FARIHA SHAD, Dr., Kaiser Permanente, Cleveland, Ohio

MICHAEL C. SMITH, Doc, Case Western Reserve University School of Medicine, Cleveland, Ohio

Am Fam Physician. 2012 Oct one;86(7):631-639.

Article Sections

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

Astute kidney injury is characterized past precipitous deterioration in kidney office, manifested past an increment 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 tin can be used to classify acute kidney injury every bit prerenal, intrinsic renal, or postrenal. The initial workup includes a patient history to place the use of nephrotoxic medications or systemic illnesses that might cause poor renal perfusion or directly impair renal office. Physical examination should assess intravascular volume status and identify pare rashes indicative of systemic illness. The initial laboratory evaluation should include measurement of serum creatinine level, complete claret count, urinalysis, and fractional excretion of sodium. Ultrasonography of the kidneys should be performed in most patients, particularly in older men, to rule out obstruction. 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; volume overload; intractable acidosis; uremic encephalopathy, pericarditis, or pleuritis; and removal of certain toxins. Recognition of risk factors (e.k., older age, sepsis, hypovolemia/stupor, cardiac surgery, infusion of contrast agents, diabetes mellitus, preexisting chronic kidney disease, cardiac failure, liver failure) is important. Squad-based approaches for prevention, early diagnosis, and aggressive management are critical for improving outcomes.

The incidence of acute kidney injury has increased in recent years, both in the customs and in hospital settings.ane,2 The estimated incidence of astute kidney injury is 2 to three cases per 1,000 persons.3 Seven percent of hospitalized patients and about ii-thirds of patients in intensive care units develop acute kidney injury,2 often as part of the multiple organ dysfunction syndrome.iv

SORT: Cardinal 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 be performed in most patients with acute kidney injury to rule out obstruction.

C

17

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

C

nineteen

Dopamine use is not recommended for the prevention of acute kidney injury.

A

21

Diuretics do not improve morbidity, mortality, or renal outcomes, and should not be used to forestall or care for astute kidney injury in the absenteeism of volume overload.

A

22

Consider therapy with immunosuppressive agents (due east.1000., cyclophosphamide, prednisone) in patients with rapidly progressive glomerulonephritis.

C

23

Astute kidney injury is associated with a loftier rate of agin outcomes; mortality rates range between 25 and eighty percent, depending on the cause and the clinical status of the patient.5–7 These data highlight the importance of recognition and appropriate management, usually in collaboration with nephrologists and other subspecialists.

Definition

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

Acute kidney injury is divers as an abrupt (inside 48 hours) reduction in kidney function based on an top 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 3 stages (Table 1).eight 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 same clinical condition.

Table 1.

Stages of Acute Kidney Injury

Stage Change in serum creatinine level Urine output Other

ane

Increase ≥ 0.iii mg per dL (26.52 μmol per L) or ≥ 1.5- to twofold from baseline

< 0.five mL per kg per hour for more than six hours

—

2

Increase > 2- to threefold from baseline

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

—

iii

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

< 0.3 mL per kg per hour 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 be divided into iii categories (Tabular array ii9): prerenal (acquired past decreased renal perfusion, often because of volume depletion), intrinsic renal (caused past a process inside the kidneys), and postrenal (caused by inadequate drainage of urine distal to the kidneys). In patients who already have underlying chronic kidney disease, any of these factors, just especially book depletion, may crusade astute kidney injury in addition to the chronic impairment of renal function.

Table two.

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 (eastward.thou., diabetic ketoacidosis*)

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

Intrinsic renal

Glomerular (e.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 (due east.g., directly 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 disease: 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.yard., hemolysis and rhabdomyolysis [paint 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 obstruction: stones,* crystals (acyclovir, indinavir [Crixivan]), clots, tumors

PRERENAL CAUSES

Approximately seventy per centum of community-acquired cases of acute kidney injury are attributed to prerenal causes.10 In these cases, underlying kidney function may be normal, but decreased renal perfusion associated with intravascular book depletion (e.g., from vomiting or diarrhea) or decreased arterial pressure (eastward.g., from heart failure or sepsis) results in a reduced glomerular filtration rate. Autoregulatory mechanisms often 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, however, these mechanisms are impaired, and the susceptibility to develop acute-on-chronic renal failure is higher.11

Several medications tin cause prerenal astute kidney injury. Notably, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers tin can impair renal perfusion by causing dilation of the efferent arteriole and reduce intraglomerular pressure. Nonsteroidal anti-inflammatory drugs also tin decrease the glomerular filtration charge per unit 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 tin can be associated with a decline in renal part. In patients with prerenal astute kidney injury, kidney function typically returns to baseline after acceptable book status is established, the underlying cause is treated, or the offending drug is discontinued.

