disease you have and how much damage there is.
GFR – Your blood test will also help find your GFR (glomerular filtration rate) to estimate the decrease in kidney function
Kidney biopsy – In some situations, your healthcare provider will do a procedure where a tiny piece of your kidney is removed with a special needle, and looked at under a microscope.
Removing a sample of kidney tissue for testing. In some situations, your doctor may recommend a kidney biopsy to remove a small sample of kidney tissue for lab testing. Your doctor inserts a needle through your skin and into your kidney to remove the sample.

Evaluation of AKI should include a thorough search for all possible etiologies of AKI, including prerenal, renal, and post renal disease. The timing of the onset of AKI can be especially helpful when dealing with hospitalized patients. For example, if a patient’s labs are being checked every day and creatinine suddenly starts to rise on the fourth day of admission then an inciting factor can usually be found in 24-48 hours preceding the onset. It is especially important to look for any radiologic studies that might have been done involving the use of iodinated contrast agents which are not an uncommon cause of AKI. It is also imperative to review the list of medications that the patient is receiving as they may be contributing to renal failure, therefore in view of decreased renal function, the doses of such drugs need to be modified. ACE inhibitors and ARBs are often the co-contributors to AKI. A good physical exam can also be helpful sometimes e.g. the presence of a drug rash may point to acute interstitial nephritis being the etiology, cyanotic toes could suggest cholesterol emboli in a patient post cardiac catheterization.

All patients presenting with AKI warrant a basic lab panel including a basic metabolic panel. Sometimes, urine electrolytes can be helpful in suggesting an etiology of the AKI. Urine protein, urine osmolality, and urine albumin to creatinine ratios can also be helpful clues in determining the etiology of AKI. Older patients without any obvious etiology should also be subjected to serum and urine protein electrophoresis (SPEP and UPEP) to rule out monoclonal gammopathy and multiple myeloma. Renal ultrasound can be helpful if obstructive causes are suspected. However, routine renal ultrasound for every patient with AKI is not warranted. CT non-contrast is another important radiographic modality and can be used to look for nephrolithiasis or urolithiasis. Urine sediment examination can also provide important clues as to the etiology such as muddy brown casts seen in acute tubular necrosis. Sterile pyuria is the most sensitive sign of acute interstitial nephritis.[rx][rx]

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A kidney biopsy is an excellent but infrequently utilized tool. It is usually indicated in patients with rapidly declining renal function without apparent cause or to find out the exact etiology of AKI in a setting where multiple etiologies could be responsible. It is a test with a number of risks such as bleeding particularly in patients with platelet dysfunction from uremia.

There are markers of tubular function that can be calculated to help distinguish prerenal causes from renal/postrenal, like the fractional excretion of sodium and urea, and urine osmolality; however, the sensitivity of all these markers is very poor, and they are affected by many drugs very commonly used in clinical practice such as diuretics. Therefore, no single marker can be reliably used in isolation to distinguish prerenal from renal causes of AKI, which is a common misconception in clinical practice.

Lastly, attention also needs to be paid to the overall clinical picture. It is important to assess the volume status of the patient to exclude possible cardiorenal or hepatorenal syndrome. The cardiorenal syndrome is usually due to poor glomerular filtration due to venous congestion along with a lack of forwarding flow in some cases due to poor cardiac output. Hepatorenal syndrome is due to the differential distribution of circulation volume with systemic vasodilation and splanchnic vasoconstriction leading to the diversion of blood into the periphery and paucity of blood supply to the kidneys.

Treatment of Acute Kidney Injury

With the exception of post-renal AKI, most cases are an overlap between pre-renal and acute tubular necrosis type of AKI. [rx][rx] The best way to determine if the AKI is pre-renal or not is a fluid challenge. If the clinical scenario doesn’t contradict it, all patients with acute renal dysfunction should receive a fluid challenge. They require close monitoring of urine output and renal function. If the renal function improves with fluid, that is the best indicator of a pre-Renal AKI. Acute tubular necrosis is very slow to recover and can take weeks to months for complete recovery of renal function. It may not normalize at all sometimes. Diuretics may be required during the oliguric phase of ATN if significant volume overload develops. Another important thing to consider for these patients is to avoid any further insult to the kidneys, such as nephrotoxic drugs. Any and the doses of all medications need to be really adjusted once a patient develops AKI. Another vital step is to limit the dietary ingestion of potassium and phosphorus.

