FARIHA SHAD, MD, Kaiser Permanente, Cleveland, Ohio

MICHAEL C. SMITH, MD, Case Western Reserve Academy School of Medicine, Cleveland, Ohio

Am Fam Physician. 2012 Oct 1;86(seven):631-639.

Commodity Sections

  • Abstract
  • Definition
  • Etiology
  • Clinical Presentation
  • Diagnosis
  • Management
  • Prognosis
  • Prevention
  • References

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, sometimes requiring renal replacement therapy. The diagnostic evaluation can be used to classify astute 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. Concrete examination should assess intravascular volume status and identify skin rashes indicative of systemic affliction. The initial laboratory evaluation should include measurement of serum creatinine level, complete blood count, urinalysis, and fractional excretion of sodium. Ultrasonography of the kidneys should be performed in well-nigh patients, particularly in older men, to rule out obstacle. Direction of acute kidney injury involves fluid resuscitation, abstention of nephrotoxic medications and contrast media exposure, and correction of electrolyte imbalances. Renal replacement therapy (dialysis) is indicated for refractory hyperkalemia; book overload; intractable acidosis; uremic encephalopathy, pericarditis, or pleuritis; and removal of certain toxins. Recognition of risk factors (east.one thousand., older historic period, sepsis, hypovolemia/daze, cardiac surgery, infusion of contrast agents, diabetes mellitus, preexisting chronic kidney disease, cardiac failure, liver failure) is important. Team-based approaches for prevention, early on diagnosis, and aggressive management are critical for improving outcomes.

The incidence of astute kidney injury has increased in recent years, both in the community and in hospital settings.one,ii The estimated incidence of acute kidney injury is two to three cases per 1,000 persons.three Vii percent of hospitalized patients and about two-thirds of patients in intensive care units develop acute kidney injury,two ofttimes as part of the multiple organ dysfunction syndrome.4

SORT: KEY RECOMMENDATIONS FOR Practice

Clinical recommendation Evidence rating References

The diagnosis of acute kidney injury is based on serum creatinine levels, urine output, and the need for renal replacement therapy.

C

8

Renal ultrasonography should exist performed in nearly patients with acute kidney injury to rule out obstruction.

C

17

Adequate fluid residue should be maintained in patients with astute kidney injury by using isotonic solutions (e.g., normal saline) instead of hyperoncotic solutions (eastward.g., dextrans, hydroxyethyl starch, albumin).

C

nineteen

Dopamine utilize is non recommended for the prevention of astute kidney injury.

A

21

Diuretics do not ameliorate morbidity, mortality, or renal outcomes, and should not be used to prevent or care for acute kidney injury in the absence of volume overload.

A

22

Consider therapy with immunosuppressive agents (e.yard., cyclophosphamide, prednisone) in patients with apace progressive glomerulonephritis.

C

23

Astute kidney injury is associated with a high rate of adverse outcomes; mortality rates range between 25 and 80 percent, depending on the cause and the clinical condition of the patient.v–7 These information highlight the importance of recognition and advisable management, usually in collaboration with nephrologists and other subspecialists.

Definition

  • Abstract
  • Definition
  • Etiology
  • Clinical Presentation
  • Diagnosis
  • Management
  • Prognosis
  • Prevention
  • References

Acute kidney injury is defined every bit an abrupt (inside 48 hours) reduction in kidney role based on an elevation in serum creatinine level, a reduction in urine output, the need for renal replacement therapy (dialysis), or a combination of these factors. It is classified in three stages (Table i).viii The term acute kidney injury should replace terms such as acute renal failure and acute renal insufficiency, which previously have been used to describe the aforementioned clinical status.

Table 1.

Stages of Acute Kidney Injury

Stage Change in serum creatinine level Urine output Other

1

Increase ≥ 0.3 mg per dL (26.52 μmol per L) or ≥ 1.5- to twofold from baseline

< 0.5 mL per kg per hour for more than 6 hours

—

2

Increment > two- to threefold from baseline

< 0.5 mL per kg per hour for more than 12 hours

—

3

Increase > threefold from baseline or ≥ four.0 mg per dL (353.60 μmol per L) with an astute rise of at least 0.5 mg per dL (44.twenty μmol per 50)

< 0.3 mL per kg per 60 minutes for 24 hours or anuria for 12 hours

Renal replacement therapy required

Etiology

  • Abstract
  • Definition
  • Etiology
  • Clinical Presentation
  • Diagnosis
  • Management
  • Prognosis
  • Prevention
  • References

The causes of acute kidney injury can exist divided into three categories (Table 29): prerenal (caused by decreased renal perfusion, ofttimes because of volume depletion), intrinsic renal (caused by a process within the kidneys), and postrenal (caused by inadequate drainage of urine distal to the kidneys). In patients who already accept underlying chronic kidney affliction, whatever of these factors, just specially book depletion, may cause astute kidney injury in addition to the chronic impairment of renal function.

