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Acute kidney injury: a guide to diagnosis and management

Acute Kidney Injury: A Guide to Diagnosis
and Management
MAHBOOB RAHMAN, MD, MS, Case Western Reserve University School of Medicine, Cleveland, Ohio
FARIHA SHAD, MD, Kaiser Permanente, Cleveland, Ohio
MICHAEL C. SMITH, MD, Case Western Reserve University School of Medicine, Cleveland, Ohio
Acute kidney injury is characterized by abrupt deterioration in kidney function, manifested by an increase in serum
creatinine level with or without reduced urine output. The spectrum of injury ranges from mild to advanced, some-
times requiring renal replacement therapy. The diagnostic evaluation can be used to classify acute kidney injury as
prerenal, intrinsic renal, or postrenal. The initial workup includes a patient history to identify the use of nephrotoxic
medications or systemic illnesses that might cause poor renal perfusion or directly impair renal function. Physi-
cal examination should assess intravascular volume status and identify skin rashes indicative of systemic illness.
The initial laboratory evaluation should include measurement of serum creatinine level, complete blood count, uri-
nalysis, and fractional excretion of sodium. Ultrasonography of the
kidneys should be performed in most patients, particularly in older
men, to rule out obstruction. Management of acute kidney injury
involves fluid resuscitation, avoidance of nephrotoxic medications
and contrast media exposure, and correction of electrolyte imbal-
ances. Renal replacement therapy (dialysis) is indicated for refrac-
tory hyperkalemia; volume overload; intractable acidosis; uremic
encephalopathy, pericarditis, or pleuritis; and removal of certain
toxins. Recognition of risk factors (e.g., older age, sepsis, hypovo-
lemia/shock, cardiac surgery, infusion of contrast agents, diabetes

mellitus, preexisting chronic kidney disease, cardiac failure, liver
failure) is important. Team-based approaches for prevention, early
diagnosis, and aggressive management are critical for improving
outcomes. (Am Fam Physician. 2012;86(7):631-639. Copyright
2012 American Academy of Family Physicians.)
The incidence of acute kidney injury Definition
has increased in recent years, both Acute kidney injury is defined as an abrupt in the community and in hospi- (within 48 hours) reduction in kidney func- tal settings.1,2 The estimated inci- tion based on an elevation in serum creati- dence of acute kidney injury is two to three nine level, a reduction in urine output, the cases per 1,000 persons.3 Seven percent of need for renal replacement therapy (dialy-hospitalized patients and about two-thirds sis), or a combination of these factors. It is of patients in intensive care units develop classified in three stages (Table 1).8 The term acute kidney injury,2 often as part of the acute kidney injury should replace terms multiple organ dysfunction syndrome.4 such as acute renal failure and acute renal Acute kidney injury is associated with insufficiency, which previously have been a high rate of adverse outcomes; mortal- used to describe the same clinical condition.
ity rates range between 25 and 80 percent, depending on the cause and the clinical sta- tus of the patient.5-7 These data highlight the The causes of acute kidney injury can be importance of recognition and appropriate divided into three categories (Table 2 management, usually in collaboration with prerenal (caused by decreased renal perfu-nephrologists and other subspecialists.
sion, often because of volume depletion), Downloaded from the American Family Physician Web site at www.aafp.org/afp. Copyright 2012 American Academy of Family Physicians. For the private, noncommercial October 1, 20 f th ber 7 b site. All other rights reserw s@aafp.org for copyright questioA
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Acute Kidney Injury
SORT: KEY RECOMMENDATIONS FOR PRACTICE
The diagnosis of acute kidney injury is based on serum creatinine levels, urine output, and the need for renal replacement therapy.
Renal ultrasonography should be performed in most patients with acute kidney injury to rule out obstruction. Adequate fluid balance should be maintained in patients with acute kidney injury by using isotonic solutions (e.g., normal saline) instead of hyperoncotic solutions (e.g., dextrans, hydroxyethyl starch, albumin).
Dopamine use is not recommended for the prevention of acute kidney injury.
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.
Consider therapy with immunosuppressive agents (e.g., cyclophosphamide, prednisone) in patients with rapidly progressive glomerulonephritis. A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to http://www.
aafp.org/afpsort.xml.