If hyperkalemia develops, it needs to be managed in a robust manner because, in AKI patients, it can be catastrophic. Approaches to lower potassium in the body include:

Dietary restriction
Insulin, IV dextrose and beta-agonists
potassium-binding resins
Calcium gluconate to stabilize cardiac membrane
Dialysis for nonresponsive hyperkalemia

Some AKI patients would tend to develop volume overload, which should be corrected as early as possible to avoid pulmonary and cardiac complications. Euvolemic state can be achieved with the help of furosemide, which is a cornerstone in the management of such patients. Usually, high doses of IV furosemide are needed to correct volume overload in AKI patients; however, it plays no role in the conversion of oliguric AKI to non-oliguric AKI.

Sometimes, AKI may need short-term renal replacement therapy until the kidney function recovers. Dialysis is usually required to manage the complications of AKI, such as severe and nonresponsive hyperkalemia, uremic pericarditis, and pulmonary edema. This is seen especially in the oliguric phase of acute tubular necrosis, where the patient is prone to develop multiple electrolyte and acid-base abnormalities as well as fluid overload.[rx] When required, dialysis in this setting is usually performed through a double-lumen central venous catheter. Continuous renal replacement therapy can also be utilized in patients who cannot tolerate hemodialysis due to hypotension. It is a much slower, continuous type of dialysis. Correction of some of the metabolic abnormalities, along with dialysis, may be required. Metabolic acidosis is one such instance where systemic administration of citrate or bicarbonate is often required to maintain a suitable blood pH. The requirement for renal replacement therapy should be reevaluated in these patients daily while they are hospitalized and at least weekly thereafter until the kidney function is stable. Renal replacement therapy is usually required for the short term ranging from a few days to a few weeks in most cases; however, acute tubular necrosis can take up to months to recover and may, therefore, require intermittent hemodialysis support during that time.

There are certain specific treatments that are required for acute kidney injury in specific circumstances, such as administration of vasoactive medications and colloids for treatment of hepatorenal syndrome and cautious diuresis in cardiorenal syndrome. Acute kidney injury from various glomerulonephritides may require immunosuppressive medications for treatment. Acute interstitial nephritis, which does not recover with supportive care, may benefit from a trial of steroids. Post renal obstruction may need to be relieved operatively in certain situations. For example, benign prostatic hypertrophy may require surgical relief of bladder outlet obstruction. Urethral calculi may require stenting and lithotripsy.

It is also important to note that in a certain situation, the risk of acute kidney injury may be decreased by taking some measures. For example, in high-risk patients such as those with compromised renal function at baseline, it may be beneficial to administer peri-procedure intravenous fluids to prevent contrast-induced nephropathy when performing cardiac catheterization.

Treating complications until your kidneys recover

Your doctor will also work to prevent complications and allow your kidneys time to heal. Treatments that help prevent complications include:

Treatments to balance the number of fluids in your blood – If your acute kidney failure is caused by a lack of fluids in your blood, your doctor may recommend intravenous (IV) fluids. In other cases, acute kidney failure may cause you to have too much fluid, leading to swelling in your arms and legs. In these cases, your doctor may recommend medications (diuretics) to cause your body to expel extra fluids.
Medications to control blood potassium – If your kidneys aren’t properly filtering potassium from your blood, your doctor may prescribe calcium, glucose or sodium polystyrene sulfonate (Kionex) to prevent the accumulation of high levels of potassium in your blood. Too much potassium in the blood can cause dangerous irregular heartbeats (arrhythmias) and muscle weakness.
Medications to restore blood calcium levels – If the levels of calcium in your blood drop too low, your doctor may recommend an infusion of calcium.
Dialysis to remove toxins from your blood – If toxins build up in your blood, you may need temporary hemodialysis — often referred to simply as dialysis — to help remove toxins and excess fluids from your body while your kidneys heal. Dialysis may also help remove excess potassium from your body. During dialysis, a machine pumps blood out of your body through an artificial kidney (dialyzer) that filters out waste. The blood is then returned to your body.

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Prerenal

In prerenal AKI without fluid overload, administration of intravenous fluids is typically the first step to improving kidney function. Volume status may be monitored with the use of a central venous catheter to avoid over-or under-replacement of fluid.
If low blood pressure persists despite providing a person with adequate amounts of intravenous fluid, medications that increase blood pressure (vasopressors) such as norepinephrine, and in certain circumstances medications that improve the heart’s ability to pump (known as inotropes) such as dobutamine may be given to improve blood flow to the kidney. While a useful vasopressor, there is no evidence to suggest that dopamine is of any specific benefit and may in fact be harmful.^[rx]

Intrinsic

The myriad causes of intrinsic AKI require specific therapies. For example, intrinsic AKI due to vasculitis or glomerulonephritis may respond to steroid medication, cyclophosphamide, and (in some cases) plasma exchange. Toxin-induced prerenal AKI often responds to discontinuation of the offending agent, such as ACE inhibitors, ARB antagonists, aminoglycosides, penicillins, NSAIDs, or paracetamol.^[rx]
The use of diuretics such as furosemide is widespread and sometimes convenient in improving fluid overload. It is not associated with higher mortality (risk of death),^[rx] nor with any reduced mortality or length of intensive care unit or hospital stay.^[rx]

Postrenal

If the cause is obstruction of the urinary tract, relief of the obstruction (with a nephrostomy or urinary catheter) may be necessary.