Table 2.

Causes of Acute Kidney Injury

Prerenal

Intrarenal vasoconstriction (hemodynamically mediated)

Medications: nonsteroidal anti-inflammatory drugs,* angiotensin-converting enzyme inhibitors,* angiotensin receptor blockers,* cyclosporine (Sandimmune), tacrolimus (Prograf)

Cardiorenal syndrome*

Hepatorenal syndrome

Abdominal compartment syndrome

Hypercalcemia

Systemic vasodilation (e.g., sepsis,* neurogenic shock)

Volume depletion

Renal loss from diuretic overuse,* osmotic diuresis (e.k., diabetic ketoacidosis*)

Extrarenal loss from vomiting, diarrhea,* burns, sweating, claret loss

Intrinsic renal

Glomerular (due east.one thousand., postinfectious and other glomerulonephritis)

Interstitial

Medications: penicillin analogues,* cephalosporins,* sulfonamides, ciprofloxacin (Cipro), acyclovir (Zovirax), rifampin, phenytoin (Dilantin), interferon, proton pump inhibitors, nonsteroidal anti-inflammatory drugs

Infections (e.g., direct infection of renal parenchyma or associated with systemic infections)

Viruses: Epstein-Barr virus, cytomegalovirus, human immunodeficiency virus

Bacteria: Streptococcus species, Legionella species

Fungi: candidiasis, histoplasmosis

Systemic illness: sarcoidosis, lupus

Tubular

Ischemic: prolonged hypotension*

Nephrotoxic: exogenous toxins (e.g., radiographic contrast agents,* aminoglycosides,* cisplatin, methotrexate, ethylene glycol, amphotericin B) and endogenous toxins (due east.g., hemolysis and rhabdomyolysis [pigment nephropathy], tumor lysis syndrome, myeloma)

Vascular

Renal vein thrombosis, malignant hypertension, scleroderma renal crisis, renal atheroembolic disease,* and renal infarction

Postrenal

Extrarenal obstruction: prostate hypertrophy*; neurogenic bladder; retroperitoneal fibrosis; bladder, prostate, or cervical cancer

Intrarenal obstacle: stones,* crystals (acyclovir, indinavir [Crixivan]), clots, tumors

PRERENAL CAUSES

Approximately 70 percent of community-acquired cases of astute kidney injury are attributed to prerenal causes.10 In these cases, underlying kidney function may be normal, just decreased renal perfusion associated with intravascular volume depletion (e.thou., from vomiting or diarrhea) or decreased arterial pressure (eastward.thou., from eye failure or sepsis) results in a reduced glomerular filtration rate. Autoregulatory mechanisms oft can compensate for some degree of reduced renal perfusion in an attempt to maintain the glomerular filtration rate. In patients with preexisting chronic kidney disease, all the same, these mechanisms are dumb, and the susceptibility to develop acute-on-chronic renal failure is college.11

Several medications can crusade prerenal acute kidney injury. Notably, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers can impair renal perfusion by causing dilation of the efferent arteriole and reduce intraglomerular pressure. Nonsteroidal anti-inflammatory drugs likewise can decrease the glomerular filtration rate by changing the balance of vasodilatory/vasoconstrictive agents in the renal microcirculation. These drugs and others limit the normal homeostatic responses to volume depletion and can exist associated with a decline in renal part. In patients with prerenal acute kidney injury, kidney function typically returns to baseline after adequate volume condition is established, the underlying cause is treated, or the offending drug is discontinued.

INTRINSIC RENAL CAUSES

Intrinsic renal causes are likewise of import sources of astute kidney injury and tin can be categorized by the component of the kidney that is primarily affected (i.e., tubular, glomerular, interstitial, or vascular).