Table 1. Stages of Acute Kidney Injury
Change in serum creatinine level Urine output Increase ≥ 0.3 mg per dL (26.52 µmol per L) or < 0.5 mL per kg per hour for more ≥ 1.5- to twofold from baseline Increase > two- to threefold from baseline < 0.5 mL per kg per hour for more Increase > threefold from baseline or ≥ 4.0 mg < 0.3 mL per kg per hour for 24 hours Renal replacement per dL (353.60 µmol per L) with an acute rise or anuria for 12 hours of at least 0.5 mg per dL (44.20 µmol per L) NOTE: Each stage is defined by the change in serum creatinine level, the change in urine output, or the need for renal replacement therapy. Adapted with permission from Mehta RL, Kel um JA, Shah SV, et al. Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury. Crit Care. 2007;11(2):R31. intrinsic renal (caused by a process within the kidneys), In patients with preexisting chronic kidney disease, and postrenal (caused by inadequate drainage of urine however, these mechanisms are impaired, and the sus-distal to the kidneys). In patients who already have ceptibility to develop acute-on-chronic renal failure is underlying chronic kidney disease, any of these factors, higher.11but especially volume depletion, may cause acute kidney Several medications can cause prerenal acute kidney injury in addition to the chronic impairment of renal injury. Notably, angiotensin-converting enzyme inhibi-function.
tors and angiotensin receptor blockers can impair renal perfusion by causing dilation of the efferent arteriole and reduce intraglomerular pressure. Nonsteroidal anti- Approximately 70 percent of community-acquired cases inflammatory drugs also can decrease the glomerular of acute kidney injury are attributed to prerenal causes.10 filtration rate by changing the balance of vasodilatory/In these cases, underlying kidney function may be nor- vasoconstrictive agents in the renal microcirculation. mal, but decreased renal perfusion associated with These drugs and others limit the normal homeostatic intravascular volume depletion (e.g., from vomiting or responses to volume depletion and can be associated diarrhea) or decreased arterial pressure (e.g., from heart with a decline in renal function. In patients with pre-failure or sepsis) results in a reduced glomerular filtra- renal acute kidney injury, kidney function typically tion rate. Autoregulatory mechanisms often can com- returns to baseline after adequate volume status is estab- pensate for some degree of reduced renal perfusion in lished, the underlying cause is treated, or the offending an attempt to maintain the glomerular filtration rate. drug is discontinued.
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Table 2. Causes of Acute Kidney Injury
Prerenal
Intrarenal vasoconstriction (hemodynamical y mediated)
INTRINSIC RENAL CAUSES
Medications: nonsteroidal anti-inflammatory drugs,* Intrinsic renal causes are also important sources of acute angiotensin-converting enzyme inhibitors,* angiotensin kidney injury and can be categorized by the component receptor blockers,* cyclosporine (Sandimmune), of the kidney that is primarily affected (i.e., tubular, glo- tacrolimus (Prograf) merular, interstitial, or vascular).
Cardiorenal syndrome* Acute tubular necrosis is the most common type of Hepatorenal syndrome intrinsic acute kidney injury in hospitalized patients. Abdominal compartment syndrome The cause is usually ischemic (from prolonged hypoten- sion) or nephrotoxic (from an agent that is toxic to the Systemic vasodilation (e.g., sepsis,* neurogenic shock) tubular cells). In contrast to a prerenal etiology, acute kidney injury caused by acute tubular necrosis does not Renal loss from diuretic overuse,* osmotic diuresis improve with adequate repletion of intravascular vol- (e.g., diabetic ketoacidosis*) ume and blood flow to the kidneys. Both ischemic and Extrarenal loss from vomiting, diarrhea,* burns, sweating, nephrotoxic acute tubular necrosis can resolve over time, although temporary renal replacement therapy may be required, depending on the degree of renal injury and Glomerular (e.g., postinfectious and other the presence of preexisting chronic kidney disease.