INTRINSIC RENAL CAUSES

Intrinsic renal causes are also important sources of acute 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 mutual type of intrinsic acute kidney injury in hospitalized patients. The cause is usually 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 past astute tubular necrosis does non improve with adequate repletion of intravascular book and blood flow to the kidneys. Both ischemic and nephrotoxic astute tubular necrosis can resolve over time, although temporary renal replacement therapy may be required, depending on the caste of renal injury and the presence of preexisting chronic kidney disease.

Glomerular causes of acute kidney injury are the outcome of acute inflammation of blood vessels and glomeruli. Glomerulonephritis is usually a manifestation of a systemic affliction (east.g., systemic lupus erythematosus) or pulmonary renal syndromes (e.g., Goodpasture syndrome, Wegener granulomatosis). History, concrete exam, and urinalysis are crucial for diagnosing glomerulonephritis (Table threeix and Figure ane 12). Because management frequently involves administration of immunosuppressive or cytotoxic medications with potentially severe adverse effects, renal biopsy is often required to confirm the diagnosis before initiating therapy.

Table 3.

History and Concrete Examination Findings for Categorizing Acute Kidney Injury

Type of acute kidney injury History findings Physical exam findings

Prerenal

Book loss (east.g., history of vomiting, diarrhea, diuretic overuse, hemorrhage, burns)

Weight loss, orthostatic hypotension and tachycardia

Thirst and reduced fluid intake

Poor skin turgor

Cardiac affliction

Dilated neck veins, S3 heart sound, pulmonary rales, peripheral edema

Liver disease

Ascites, caput medusae, spider angiomas

Intrinsic renal

Astute tubular necrosis

History of receiving nephrotoxic medications (including over-the-counter, illicit, and herbal), hypotension, trauma or myalgias suggesting rhabdomyolysis, contempo exposure to radiographic contrast agents

Musculus tenderness, compartment syndrome, assessment of volume status

Glomerular

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

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

Interstitial

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

Fever, drug-related rash

Vascular

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

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

Postrenal

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

Bladder distention, pelvic mass, prostate enlargement

Diagnosis and Handling of Astute Kidney Injury

Figure ane.

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. tertiary ed. Hamilton, Ontario, Canada: BC Decker, Inc.; 2004:61.

Acute interstitial nephritis can be secondary to many conditions, only most cases are related to medication use, making patient history the key to diagnosis. In almost one-third of cases, there is a history of maculopapular erythematous rash, fever, arthralgias, or a combination of these symptoms.13 Eosinophiluria may be institute in patients with acute interstitial nephritis, but information technology is not pathognomonic of this affliction. A kidney biopsy may be needed to distinguish between allergic interstitial nephritis and other renal causes of astute kidney injury. In improver to discontinuing offending agents, steroids may exist beneficial if given early on in the form of disease.xiv

Acute events involving renal arteries or veins can as well lead to intrinsic acute kidney injury. Renal atheroembolic disease is the about common crusade and is suspected with a recent history of arterial catheterization, the presence of a status requiring anticoagulation, or later vascular surgery. Physical exam and history provide of import clues to the diagnosis (Table 39). Vascular causes of acute kidney injury usually crave imaging to confirm the diagnosis.

POSTRENAL CAUSES

Postrenal causes typically result from obstruction of urinary flow, and prostatic hypertrophy is the well-nigh mutual cause of obstruction in older men. Prompt diagnosis followed by early on relief of obstruction is associated with improvement in renal role 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. Most patients with mild to moderate astute 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, airsickness, weight gain, or edema.15 Patients can also 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 astute kidney injury). Other presentations of acute kidney injury may include development of uremic encephalopathy (manifested by a refuse in mental status, asterixis, or other neurologic symptoms), anemia, or haemorrhage caused by uremic platelet dysfunction.

Diagnosis

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

A patient history and physical examination, with an emphasis on assessing the patient'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 direct impair renal role. Physical exam should assess intravascular book status and whatever skin rashes indicative of systemic affliction. The initial laboratory evaluation should include urinalysis, complete blood count, and measurement of serum creatinine level and partial excretion of sodium (Atomic number 26Na). Imaging studies can help dominion out obstruction. Useful tests are summarized in Tabular array iv.16 Figure i 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 consequence When to club Associated diseases/conditions

Elevated antineutrophil cytoplasmic antibody, antiglomerular basement membrane antibody

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 just negative for red blood cells

Recent trauma, musculus 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

Testify 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 acute 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 antibody, double-stranded DNA antibody

