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Glomerular causes of acute kidney injury are the result of acute inflammation of blood vessels and glomeruli.
Glomerulonephritis is usually a manifestation of a systemic illness e. History, physical examination, and urinalysis are crucial for diagnosing glomerulonephritis Table 3 9 and Figure 1 Because management often involves administration of immunosuppressive or cytotoxic medications with potentially severe adverse effects, renal biopsy is often required to confirm the diagnosis before initiating therapy.
Volume loss e. Dilated neck veins, S 3 heart sound, pulmonary rales, peripheral edema. 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.
Acute kidney injury AKI , also known as acute renal failure ARF , is a sudden episode of kidney failure or kidney damage that happens within a few hours or a few days.
AKI causes a build-up of waste products in your blood and makes it hard for your kidneys to keep the right balance of fluid in your body.
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.
The odds ratios ORs and hazard ratios for AKI and all-cause mortality were calculated after adjusting for multiple covariates.
The OR of AKI increased depending on the decrease in hemoglobin level and the ideal threshold point of hemoglobin linked to increasing AKI risk was 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.
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.
Metabolic acidosis , hyperkalemia , and pulmonary edema may require medical treatment with sodium bicarbonate , antihyperkalemic measures, and diuretics.
Lack of improvement with fluid resuscitation , therapy-resistant hyperkalemia, metabolic acidosis, or fluid overload may necessitate artificial support in the form of dialysis or hemofiltration.
Each year, around two million people die of AKI worldwide. Patients with AKI are more likely to die prematurely after being discharged from hospital, even if their kidney function has recovered.
The risk of developing chronic kidney disease is increased 8. New cases of AKI are unusual but not rare, affecting approximately 0. There is an increased incidence of AKI in agricultural workers, particularly those paid by the piece.
Agricultural workers are at increased risk for AKI because of occupational hazards such as dehydration and heat illness. Acute kidney injury is common among hospitalized patients.
Acute kidney injury was one of the most expensive conditions seen in U. Before the advancement of modern medicine , acute kidney injury was referred to as uremic poisoning while uremia was contamination of the blood with urine.
Starting around , uremia came to be used for reduced urine output, a condition now called oliguria , which was thought to be caused by the urine's mixing with the blood instead of being voided through the urethra.
Acute kidney injury due to acute tubular necrosis ATN was recognized in the s in the United Kingdom , where crush injury victims during the London Blitz developed patchy necrosis of kidney tubules, leading to a sudden decrease in kidney function.
From Wikipedia, the free encyclopedia. Acute kidney injury Other names Acute renal failure ARF Pathologic kidney specimen showing marked pallor of the cortex, contrasting to the darker areas of surviving medullary tissue.
The patient died with acute kidney injury. Specialty Nephrology , Urology Acute kidney injury AKI , previously called acute renal failure ARF ,   is an abrupt loss of kidney function that develops within 7 days.
BUN-to-creatinine ratio Chronic kidney disease Dialysis Kidney failure Rhabdomyolysis Contrast-induced nephropathy Ischemia-reperfusion injury of the appendicular musculoskeletal system.