Glomerular causes of acute kidney injury are the result of acute inflammation of blood vessels and glom- Medications: penicillin analogues,* cephalosporins,* eruli. Glomerulonephritis is usually a manifestation sulfonamides, ciprofloxacin (Cipro), acyclovir (Zovirax), of a systemic illness (e.g., systemic lupus erythemato- rifampin, phenytoin (Dilantin), interferon, proton pump sus) or pulmonary renal syndromes (e.g., Goodpasture inhibitors, nonsteroidal anti-inflammatory drugs syndrome, Wegener granulomatosis). History, physical Infections (e.g., direct infection of renal parenchyma or associated with systemic infections) examination, and urinalysis are crucial for diagnosing glomerulonephritis (Table 3 9 and Figure 112). Because Viruses: Epstein-Barr virus, cytomegalovirus, human immunodeficiency virus management often involves administration of immu- Bacteria: Streptococcus species, Legionel a species nosuppressive or cytotoxic medications with potentially Fungi: candidiasis, histoplasmosis severe adverse effects, renal biopsy is often required to confirm the diagnosis before initiating therapy. Systemic disease: sarcoidosis, lupus Acute interstitial nephritis can be secondary to many conditions, but most cases are related to medication Ischemic: prolonged hypotension* use, making patient history the key to diagnosis. In Nephrotoxic: exogenous toxins (e.g., radiographic contrast agents,* aminoglycosides,* cisplatin, methotrexate, about one-third of cases, there is a history of macu- ethylene glycol, amphotericin B) and endogenous lopapular erythematous rash, fever, arthralgias, or a toxins (e.g., hemolysis and rhabdomyolysis [pigment combination of these symptoms.13 Eosinophiluria may nephropathy], tumor lysis syndrome, myeloma) be found in patients with acute interstitial nephritis, but it is not pathognomonic of this disease. A kidney Renal vein thrombosis, malignant hypertension, biopsy may be needed to distinguish between allergic scleroderma renal crisis, renal atheroembolic disease,* interstitial nephritis and other renal causes of acute and renal infarction kidney injury. In addition to discontinuing offending agents, steroids may be beneficial if given early in the Extrarenal obstruction: prostate hypertrophy*; neurogenic course of disease.14 bladder; retroperitoneal fibrosis; bladder, prostate, or Acute events involving renal arteries or veins can also lead to intrinsic acute kidney injury. Renal atheroem- Intrarenal obstruction: stones,* crystals (acyclovir, indinavir bolic disease is the most common cause and is suspected [Crixivan]), clots, tumors with a recent history of arterial catheterization, the pres-ence of a condition requiring anticoagulation, or after *—Most common causes. vascular surgery. Physical examination and history pro- Adapted with permission from Hol ey JL. Clinical approach to the diagnosis of acute renal failure. In: Greenberg A, Cheung AK, eds. vide important clues to the diagnosis (Table 3 9). Vascular Primer on Kidney Diseases. 5th ed. Philadelphia, Pa.: National Kidney causes of acute kidney injury usually require imaging to confirm the diagnosis.
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Postrenal causes typically result from obstruction of uri- A patient history and physical examination, with an nary flow, and prostatic hypertrophy is the most com- emphasis on assessing the patient's volume status, are mon cause of obstruction in older men. Prompt diagnosis crucial for determining the cause of acute kidney injury followed by early relief of obstruction is associated with (Table 3 9). The history should identify use of nephrotoxic improvement in renal function in most patients.
medications or systemic illnesses that might cause poor renal perfusion or directly impair renal function. Physi- cal examination should assess intravascular volume status Clinical presentation varies with the cause and sever- and any skin rashes indicative of systemic illness. The ini- ity of renal injury, and associated diseases. Most patients tial laboratory evaluation should include urinalysis, com-with mild to moderate acute kidney injury are asymp- plete blood count, and measurement of serum creatinine tomatic and are identified on laboratory testing. Patients level and fractional excretion of sodium (FE ). Imaging with severe cases, however, may be symptomatic and pres- studies can help rule out obstruction. Useful tests are ent with listlessness, confusion, fatigue, anorexia, nausea, summarized in Table 4.16 Figure 1 presents an overview of vomiting, weight gain, or edema.15 Patients can also pres- the diagnosis and management of acute kidney injury.12 ent with oliguria (urine output less than 400 mL per day),
anuria (urine output less than 100 mL per day), or normal SERUM CREATININE LEVEL
volumes of urine (nonoliguric acute kidney injury). Other It is important to compare the patient's current serum cre-
presentations of acute kidney injury may include develop-
atinine level with previous levels to determine the duration ment of uremic encephalopathy (manifested by a decline and acuity of the disease. The definition of acute kidney in mental status, asterixis, or other neurologic symptoms), injury indicates that a rise in creatinine has occurred within anemia, or bleeding caused by uremic platelet dysfunction.
