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However, the relationship between anemia and AKI and the effect of anemia on long-term mortality are unresolved in critically ill patients. A total of 2, patients admitted to the intensive care unit were retrospectively analyzed.
We calculated a threshold value of hemoglobin associated with an increased risk of AKI and used this value to define anemia. Your healthcare provider will work to treat all of your symptoms and complications until your kidneys recover.
After having AKI, your chances are higher for other health problems such as kidney disease, stroke, heart disease or having AKI again in the future.
The chances for developing kidney disease and kidney failure increase every time AKI occurs. To protect yourself, you should follow up with your healthcare provider to keep track of your kidney function and recovery.
The best ways to lower your chances of having kidney damage and to save kidney function are to prevent acute kidney injury or to find and treat it as early as possible.
Skip to main content. What are the signs and symptoms of acute kidney injury? Signs and symptoms of acute kidney injury differ depending on the cause and may include: 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.
A diagnosis is made when there is a rapid reduction in kidney function , as measured by serum creatinine , or based on a rapid reduction in urine output, termed oliguria less than mLs of urine per 24 hours.
AKI can be caused by systemic disease such as a manifestation of an autoimmune disease, e. AKI often occurs due to multiple processes.
The most common cause is dehydration and sepsis combined with nephrotoxic drugs, especially following surgery or contrast agents.
The causes of acute kidney injury are commonly categorized into prerenal , intrinsic , and postrenal. Preoperative creatinine greater than 1.
Other well-known minor risk factors include: female gender, congestive heart failure, chronic obstructive pulmonary disease, insulin-requiring diabetes, and depressed left ventricular ejection fraction.
Prerenal causes of AKI "pre-renal azotemia" are those that decrease effective blood flow to the kidney and cause a decrease in the glomerular filtration rate GFR.
Both kidneys need to be affected as one kidney is still more than adequate for normal kidney function. Notable causes of prerenal AKI include low blood volume e.
The latter include renal artery stenosis , or the narrowing of the renal artery which supplies the kidney with blood, and renal vein thrombosis , which is the formation of a blood clot in the renal vein that drains blood from the kidney.
Intrinsic AKI refers to disease processes which directly damage the kidney itself. Intrinsic AKI can be due to one or more of the kidney's structures including the glomeruli , kidney tubules , or the interstitium.
Common causes of each are glomerulonephritis , acute tubular necrosis ATN , and acute interstitial nephritis AIN , respectively. Other causes of intrinsic AKI are rhabdomyolysis and tumor lysis syndrome.
Postrenal AKI refers to acute kidney injury caused by disease states downstream of the kidney and most often occurs as a consequence of urinary tract obstruction.
This may be related to benign prostatic hyperplasia , kidney stones , obstructed urinary catheter , bladder stones , or cancer of the bladder , ureters , or prostate.
The deterioration of kidney function may be signaled by a measurable decrease in urine output. Often, it is diagnosed on the basis of blood tests for substances normally eliminated by the kidney: urea and creatinine.
Additionally, the ratio of BUN to creatinine is used to evaluate kidney injury. Both tests have their disadvantages.
For instance, it takes about 24 hours for the creatinine level to rise, even if both kidneys have ceased to function. A number of alternative markers have been proposed such as NGAL , KIM-1 , IL18 and cystatin C , but none of them are currently established enough to replace creatinine as a marker of kidney function.
Once the diagnosis of AKI is made, further testing is often required to determine the underlying cause. It is useful to perform a bladder scan or a post void residual to rule out urinary retention.
In post void residual, a catheter is inserted into the urinary tract immediately after urinating to measure fluid still in the bladder. Indications for kidney biopsy in the setting of AKI include the following: .
In medical imaging , the acute changes in the kidney are often examined with renal ultrasonography as the first-line modality, where CT scan and magnetic resonance imaging MRI are used for the follow-up examinations and when US fails to demonstrate abnormalities.
