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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.
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.
Et al. Clinical Journal of the American Society of Nephrology. Spence; Miranda Payne 1 January Oxford Handbook of Oncology. Oxford University Press.
Kidney inter. Crit Care. Health Technol Assess. Current Medical Diagnosis and Treatment. CC-BY 4. The New England Journal of Medicine.
Emergency Medicine Journal. Archived from the original on 8 August Retrieved 8 August Intensive Care Medicine. Scientific Reports. Bibcode : NatSR Joseph; Bihorac Azra Kidney International.
Archived from the original on Retrieved Philadelphia: Saunders. August Most Frequent Conditions in U. Hospitals, September Hospitals, ".
Kidney International Review. Br Med J. Kidney disease. See Template:Glomerular disease. Renal tubular acidosis proximal distal Acute tubular necrosis Genetic Fanconi syndrome Bartter syndrome Gitelman syndrome Liddle's syndrome.
Interstitial nephritis Pyelonephritis Balkan endemic nephropathy. Renal artery stenosis Renal ischemia Hypertensive nephropathy Renovascular hypertension Renal cortical necrosis.
Acute kidney injury AKI is a major health concern, because AKI is related with an increase in morbidity and mortality.
Anemia is related to AKI in several clinical settings. However, the relationship between anemia and AKI and the effect of anemia on long-term mortality are unresolved in critically ill patients.
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. 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?