48 hours, although in the outpatient setting, it may be hard Table 3. History and Physical Examination Findings for Categorizing Acute Kidney Injury
Type of acute kidney injury History findings Physical examination findings Volume loss (e.g., history of vomiting, diarrhea, diuretic overuse, Weight loss, orthostatic hypotension hemorrhage, burns) Thirst and reduced fluid intake Dilated neck veins, S3 heart sound, pulmonary rales, peripheral edema Ascites, caput medusae, spider angiomas History of receiving nephrotoxic medications (including over-the- Muscle tenderness, compartment counter, il icit, and herbal), hypotension, trauma or myalgias syndrome, assessment of volume suggesting rhabdomyolysis, recent exposure to radiographic Lupus, systemic sclerosis, rash, arthritis, uveitis, weight loss, fatigue, Periorbital, sacral, and lower-extremity hepatitis C virus infection, human immunodeficiency virus edema; rash; oral/nasal ulcers infection, hematuria, foamy urine, cough, sinusitis, hemoptysis Medication use (e.g., antibiotics, proton pump inhibitors), rash, Fever, drug-related rash arthralgias, fever, infectious il ness Nephrotic syndrome, trauma, flank pain, anticoagulation Livedo reticularis, funduscopic (atheroembolic disease), vessel catheterization or vascular surgery examination (showing malignant hypertension), abdominal bruits Urinary urgency or hesitancy, gross hematuria, polyuria, stones, Bladder distention, pelvic mass, prostate medications, cancer Adapted with permission from Hol ey JL. Clinical approach to the diagnosis of acute renal failure. In: Greenberg A, Cheung AK, eds. Primer on Kidney Diseases. 5th ed. Philadelphia, Pa.: National Kidney Foundation; 2009:280. 634 American Family Physician
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Diagnosis and Treatment of Acute Kidney Injury
Patient presents with acute kidney injury Progressive increase in blood urea nitrogen and creatinine levels Take history and perform physical examinationObtain serial measurement of blood urea nitrogen, creatinine, and electrolyte levels Patient has oliguria? Measure urinary and serum sodium and creatinine levels and osmolality Perform renal ultrasonography Normal-size kidneys Bilateral smal kidneys Renal parenchymal disease Relieve obstruction Chronic renal failure Administer diuretics and perform afterload reduction Perform urinalysis Renal tubular cel s, renal tubular Eosinophils, white Red blood cell casts; Orthotolidine positive cell casts, or pigmented casts proteinuria > 3 g but no red blood cel s Acute tubular necrosis Al ergic interstitial nephritis Myoglobinuria or hemoglobinuria Glomerulonephritis Eliminate nephrotoxins; Eliminate offending drug, treat underlying cause Administer fluids, mannitol; perform Perform renal biopsy urine alkalinization Supportive management Unresponsive volume overload, acidosis, or hyperkalemia renal insufficiency Signs and symptoms of uremia (blood urea nitrogen > 100 mg per dL [35.70 mmol per L]) Perform renal replacement therapy (dialysis) Figure 1. Algorithm for the diagnosis and treatment of acute kidney injury.
Adapted with permission from Smith MC. Acute renal failure. In: Resnick MI, Elder JS, Spirnak JP, eds. Clinical Decisions in Urology. 3rd ed. Hamilton,
Ontario, Canada: BC Decker, Inc.; 2004:61.