In evaluation of the acute changes in the kidney, the echogenicity of the renal structures, the delineation of the kidney, the renal vascularity, kidney size and focal abnormalities are observed.
A CT scan of the abdomen will also demonstrate bladder distension or hydronephrosis. However, in AKI, the use of IV contrast is contraindicated as the contrast agent used is nephrotoxic.
Renal ultrasonograph of acute pyelonephritis with increased cortical echogenicity and blurred delineation of the upper pole. Renal ultrasonograph in renal failure after surgery with increased cortical echogenicity and kidney size.
Biopsy showed acute tubular necrosis. History of receiving nephrotoxic medications including over-the-counter, illicit, and herbal , hypotension, trauma or myalgias suggesting rhabdomyolysis, recent exposure to radiographic contrast agents.
Lupus, systemic sclerosis, rash, arthritis, uveitis, weight loss, fatigue, hepatitis C virus infection, human immunodeficiency virus infection, hematuria, foamy urine, cough, sinusitis, hemoptysis.
Medication use e. Nephrotic syndrome, trauma, flank pain, anticoagulation atheroembolic disease , vessel catheterization or vascular surgery.
Livedo reticularis, funduscopic examination showing malignant hypertension , abdominal bruits. Urinary urgency or hesitancy, gross hematuria, polyuria, stones, medications, cancer.
Adapted with permission from Smith MC. Acute renal failure. Clinical Decisions in Urology. Acute interstitial nephritis can be secondary to many conditions, but most cases are related to medication use, making patient history the key to diagnosis.
In about one-third of cases, there is a history of maculopapular erythematous rash, fever, arthralgias, or a combination of these symptoms.
A kidney biopsy may be needed to distinguish between allergic interstitial nephritis and other renal causes of acute kidney injury.
In addition to discontinuing offending agents, steroids may be beneficial if given early in the course of disease. Acute events involving renal arteries or veins can also lead to intrinsic acute kidney injury.
Renal atheroembolic disease is the most common cause and is suspected with a recent history of arterial catheterization, the presence of a condition requiring anticoagulation, or after vascular surgery.
Physical examination and history provide important clues to the diagnosis Table 3 9. Vascular causes of acute kidney injury usually require imaging to confirm the diagnosis.
Postrenal causes typically result from obstruction of urinary flow, and prostatic hypertrophy is the most common cause of obstruction in older men.
Prompt diagnosis followed by early relief of obstruction is associated with improvement in renal function in most patients. Clinical presentation varies with the cause and severity of renal injury, and associated diseases.
Most patients with mild to moderate acute kidney injury are asymptomatic and are identified on laboratory testing. Patients with severe cases, however, may be symptomatic and present with listlessness, confusion, fatigue, anorexia, nausea, vomiting, weight gain, or edema.
Other presentations of acute kidney injury may include development of uremic encephalopathy manifested by a decline in mental status, asterixis, or other neurologic symptoms , anemia, or bleeding caused by uremic platelet dysfunction.
The history should identify use of nephrotoxic medications or systemic illnesses that might cause poor renal perfusion or directly impair renal function.
Physical examination should assess intravascular volume status and any skin rashes indicative of systemic illness. The initial laboratory evaluation should include urinalysis, complete blood count, and measurement of serum creatinine level and fractional excretion of sodium FE Na.
Imaging studies can help rule out obstruction. Useful tests are summarized in Table 4. Elevated antineutrophil cytoplasmic antibody, antiglomerular basement membrane antibody.
Elevated creatine kinase level, elevated myoglobin level, dipstick positive for blood but negative for red blood cells.
Evidence of hemolysis schistocytes on peripheral smear, decreased haptoglobin level, elevated indirect bilirubin level, elevated lactate dehydrogenase level.
Hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, systemic lupus erythematosus, other autoimmune diseases. Malignancy, prostate hypertrophy, uterine fibroids, nephrolithiasis, ureterolithiasis.
Adapted with permission from Agrawal M, Swartz R. Acute renal failure [published correction appears in Am Fam Physician. Am Fam Physician.