Acute tubular necrosis is the most common type of intrinsic acute kidney injury in hospitalized patients. The crusade is unremarkably ischemic (from prolonged hypotension) or nephrotoxic (from an amanuensis that is toxic to the tubular cells). In contrast to a prerenal etiology, acute kidney injury caused by acute tubular necrosis does not improve with adequate repletion of intravascular book and blood catamenia to the kidneys. Both ischemic and nephrotoxic acute tubular necrosis can resolve over time, although temporary renal replacement therapy may be required, depending on the degree of renal injury and the presence of preexisting chronic kidney disease.

Glomerular causes of astute kidney injury are the result of acute inflammation of blood vessels and glomeruli. Glomerulonephritis is usually a manifestation of a systemic disease (e.g., systemic lupus erythematosus) or pulmonary renal syndromes (e.chiliad., Goodpasture syndrome, Wegener granulomatosis). History, physical examination, and urinalysis are crucial for diagnosing glomerulonephritis (Table 39 and Figure 1 12). Because management often involves administration of immunosuppressive or cytotoxic medications with potentially astringent adverse effects, renal biopsy is ofttimes required to confirm the diagnosis before initiating therapy.

Table 3.

History and Physical Examination Findings for Categorizing Astute Kidney Injury

Blazon of acute kidney injury History findings Physical examination findings

Prerenal

Volume loss (e.k., history of vomiting, diarrhea, diuretic overuse, hemorrhage, burns)

Weight loss, orthostatic hypotension and tachycardia

Thirst and reduced fluid intake

Poor skin turgor

Cardiac disease

Dilated cervix veins, Sthree heart sound, pulmonary rales, peripheral edema

Liver affliction

Ascites, caput medusae, spider angiomas

Intrinsic renal

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

Muscle tenderness, compartment syndrome, assessment of volume status

Glomerular

Lupus, systemic sclerosis, rash, arthritis, uveitis, weight loss, fatigue, hepatitis C virus infection, human immunodeficiency virus infection, hematuria, foamy urine, cough, sinusitis, hemoptysis

Periorbital, sacral, and lower-extremity edema; rash; oral/nasal ulcers

Interstitial

Medication use (e.k., antibiotics, proton pump inhibitors), rash, arthralgias, fever, infectious illness

Fever, drug-related rash

Vascular

Nephrotic syndrome, trauma, flank pain, anticoagulation (atheroembolic illness), vessel catheterization or vascular surgery

Livedo reticularis, funduscopic examination (showing cancerous hypertension), abdominal bruits

Postrenal

Urinary urgency or hesitancy, gross hematuria, polyuria, stones, medications, cancer

Bladder distention, pelvic mass, prostate enlargement

Diagnosis and Treatment of Acute Kidney Injury

Figure 1.

Algorithm for the diagnosis and handling of acute kidney injury.

Adjusted with permission from Smith MC. Astute 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 interstitial nephritis tin be secondary to many conditions, but most cases are related to medication employ, making patient history the key to diagnosis. In nigh 1-3rd of cases, there is a history of maculopapular erythematous rash, fever, arthralgias, or a combination of these symptoms.13 Eosinophiluria may be plant in patients with astute interstitial nephritis, but it is not pathognomonic of this disease. A kidney biopsy may be needed to distinguish between allergic interstitial nephritis and other renal causes of acute kidney injury. In improver to discontinuing offending agents, steroids may be beneficial if given early in the course of disease.14

Acute events involving renal arteries or veins can also atomic number 82 to intrinsic astute 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 exam and history provide important clues to the diagnosis (Tabular array 3nine). Vascular causes of acute kidney injury usually require imaging to confirm the diagnosis.

POSTRENAL CAUSES

Postrenal causes typically result from obstacle of urinary menstruum, and prostatic hypertrophy is the most common cause of obstacle in older men. Prompt diagnosis followed by early relief of obstruction is associated with improvement in renal function in most patients.

Clinical Presentation

  • Abstract
  • Definition
  • Etiology
  • Clinical Presentation
  • Diagnosis
  • Management
  • Prognosis
  • Prevention
  • References

Clinical presentation varies with the crusade and severity of renal injury, and associated diseases. Nearly 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.15 Patients can likewise present with oliguria (urine output less than 400 mL per day), anuria (urine output less than 100 mL per day), or normal volumes of urine (nonoliguric acute kidney injury). Other presentations of astute kidney injury may include development of uremic encephalopathy (manifested by a pass up in mental status, asterixis, or other neurologic symptoms), anemia, or bleeding caused by uremic platelet dysfunction.