Acute Kidney Injury
Table 4. Diagnostic Test Results and Corresponding Diseases in Patients with Acute Kidney Injury
Test result When to order Elevated antineutrophil cytoplasmic Suspected acute glomerulonephritis, Vasculitis, Goodpasture syndrome antibody, antiglomerular basement pulmonary renal syndromes membrane antibody Elevated antistreptolysin O titer Recent infection and clinical picture of acute glomerulonephritis Elevated creatine kinase level, elevated Recent trauma, muscle injury myoglobin level, dipstick positive for blood but negative for red blood cel s Elevated prostate-specific antigen level Older men with symptoms Prostate hypertrophy, prostate cancer suggestive of urinary obstruction Elevated uric acid level History of rapidly proliferating Malignancy, tumor lysis syndrome tumors, recent chemotherapy Al ergic interstitial nephritis Evidence of hemolysis (schistocytes on Fever, anemia, thrombocytopenia, Hemolytic uremic syndrome, thrombotic peripheral smear, decreased haptoglobin thrombocytopenic purpura, systemic lupus level, elevated indirect bilirubin level, erythematosus, other autoimmune diseases elevated lactate dehydrogenase level) Hydronephrosis on renal ultrasonography Suspected obstruction Malignancy, prostate hypertrophy, uterine fibroids, nephrolithiasis, ureterolithiasis Increased anion gap with increased Suspected poisoning, unresponsive Ethylene glycol or methanol poisoning Low complement level Suspected acute glomerulonephritis Systemic lupus erythematosus, endocarditis, Monoclonal spike on serum protein Anemia, proteinuria, acute kidney injury in older patients Positive antinuclear antibody, double- Proteinuria, skin rash, arthritis Autoimmune diseases, systemic lupus stranded DNA antibody Positive blood cultures Intravenous drug use, recent infection, new cardiac murmur Positive HIV test Risk factors for HIV infection HIV = human immunodeficiency virus. *—Calculations are as fol ows: Anion gap = sodium – (chloride + bicarbonate)Calculated serum osmolality = 2(sodium [in mEq per L]) + (blood urea nitrogen [in mg per dL] ÷ 2.8) + (glucose [in mg per dL] ÷ 18) Osmolar gap = measured serum osmolality – calculated serum osmolality. Adapted with permission from Agrawal M, Swartz R. Acute renal failure [published correction appears in Am Fam Physician. 2001;63(3):445]. Am Fam Physician. 2000;61(7):2081. to ascertain when the rise actually happened. A high serum urinalysis guide the differential diagnosis and direct fur-creatinine level in a patient with a previously normal docu- ther workup (Figure 112).
mented level suggests an acute process, whereas a rise over weeks to months represents a subacute or chronic process. COMPLETE BLOOD COUNT
The presence of acute hemolytic anemia with the periph- eral smear showing schistocytes in the setting of acute kid- Urinalysis is the most important noninvasive test in ney injury should raise the possibility of hemolytic uremic the initial workup of acute kidney injury. Findings on syndrome or thrombotic thrombocytopenic purpura.
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In patients with oliguria, measurement of FE is help- Optimal management of acute kidney injury requires ful in distinguishing prerenal from intrinsic renal causes close collaboration among primary care physicians, of acute kidney injury. FE is defined by the following nephrologists, hospitalists, and other subspecialists par- ticipating in the care of the patient. After acute kidney injury is established, management is primarily supportive.
(urinary sodium × serum creatinine) Patients with acute kidney injury generally should (serum sodium × urinary creatinine) be hospitalized unless the condition is mild and clearly Online calculators are also available. A value less than resulting from an easily reversible cause. The key to 1 percent indicates a prerenal cause of acute kidney management is assuring adequate renal perfusion by injury, whereas a value greater than 2 percent indicates achieving and maintaining hemodynamic stability and an intrinsic renal cause. In patients on diuretic therapy, avoiding hypovolemia. In some patients, clinical assess-however, a FE higher than 1 percent may be caused ment of intravascular volume status and avoidance of by natriuresis induced by the diuretic, and is a less reli- volume overload may be difficult, in which case mea- able measure of a prerenal state. In such cases, fractional surement of central venous pressures in an intensive care excretion of urea may be helpful, with values less than setting may be helpful.
35 percent indicating a prerenal cause. FE values less If fluid resuscitation is required because of intravas- than 1 percent are not specific for prerenal causes of acute cular volume depletion, isotonic solutions (e.g., normal kidney injury because these values can occur in other con- saline) are preferred over hyperoncotic solutions (e.g., ditions, such as contrast nephropathy, rhabdomyolysis, dextrans, hydroxyethyl starch, albumin).19 A reasonable acute glomerulonephritis, and urinary tract obstruction.
goal is a mean arterial pressure greater than 65 mm Hg, which may require the use of vasopressors in patients with persistent hypotension.20 Renal-dose dopamine is Renal ultrasonography should be performed in most associated with poorer outcomes in patients with acute patients with acute kidney injury, particularly in older kidney injury; it is no longer recommended.21 Cardiac men, to rule out obstruction (i.e., a postrenal cause).17,18 function can be optimized as needed with positive ino-The presence of postvoid residual urine greater than tropes, or afterload and preload reduction.
