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The risk of AKI was higher in the anemia group than the non-anemia group and this trend remained significant irrespective of the AKI development time early vs.
Both anemia and AKI increased the year mortality risk and this risk prediction was significantly separated by the presence of anemia and AKI.
Furthermore, the risk prediction remained consistent irrespective of the AKI severity i. 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. Avoidance of iodinated contrast media and gadolinium is important and, if imaging is needed, noncontrast studies are recommended.
Supportive therapies e. In patients with rapidly progressive glomerulonephritis, treatment with pulse steroids, cytotoxic therapy, or a combination may be considered, often after confirmation of the diagnosis by kidney biopsy.
The indications for initiation of renal replacement therapy include refractory hyperkalemia, volume overload refractory to medical management, uremic pericarditis or pleuritis, uremic encephalopathy, intractable acidosis, and certain poisonings and intoxications e.
Patients with acute kidney injury are more likely to develop chronic kidney disease in the future. They are also at higher risk of end-stage renal disease and premature death.
Because of the morbidity and mortality associated with acute kidney injury, it is important for primary care physicians to identify patients who are at high risk of developing this type of injury and to implement preventive strategies.
Those at highest risk include adults older than 75 years; persons with diabetes or preexisting chronic kidney disease; persons with medical problems such as cardiac failure, liver failure, or sepsis; and those who are exposed to contrast agents or who are undergoing cardiac surgery.
Cancer chemotherapy with risk of tumor lysis syndrome Hydration and allopurinol Zyloprim administration a few days before chemotherapy initiation in patients at high risk of tumor lysis syndrome to prevent uric acid nephropathy.
Exposure to radiographic contrast agents If use of contrast media is essential, use iso-osmolar or low-osmolar contrast agent with lowest volume possible.
Optimize volume status before administration of contrast media; use of isotonic normal saline or sodium bicarbonate may be considered in high-risk patients who are not at risk of volume overload.
Dopamine is not recommended Hepatic failure Early recognition and treatment of spontaneous bacterial peritonitis; use albumin, 1.
Rhabdomyolysis Alkalinization of the urine with intravenous sodium bicarbonate in select patients normal calcium, bicarbonate less than 30 mEq per L [30 mmol per L], and arterial pH less than 7.
Information from references 19 through 21 , 27 , and 29 through Search date: February Already a member or subscriber?
Log in. At the time the article was written, Dr. Reprints are not available from the authors. Community-based incidence of acute renal failure.
Kidney Int. Hospital-acquired renal insufficiency. Am J Kidney Dis. Hoste EA, Schurgers M. Epidemiology of acute kidney injury: how big is the problem?
Crit Care Med. RIFLE criteria for acute kidney injury are associated with hospital mortality in critically ill patients: a cohort analysis. Has mortality from acute renal failure decreased?
A systematic review of the literature. Am J Med. Impact of renal function on morbidity and mortality after percutaneous aortocoronary saphenous vein graft intervention.
Am Heart J. It is important that AKI is found as soon as possible because it can lead to chronic kidney disease, or even kidney failure. It may also lead to heart disease or death.
Treatment for AKI usually requires you to stay in a hospital. Most people with acute kidney injury are already in the hospital for another reason.
How long you will stay in the hospital depends on the cause of your AKI and how quickly your kidneys recover.
In more serious cases, dialysis may be needed to help replace kidney function until your kidneys recover. The main goal of your healthcare provider is to treat what is causing your acute kidney injury.
Your healthcare provider will work to treat all of your symptoms and complications until your kidneys recover. 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. Renal ultrasonograph in renal trauma with laceration of the lower pole and subcapsular fluid collection below the kidney.
The management of AKI hinges on identification and treatment of the underlying cause. The main objectives of initial management are to prevent cardiovascular collapse and death and to call for specialist advice from a nephrologist.
In addition to treatment of the underlying disorder, management of AKI routinely includes the avoidance of substances that are toxic to the kidneys, called nephrotoxins.
These include NSAIDs such as ibuprofen or naproxen , iodinated contrasts such as those used for CT scans , many antibiotics such as gentamicin , and a range of other substances.
Monitoring of kidney function, by serial serum creatinine measurements and monitoring of urine output, is routinely performed.
In the hospital, insertion of a urinary catheter helps monitor urine output and relieves possible bladder outlet obstruction, such as with an enlarged prostate.
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 be harmful. 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.
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 ,  nor with any reduced mortality or length of intensive care unit or hospital stay.
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 , such as with hemodialysis , may be instituted in some cases of AKI.
A systematic review of the literature in demonstrated no difference in outcomes between the use of intermittent hemodialysis and continuous venovenous hemofiltration CVVH a type of continuous hemodialysis.