Diagnosis

  • Abstract
  • Definition
  • Etiology
  • Clinical Presentation
  • Diagnosis
  • Management
  • Prognosis
  • Prevention
  • References

A patient history and physical examination, with an accent on assessing the patient'due south volume status, are crucial for determining the cause of acute kidney injury (Table 39). The history should identify use of nephrotoxic medications or systemic illnesses that might cause poor renal perfusion or directly impair renal office. Physical examination should appraise intravascular book condition 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 (FENa). Imaging studies can aid rule out obstacle. Useful tests are summarized in Tabular array 4.sixteen Figure 1 presents an overview of the diagnosis and management of acute kidney injury.12

Table 4.

Diagnostic Test Results and Corresponding Diseases in Patients with Acute Kidney Injury

Test result When to order Associated diseases/conditions

Elevated antineutrophil cytoplasmic antibody, antiglomerular basement membrane antibiotic

Suspected acute glomerulonephritis, pulmonary renal syndromes

Vasculitis, Goodpasture syndrome

Elevated antistreptolysin O titer

Recent infection and clinical picture of acute glomerulonephritis

Poststreptococcal glomerulonephritis

Elevated creatine kinase level, elevated myoglobin level, dipstick positive for blood but negative for red blood cells

Contempo trauma, muscle injury

Rhabdomyolysis

Elevated prostate-specific antigen level

Older men with symptoms suggestive of urinary obstruction

Prostate hypertrophy, prostate cancer

Elevated uric acid level

History of rapidly proliferating tumors, recent chemotherapy

Malignancy, tumor lysis syndrome

Eosinophiluria

Fever, rash

Allergic interstitial nephritis

Prove of hemolysis (schistocytes on peripheral smear, decreased haptoglobin level, elevated indirect bilirubin level, elevated lactate dehydrogenase level)

Fever, anemia, thrombocytopenia, neurologic signs

Hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, systemic lupus erythematosus, other autoimmune diseases

Hydronephrosis on renal ultrasonography

Suspected obstruction

Malignancy, prostate hypertrophy, uterine fibroids, nephrolithiasis, ureterolithiasis

Increased anion gap with increased osmolar gap*

Suspected poisoning, unresponsive patient

Ethylene glycol or methanol poisoning

Low complement level

Suspected astute glomerulonephritis

Systemic lupus erythematosus, endocarditis, postinfectious glomerulonephritis

Monoclonal spike on serum poly peptide electrophoresis

Anemia, proteinuria, astute kidney injury in older patients

Multiple myeloma

Positive antinuclear antibiotic, double-stranded DNA antibiotic

Proteinuria, peel rash, arthritis

Autoimmune diseases, systemic lupus erythematosus

Positive claret cultures

Intravenous drug utilize, recent infection, new cardiac murmur

Endocarditis

Positive HIV test

Take a chance factors for HIV infection

HIV nephropathy

SERUM CREATININE LEVEL

It is important to compare the patient's electric current serum creatinine level with previous levels to make up one's mind the duration and acuity of the disease. The definition of acute kidney injury indicates that a ascent in creatinine has occurred within 48 hours, although in the outpatient setting, it may be hard to ascertain when the ascent actually happened. A loftier serum creatinine level in a patient with a previously normal documented level suggests an acute process, whereas a rising over weeks to months represents a subacute or chronic process.

URINALYSIS

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 12).

COMPLETE BLOOD COUNT

The presence of acute hemolytic anemia with the peripheral smear showing schistocytes in the setting of astute kidney injury should heighten the possibility of hemolytic uremic syndrome or thrombotic thrombocytopenic purpura.

URINE ELECTROLYTES

In patients with oliguria, measurement of IronNa is helpful in distinguishing prerenal from intrinsic renal causes of acute kidney injury. Atomic number 26Na is defined by the following formula:

Online calculators are too available. A value less than ane percent indicates a prerenal cause of acute kidney injury, whereas a value greater than 2 percent indicates an intrinsic renal crusade. In patients on diuretic therapy, notwithstanding, a IronNa higher than 1 percent may be acquired by natriuresis induced by the diuretic, and is a less reliable measure of a prerenal state. In such cases, fractional excretion of urea may exist helpful, with values less than 35 percentage indicating a prerenal cause. FeNa values less than 1 percent are not specific for prerenal causes of acute kidney injury because these values can occur in other weather condition, such equally dissimilarity nephropathy, rhabdomyolysis, acute glomerulonephritis, and urinary tract obstruction.