100 mL (determined by a bladder scan or via urethral Attention to electrolyte imbalances (e.g., hyperkale- catheterization if bladder scan is unavailable) suggests mia, hyperphosphatemia, hypermagnesemia, hypona-postrenal acute kidney injury and requires renal ultra- tremia, hypernatremia, metabolic acidosis) is important. sonography to detect hydronephrosis or outlet obstruc- Severe hyperkalemia is defined as potassium levels of tion. To diagnose extrarenal causes of obstruction (e.g., 6.5 mEq per L (6.5 mmol per L) or greater, or less than pelvic tumors), other imaging modalities, such as com- 6.5 mEq per L with electrocardiographic changes typi- puted tomography or magnetic resonance imaging, may cal of hyperkalemia (e.g., tall, peaked T waves). In severe be required.
hyperkalemia, 5 to 10 units of regular insulin and dex-trose 50% given intravenously can shift potassium out of RENAL BIOPSY
circulation and into the cells. Calcium gluconate (10 mL Renal biopsy is reserved for patients in whom pre- of 10% solution infused intravenously over five minutes) renal and postrenal causes of acute kidney injury have is also used to stabilize the membrane and reduce the been excluded and the cause of intrinsic renal injury is risk of arrhythmias when there are electrocardiographic unclear. Renal biopsy is particularly important when changes showing hyperkalemia. In patients without clinical assessment and laboratory investigations suggest electrocardiographic evidence of hyperkalemia, calcium a diagnosis that requires confirmation before disease- gluconate is not necessary, but sodium polystyrene sulfo- specific therapy (e.g., immunosuppressive medications) nate (Kayexalate) can be given to lower potassium levels is instituted. Renal biopsy may need to be performed gradually, and loop urgently in patients with oliguria who have rapidly wors- diuretics can be used ening acute kidney injury, hematuria, and red blood cell in patients who are Patients with acute kidney
casts. In this setting, in addition to indicating a diagno- responsive to diuret- injury are more likely to
sis that requires immunosuppressive therapy, the biopsy ics. Dietary intake of develop chronic kidney
may support the initiation of special therapies, such as potassium should be disease in the future.
plasmapheresis if Goodpasture syndrome is present.
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Table 5. Preventive Strategies for Patients at High Risk of Acute Kidney Injury
Risk factors Cancer chemotherapy Hydration and al opurinol (Zyloprim) administration a few days before chemotherapy initiation in with risk of tumor lysis patients at high risk of tumor lysis syndrome to prevent uric acid nephropathy Exposure to nephrotoxic Avoid nephrotoxic medications if possible Measure and fol ow drug levels if availableUse appropriate dosing, intervals, and duration of therapy Exposure to radiographic Avoid use of intravenous contrast media when risks outweigh benefits contrast agents29 If use of contrast media is essential, use iso-osmolar or low-osmolar contrast agent with lowest 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 Use of N-acetylcysteine may be considered Hemodynamic instability Optimal fluid resuscitation; although there is no consensus, a mean arterial pressure goal of > 65 mm Hg is widely used; isotonic solutions (e.g., normal saline) are preferred over hyperoncotic solutions (e.g., albumin)19 Vasopressors are recommended for persistent hypotension (mean arterial pressure < 65 mm Hg) despite fluid resuscitation; choice of vasoactive agent should be tailored to patients' needs20 Dopamine is not recommended21 Hepatic failure30 Avoid hypotension and gastrointestinal bleedingEarly recognition and treatment of spontaneous bacterial peritonitis; use albumin, 1.5 g per kg at diagnosis and 1 g per kg at 48 hours Early recognition and management of ascitesAlbumin infusion during large volume paracentesisAvoid nephrotoxic medications Maintain adequate hydrationAlkalinization 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 7.5) Undergoing surgery Adequate volume resuscitation/prevention of hypotension, sepsis, optimizing cardiac functionConsider holding renin-angiotensin system antagonists preoperatively 31 Information from references 19 through 21, 27, and 29 through 31. The main indication for use of diuretics is manage- progressive glomerulonephritis, treatment with pulse ste- ment of volume overload. Intravenous loop diuretics, as roids, cytotoxic therapy, or a combination may be consid-a bolus or continuous infusion, can be helpful for this ered, often after confirmation of the diagnosis by kidney purpose. However, it is important to note that diuretics biopsy.23 In some patients, the metabolic consequences do not improve morbidity, mortality, or renal outcomes, of acute kidney injury cannot be adequately controlled and should not be used to prevent or treat acute kidney with conservative management, and renal replacement injury in the absence of volume overload.22 therapy will be required. The indications for initiation of All medications that may potentially affect renal func- renal replacement therapy include refractory hyperkale- tion by direct toxicity or by hemodynamic mechanisms mia, volume overload refractory to medical management, should be discontinued, if possible. For example, metfor- uremic pericarditis or pleuritis, uremic encephalopathy, min (Glucophage) should not be given to patients with intractable acidosis, and certain poisonings and intoxica-
diabetes mellitus who develop acute kidney injury. The tions (e.g., ethylene glycol, lithium).24
dosages of essential medications should be adjusted for
the lower level of kidney function. Avoidance of iodinated Prognosis
contrast media and gadolinium is important and, if imag-
Patients with acute kidney injury are more likely to ing is needed, noncontrast studies are recommended.