Renal replacement therapy

Renal replacement therapy, such as with hemodialysis, may be instituted in some cases of AKI. Renal replacement therapy can be applied intermittently (IRRT) and continuously (CRRT). Study results regarding differences in outcomes between IRRT and CRRT are inconsistent.
A systematic review of the literature in 2008 demonstrated no difference in outcomes between the use of intermittent hemodialysis and continuous venovenous hemofiltration (CVVH) (a type of continuous hemodialysis).^[rx] Among critically ill patients, intensive renal replacement therapy with CVVH does not appear to improve outcomes compared to less intensive intermittent hemodialysis.^[rx]^[rx]
However, other clinical and health economic studies demonstrated that, initiation of CRRT is associated with a lower likelihood of chronic dialysis and was cost-effective compared with IRRT in patients with acute kidney injury.^[rx]^[rx]^[rx]

Complications

Several complications may associate AKI with mortality. Some of these complications are directly associated with AKI and can easily be gauged (hyperkalemia, volume overload, metabolic acidosis, hyponatremia); however, the effect of other complications on AKI-related mortality, such as inflammation and infection, is difficult to assess. Most common complications include metabolic derangements such as:

Hyperkalemia – If severe, it can lead to arrhythmias because of which renal replacement therapy is required in cases of severe hyperkalemia.
Metabolic acidosis – The kidney’s inability to excrete acids leads to metabolic acidosis and may necessitate systemic administration of bicarbonate or citrate buffers.
Hyperphosphatemia – can usually be prevented by decreasing dietary ingestion or using phosphate binders. Other effects include pulmonary edema from volume overload, peripheral edema from an inability to excrete body water. This is especially common in the oliguric phase of acute tubular necrosis. It may necessitate the use of diuretics or renal replacement therapy.
Cardiovascular – Heart failure secondary to fluid overload is attributable to oliguric AKI, arrhythmias secondary to acidotic state and electrolyte abnormalities, cardiac arrest due to metabolic derangements, and myocardial infarction, and rarely pericarditis.
Gastrointestinal (GI) – Nausea, vomiting, GI bleeding, and anorexia. A mildly raised level of amylase is commonly found in patients suffering from AKI. Elevation of amylase concentration can make the diagnosis of pancreatitis difficult, therefore measuring lipase, which is not raised in AKI, is necessary to establish AKI diagnosis.
Neurologic – CNS-related signs of uremic burden are common in AKI, and they include lethargy, somnolence, disturbed sleep-wake cycle, and cognitive impairment.
Fluid buildup – Acute kidney failure may lead to a buildup of fluid in your lungs, which can cause shortness of breath.
Chest pain – If the lining that covers your heart (pericardium) becomes inflamed, you may experience chest pain.
Muscle weakness – When your body’s fluids and electrolytes — your body’s blood chemistry — are out of balance, muscle weakness can result.
Permanent kidney damage – Occasionally, acute kidney failure causes permanent loss of kidney function or end-stage renal disease. People with the end-stage renal disease require either permanent dialysis — a mechanical filtration process used to remove toxins and wastes from the body — or a kidney transplant to survive.
Death – Acute kidney failure can lead to loss of kidney function and, ultimately, death.

Prevention

Acute kidney failure is often difficult to predict or prevent. But you may reduce your risk by taking care of your kidneys. Try to:

Pay attention to labels when taking over-the-counter (OTC) pain medications. Follow the instructions for OTC pain medications, such as aspirin, acetaminophen (Tylenol, others), ibuprofen (Advil, Motrin IB, others), and naproxen sodium (Aleve, others). Taking too much of these medications may increase your risk of kidney injury. This is especially true if you have pre-existing kidney disease, diabetes, or high blood pressure.
Work with your doctor to manage kidney and other chronic conditions. If you have kidney disease or another condition that increases your risk of acute kidney failures, such as diabetes or high blood pressure, stay on track with treatment goals and follow your doctor’s recommendations to manage your condition.
Make a healthy lifestyle a priority. Be active; eat a sensible, balanced diet; and drink alcohol only in moderation — if at all.

References

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What is the most common cause of acute kidney injury?

What is the most common cause of acute kidney injury?