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. AKI can also affect other organs such as the brain, heart, and lungs.

Acute kidney injury is common in patients who are in the hospital, in intensive care units, and especially in older adults. In some cases, AKI causes no symptoms and is only found through other tests done by your healthcare provider.

Some disease and conditions can damage your kidneys and lead to AKI. Some examples include:. In some people, conditions or diseases can block the passage of urine out of the body and can lead to AKI.

Depending on the cause of your acute kidney injury, your healthcare provider will run different tests if he or she suspects that you may have AKI.

It is important that AKI is found as soon as possible because it can lead to chronic kidney disease, or even kidney failure.

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.

The clinical picture is often dominated by the underlying cause. The various symptoms of acute kidney injury result from the various disturbances of kidney function that are associated with the disease.

Accumulation of urea and other nitrogen-containing substances in the bloodstream lead to a number of symptoms, such as fatigue , loss of appetite , headache , nausea and vomiting.

Pain in the flanks may be encountered in some conditions such as clotting of the kidneys' blood vessels or inflammation of the kidney ; this is the result of stretching of the fibrous tissue capsule surrounding the kidney.

Acute kidney injury is diagnosed on the basis of clinical history and laboratory data. 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: [15]. 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. 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.

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