develop chronic kidney disease in the future. They are Supportive therapies (e.g., antibiotics, maintenance of also at higher risk of end-stage renal disease and prema- adequate nutrition, mechanical ventilation, glycemic con- ture death.25-27 Patients who have an episode of acute kid- trol, anemia management) should be pursued based on ney injury should be monitored for the development or standard management practices. In patients with rapidly worsening of chronic kidney disease.
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report of an initiative to improve outcomes in acute kidney injury. Crit Because of the morbidity and mortality associated with Care. 2007;11(2):R31. 9. Hol ey JL. Clinical approach to the diagnosis of acute renal failure. In: acute kidney injury, it is important for primary care physi- Greenberg A, Cheung AK, eds. Primer on Kidney Diseases. 5th ed. Phil- cians to identify patients who are at high risk of developing adelphia, Pa.: National Kidney Foundation; 2009.
this type of injury and to implement preventive strategies. 10. Kaufman J, Dhakal M, Patel B, Hamburger R. Community-acquired Those at highest risk include adults older than 75 years; acute renal failure. Am J Kidney Dis. 1991;17(2):191-198.
11. Christensen PK, Hansen HP, Parving HH. Impaired autoregulation of persons with diabetes or preexisting chronic kidney dis- GFR in hypertensive non-insulin dependent diabetic patients. Kidney ease; persons with medical problems such as cardiac fail- Int. 1997;52(5):1369-1374. ure, liver failure, or sepsis; and those who are exposed to 12. Smith MC. Acute renal failure. In: Resnick MI, Elder JS, Spirnak JP, eds. contrast agents or who are undergoing cardiac surgery.28 Clinical Decisions in Urology. 3rd ed. Hamilton, Ontario, Canada: BC Decker, Inc.; 2004:60-63.
Preventive strategies can be tailored to the clinical cir- 13. Clarkson MR, Giblin L, O'Connell FP, et al. Acute interstitial nephritis: cumstances of the individual patient (Table 5).19-21,27,29-31 clinical features and response to corticosteroid therapy. Nephrol Dial Transplant. 2004;19(11):2778-2783. Data Sources: We searched PubMed (also with the Clinical Queries
14. González E, Gutiérrez E, Galeano C, et al.; Grupo Madrileño De Nefri- function), the Cochrane Database of Systematic Reviews, and the tis Intersticiales. Early steroid treatment improves the recovery of renal National Guidelines Clearinghouse using the key words AKI, acute kidney function in patients with drug-induced acute interstitial nephritis. Kid- injury, and acute renal failure. Search date: February 2012.
ney Int. 2008;73(8):940-946. 15. Meyer TW, Hostetter TH. Uremia. N Engl J Med. 2007;357(13):1316-1325. The Authors
16. Agrawal M, Swartz R. Acute renal failure [published correction appears in Am Fam Physician. 2001;63(3):445]. Am Fam Physician. 2000;61(7): MAHBOOB RAHMAN, MD, MS, is an associate professor of medicine at Case Western Reserve University School of Medicine in Cleveland, Ohio, 17. Lewington A, Kanagasundaram S. Clinical practice guidelines: acute and a staff nephrologist at University Hospitals Case Medical Center in kidney injury. 2011. http://www.renal.org/clinical/guidelinessection/ Cleveland and at Louis Stokes Cleveland VA Medical Center.
AcuteKidneyInjury.aspx. Accessed September 7, 2012.