IMAGING STUDIES

Renal ultrasonography should be performed in most patients with acute kidney injury, particularly in older men, to rule out obstacle (i.e., a postrenal cause).17,18 The presence of postvoid residual urine greater than 100 mL (determined by a bladder scan or via urethral catheterization if bladder scan is unavailable) suggests postrenal acute kidney injury and requires renal ultrasonography to detect hydronephrosis or outlet obstruction. To diagnose extrarenal causes of obstruction (east.thousand., pelvic tumors), other imaging modalities, such as computed tomography or magnetic resonance imaging, may be required.

RENAL BIOPSY

Renal biopsy is reserved for patients in whom prerenal and postrenal causes of acute kidney injury take been excluded and the cause of intrinsic renal injury is unclear. Renal biopsy is particularly important when clinical assessment and laboratory investigations advise a diagnosis that requires confirmation before disease-specific therapy (e.1000., immunosuppressive medications) is instituted. 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 back up the initiation of special therapies, such every bit plasmapheresis if Goodpasture syndrome is present.

Direction

  • Abstruse
  • Definition
  • Etiology
  • Clinical Presentation
  • Diagnosis
  • Management
  • Prognosis
  • Prevention
  • References

Optimal management of acute kidney injury requires close collaboration amidst master intendance physicians, nephrologists, hospitalists, and other subspecialists participating in the care of the patient. Subsequently astute kidney injury is established, management is primarily supportive.

Patients with astute kidney injury generally should be hospitalized unless the condition is balmy and clearly resulting from an easily reversible cause. The key to direction is assuring adequate renal perfusion by achieving and maintaining hemodynamic stability and fugitive hypovolemia. In some patients, clinical cess of intravascular volume status and abstention of volume overload may be difficult, in which example measurement of central venous pressures in an intensive care setting may be helpful.

If fluid resuscitation is required because of intravascular book depletion, isotonic solutions (due east.g., normal saline) are preferred over hyperoncotic solutions (e.thousand., dextrans, hydroxyethyl starch, albumin).xix A reasonable goal is a mean arterial pressure greater than 65 mm Hg, which may require the use of vasopressors in patients with persistent hypotension.twenty Renal-dose dopamine is associated with poorer outcomes in patients with astute kidney injury; information technology is no longer recommended.21 Cardiac function can be optimized equally needed with positive inotropes, or afterload and preload reduction.

Attending to electrolyte imbalances (e.grand., hyperkalemia, hyperphosphatemia, hypermagnesemia, hyponatremia, hypernatremia, metabolic acidosis) is important. Severe hyperkalemia is defined as potassium levels of 6.5 mEq per L (6.5 mmol per L) or greater, or less than 6.five mEq per 50 with electrocardiographic changes typical of hyperkalemia (e.yard., tall, peaked T waves). In severe hyperkalemia, five to x units of regular insulin and dextrose l% given intravenously can shift potassium out of apportionment and into the cells. Calcium gluconate (ten mL of x% solution infused intravenously over five minutes) is also used to stabilize the membrane and reduce the risk of arrhythmias when there are electrocardiographic changes showing hyperkalemia. In patients without electrocardiographic prove of hyperkalemia, calcium gluconate is non necessary, simply sodium polystyrene sulfonate (Kayexalate) can be given to lower potassium levels gradually, and loop diuretics tin 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, every bit a bolus or continuous infusion, tin exist helpful for this purpose. However, it is of import to note that diuretics do not improve morbidity, mortality, or renal outcomes, and should not be used to prevent or treat astute kidney injury in the absence of volume overload.22

All medications that may potentially touch on renal function by direct toxicity or by hemodynamic mechanisms should exist 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 exist adapted for the lower level of kidney function. Abstention of iodinated contrast media and gadolinium is of import and, if imaging is needed, noncontrast studies are recommended.