The definition of acute kidney injury indicates that a rise in creatinine has occurred within 48 hours, although in the outpatient setting, it may be hard to ascertain when the rise actually happened.
A high serum creatinine level in a patient with a previously normal documented level suggests an acute process, whereas a rise over weeks to months represents a subacute or chronic process.
Urinalysis is the most important noninvasive test in the initial workup of acute kidney injury. Findings on urinalysis guide the differential diagnosis and direct further workup Figure 1 The presence of acute hemolytic anemia with the peripheral smear showing schistocytes in the setting of acute kidney injury should raise the possibility of hemolytic uremic syndrome or thrombotic thrombocytopenic purpura.
In patients with oliguria, measurement of FE Na is helpful in distinguishing prerenal from intrinsic renal causes of acute kidney injury.
FE Na is defined by the following formula:. Online calculators are also available. A value less than 1 percent indicates a prerenal cause of acute kidney injury, whereas a value greater than 2 percent indicates an intrinsic renal cause.
In patients on diuretic therapy, however, a FE Na higher than 1 percent may be caused by natriuresis induced by the diuretic, and is a less reliable measure of a prerenal state.
In such cases, fractional excretion of urea may be helpful, with values less than 35 percent indicating a prerenal cause. FE Na values less than 1 percent are not specific for prerenal causes of acute kidney injury because these values can occur in other conditions, such as contrast nephropathy, rhabdomyolysis, acute glomerulonephritis, and urinary tract obstruction.
Renal ultrasonography should be performed in most patients with acute kidney injury, particularly in older men, to rule out obstruction i. To diagnose extrarenal causes of obstruction e.
Renal biopsy is reserved for patients in whom prerenal and postrenal causes of acute kidney injury have been excluded and the cause of intrinsic renal injury is unclear.
Renal biopsy is particularly important when clinical assessment and laboratory investigations suggest a diagnosis that requires confirmation before disease-specific therapy e.
Renal biopsy may need to be performed urgently in patients with oliguria who have rapidly worsening acute kidney injury, hematuria, and red blood cell casts.
In this setting, in addition to indicating a diagnosis that requires immunosuppressive therapy, the biopsy may support the initiation of special therapies, such as plasmapheresis if Goodpasture syndrome is present.
Optimal management of acute kidney injury requires close collaboration among primary care physicians, nephrologists, hospitalists, and other subspecialists participating in the care of the patient.
After acute kidney injury is established, management is primarily supportive. Patients with acute kidney injury generally should be hospitalized unless the condition is mild and clearly resulting from an easily reversible cause.
The key to management is assuring adequate renal perfusion by achieving and maintaining hemodynamic stability and avoiding hypovolemia. In some patients, clinical assessment of intravascular volume status and avoidance of volume overload may be difficult, in which case measurement of central venous pressures in an intensive care setting may be helpful.
If fluid resuscitation is required because of intravascular volume depletion, isotonic solutions e. Attention to electrolyte imbalances e.
Severe hyperkalemia is defined as potassium levels of 6. In patients without electrocardiographic evidence of hyperkalemia, calcium gluconate is not necessary, but sodium polystyrene sulfonate Kayexalate can be given to lower potassium levels gradually, and loop diuretics can be used in patients who are responsive to diuretics.
Dietary intake of potassium should be restricted. The main indication for use of diuretics is management of volume overload.
Intravenous loop diuretics, as a bolus or continuous infusion, can be helpful for this purpose. However, it is important to note that diuretics do not improve morbidity, mortality, or renal outcomes, and should not be used to prevent or treat acute kidney injury in the absence of volume overload.
All medications that may potentially affect renal function by direct toxicity or by hemodynamic mechanisms should be discontinued, if possible.
For example, metformin Glucophage should not be given to patients with diabetes mellitus who develop acute kidney injury.
The dosages of essential medications should be adjusted for the lower level of kidney function.