18. O'Neill WC. Sonographic evaluation of renal failure. Am J Kidney Dis. FARIHA SHAD, MD, is a nephrologist at Kaiser Permanente in Cleveland. At the time the article was written, Dr. Shad was a fel ow at Case Western 19. Schortgen F, Lacherade JC, Bruneel F, et al. Effects of hydroxyethylstarch Reserve University School of Medicine.
and gelatin on renal function in severe sepsis: a multicentre randomised MICHAEL C. SMITH, MD, is a professor of medicine at Case Western study. Lancet. 2001;357(9260):911-916. Reserve University School of Medicine, and a staff nephrologist at Univer- 20. Brochard L, Abroug F, Brenner M, et al. An Official ATS/ERS/ESICM/ sity Hospitals Case Medical Center. SCCM/SRLF Statement: Prevention and Management of Acute Renal Failure in the ICU Patient: an international consensus conference in inten- Address correspondence to Mahboob Rahman, MD, MS, Case Western sive care medicine. Am J Respir Crit Care Med. 2010;181(10):1128-1155. Reserve University, 11100 Euclid Ave., Cleveland, OH 44106. Reprints 21. Friedrich JO, Adhikari N, Herridge MS, Beyene J. Meta-analysis: low- are not available from the authors. dose dopamine increases urine output but does not prevent renal dys-function or death. Ann Intern Med. 2005;142(7):510-524. Author disclosure: No relevant financial affiliations to disclose.
22. Ho KM, Sheridan DJ. Meta-analysis of frusemide to prevent or treat acute renal failure. BMJ. 2006;333(7565):420. 23. Walters G, Wil is NS, Craig JC. Interventions for renal vasculitis in adults. Cochrane Database Syst Rev. 2008;(3):CD003232.
1. Hsu CY, McCul och CE, Fan D, Ordoñez JD, Chertow GM, Go AS. Com- 24. Mehta RL. Indications for dialysis in the ICU: renal replacement vs. renal munity-based incidence of acute renal failure. Kidney Int. 2007;72(2): support. Blood Purif. 2001;19(2):227-232. 25. Goldberg R, Dennen P. Long-term outcomes of acute kidney injury. Adv 2. Nash K, Hafeez A, Hou S. Hospital-acquired renal insufficiency. Am J Chronic Kidney Dis. 2008;15(3):297-307. Kidney Dis. 2002;39(5):930-936. 26. Coca SG, Yusuf B, Shlipak MG, Garg AX, Parikh CR. Long-term risk of 3. Hoste EA, Schurgers M. Epidemiology of acute kidney injury: how big is mortality and other adverse outcomes after acute kidney injury: a sys- the problem? Crit Care Med. 2008;36(4 suppl):S146-S151. tematic review and meta-analysis. Am J Kidney Dis. 2009;53(6):961-973. 4. Hoste EA, Clermont G, Kersten A, et al. RIFLE criteria for acute kidney 27. Pession A, Masetti R, Gaidano G, et al. Risk evaluation, prophylaxis, and injury are associated with hospital mortality in critical y ill patients: a treatment of tumor lysis syndrome: consensus of an Italian expert panel. cohort analysis. Crit Care. 2006;10(3):R73. Adv Ther. 2011;28(8):684-697. 5. Ympa YP, Sakr Y, Reinhart K, Vincent JL. Has mortality from acute renal 28. Leblanc M, Kel um JA, Gibney RT, Lieberthal W, Tumlin J, Mehta R. Risk failure decreased? A systematic review of the literature. Am J Med. factors for acute renal failure: inherent and modifiable risks. Curr Opin 2005;118(8):827-832. Crit Care. 2005;11(6):533-536. 6. Gruberg L, Weissman NJ, Pichard AD, et al. Impact of renal function on 29. Rundback JH, Nahl D, Yoo V. Contrast-induced nephropathy. J Vasc morbidity and mortality after percutaneous aortocoronary saphenous Surg. 2011;54(2):575-579. vein graft intervention. Am Heart J. 2003;145(3):529-534. 30. Nadim MK, Kel um JA, Davenport A, et al. Hepatorenal syndrome: the 7. Uchino S, Kel um JA, Bel omo R, et al.; Beginning and Ending Supportive 8th international consensus conference of the Acute Dialysis Quality Ini- Therapy for the Kidney (BEST Kidney) Investigators. Acute renal fail- tiative (ADQI) group. Crit Care. 2012;16(1):R23. ure in critical y ill patients: a multinational, multicenter study. JAMA. 31. Auron M, Harte B, Kumar A, Michota F. Renin-angiotensin system 2005;294(7):813-818. antagonists in the perioperative setting: clinical consequences and rec- 8. Mehta RL, Kel um JA, Shah SV, et al. Acute Kidney Injury Network: ommendations for practice. Postgrad Med J. 2011;87(1029):472-481. October 1, 2012Volume 86, Number 7 www.aafp.org/afp American Family Physician 639

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