Supportive therapies (eastward.g., antibiotics, maintenance of adequate nutrition, mechanical ventilation, glycemic control, anemia management) should be pursued based on standard direction practices. In patients with rapidly progressive glomerulonephritis, treatment with pulse steroids, cytotoxic therapy, or a combination may be considered, often afterwards confirmation of the diagnosis by kidney biopsy.23 In some patients, the metabolic consequences of acute kidney injury cannot be adequately controlled with conservative management, and renal replacement therapy volition exist required. 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.g., ethylene glycol, lithium).24

Prognosis

  • Abstruse
  • Definition
  • Etiology
  • Clinical Presentation
  • Diagnosis
  • Management
  • Prognosis
  • Prevention
  • References

Patients with acute kidney injury are more probable to develop chronic kidney affliction in the future. They are also at college take a chance of end-phase renal affliction and premature decease.25–27 Patients who accept an episode of acute kidney injury should be monitored for the development or worsening of chronic kidney disease.

Prevention

  • Abstruse
  • Definition
  • Etiology
  • Clinical Presentation
  • Diagnosis
  • Management
  • Prognosis
  • Prevention
  • References

Because of the morbidity and bloodshed associated with acute kidney injury, it is important for primary care physicians to identify patients who are at loftier risk of developing this blazon 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.28  Preventive strategies tin can exist tailored to the clinical circumstances of the private patient (Table five).19–21,27,29–31

Table v.

Preventive Strategies for Patients at High Risk of Acute Kidney Injury

Risk factors Preventive strategies

Cancer chemotherapy with gamble of tumor lysis syndrome27

Hydration and allopurinol (Zyloprim) administration a few days before chemotherapy initiation in patients at loftier hazard of tumor lysis syndrome to prevent uric acid nephropathy

Exposure to nephrotoxic medications

Avoid nephrotoxic medications if possible

Measure out and follow drug levels if available

Use advisable dosing, intervals, and duration of therapy

Exposure to radiographic contrast agents29

Avoid use of intravenous contrast media when risks outweigh benefits

If use of dissimilarity media is essential, utilise iso-osmolar or depression-osmolar contrast amanuensis with everyman volume possible

Optimize volume status earlier administration of contrast media; apply of isotonic normal saline or sodium bicarbonate may be considered in loftier-risk patients who are not at run a risk of volume overload

Use of N-acetylcysteine may be considered

Hemodynamic instability

Optimal fluid resuscitation; although at that place is no consensus, a mean arterial pressure goal of > 65 mm Hg is widely used; isotonic solutions (eastward.1000., 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 bleeding

Early recognition and treatment of spontaneous bacterial peritonitis; employ albumin, 1.5 g per kg at diagnosis and one thou per kg at 48 hours

Early recognition and direction of ascites

Albumin infusion during big volume paracentesis

Avoid nephrotoxic medications

Rhabdomyolysis20

Maintain acceptable hydration

Alkalinization of the urine with intravenous sodium bicarbonate in select patients (normal calcium, bicarbonate less than 30 mEq per Fifty [30 mmol per L], and arterial pH less than 7.five)

Undergoing surgery

Adequate volume resuscitation/prevention of hypotension, sepsis, optimizing cardiac function Consider holding renin-angiotensin system antagonists preoperatively31

Data Sources: We searched PubMed (also with the Clinical Queries office), the Cochrane Database of Systematic Reviews, and the National Guidelines Clearinghouse using the primal words AKI, astute kidney injury, and acute renal failure. Search date: February 2012.

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The Authors

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MAHBOOB RAHMAN, MD, MS, is an associate professor of medicine at Case Western Reserve University School of Medicine in Cleveland, Ohio, and a staff nephrologist at University Hospitals Case Medical Center in Cleveland and at Louis Stokes Cleveland VA Medical Middle....

FARIHA SHAD, Dr., is a nephrologist at Kaiser Permanente in Cleveland. At the time the commodity was written, Dr. Shad was a boyfriend at Instance Western Reserve University School of Medicine.

MICHAEL C. SMITH, MD, is a professor of medicine at Case Western Reserve University School of Medicine, and a staff nephrologist at University Hospitals Case Medical Eye.

Address correspondence to Mahboob Rahman, Md, MS, Case Western Reserve Academy, 11100 Euclid Ave., Cleveland, OH 44106. Reprints are not available from the authors.

Author disclosure: No relevant financial affiliations to disclose.

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