Proteinuria, pare rash, arthritis

Autoimmune diseases, systemic lupus erythematosus

Positive blood cultures

Intravenous drug use, recent infection, new cardiac murmur

Endocarditis

Positive HIV test

Risk factors for HIV infection

HIV nephropathy

SERUM CREATININE LEVEL

It is important to compare the patient'south electric current serum creatinine level with previous levels to determine the duration and acuity of the disease. The definition of acute kidney injury indicates that a rising in creatinine has occurred within 48 hours, although in the outpatient setting, it may be hard to ascertain when the ascent 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

Urinalysis is the most important noninvasive examination in the initial workup of acute kidney injury. Findings on urinalysis guide the differential diagnosis and straight farther workup (Effigy one 12).

Complete Blood COUNT

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

URINE ELECTROLYTES

In patients with oliguria, measurement of FeNa is helpful in distinguishing prerenal from intrinsic renal causes of acute kidney injury. FENa is defined by the following formula:

Online calculators are also available. A value less than i percent indicates a prerenal cause of acute kidney injury, whereas a value greater than 2 pct indicates an intrinsic renal cause. In patients on diuretic therapy, however, a FENa higher than i pct may exist 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 exist helpful, with values less than 35 percent indicating a prerenal crusade. FeNa values less than 1 percent are not specific for prerenal causes of astute kidney injury because these values can occur in other conditions, such as contrast nephropathy, rhabdomyolysis, acute glomerulonephritis, and urinary tract obstruction.

IMAGING STUDIES

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

RENAL BIOPSY

Renal biopsy is reserved for patients in whom prerenal and postrenal causes of astute kidney injury take been excluded and the crusade of intrinsic renal injury is unclear. Renal biopsy is particularly of import when clinical assessment and laboratory investigations propose a diagnosis that requires confirmation before disease-specific therapy (e.g., immunosuppressive medications) is instituted. Renal biopsy may need to be performed urgently in patients with oliguria who have apace worsening acute kidney injury, hematuria, and red blood jail 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 nowadays.

Management

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

Optimal management of astute kidney injury requires shut collaboration among primary care physicians, nephrologists, hospitalists, and other subspecialists participating in the care of the patient. Afterward acute kidney injury is established, management is primarily supportive.

Patients with acute kidney injury more often than not should be hospitalized unless the status is mild and conspicuously resulting from an easily reversible crusade. The fundamental to direction is assuring adequate renal perfusion past achieving and maintaining hemodynamic stability and avoiding hypovolemia. In some patients, clinical cess of intravascular volume status and avoidance of volume overload may be difficult, in which case measurement of primal venous pressures in an intensive intendance setting may be helpful.

If fluid resuscitation is required because of intravascular book depletion, isotonic solutions (e.thou., normal saline) are preferred over hyperoncotic solutions (east.g., dextrans, hydroxyethyl starch, albumin).19 A reasonable goal is a hateful arterial pressure greater than 65 mm Hg, which may require the use of vasopressors in patients with persistent hypotension.20 Renal-dose dopamine is associated with poorer outcomes in patients with acute kidney injury; it is no longer recommended.21 Cardiac function tin be optimized as needed with positive inotropes, or afterload and preload reduction.

Attending to electrolyte imbalances (east.g., hyperkalemia, hyperphosphatemia, hypermagnesemia, hyponatremia, hypernatremia, metabolic acidosis) is of import. Astringent hyperkalemia is divers equally potassium levels of vi.5 mEq per L (6.v mmol per 50) or greater, or less than 6.v mEq per L with electrocardiographic changes typical of hyperkalemia (east.thou., alpine, peaked T waves). In severe hyperkalemia, five to 10 units of regular insulin and dextrose 50% given intravenously tin shift potassium out of circulation and into the cells. Calcium gluconate (ten mL of 10% solution infused intravenously over five minutes) is also used to stabilize the membrane and reduce the take a chance of arrhythmias when in that location are electrocardiographic changes showing hyperkalemia. In patients without electrocardiographic prove 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 employ of diuretics is direction of volume overload. Intravenous loop diuretics, as a bolus or continuous infusion, can be helpful for this purpose. Nonetheless, it is important to note that diuretics practice 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.22

All medications that may potentially touch on renal function by direct toxicity or past 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 dissimilarity media and gadolinium is important and, if imaging is needed, noncontrast studies are recommended.

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

Prognosis

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

Patients with acute kidney injury are more likely to develop chronic kidney disease in the future. They are too at higher risk of end-phase renal affliction and premature death.25–27 Patients who take an episode of astute kidney injury should be monitored for the development or worsening of chronic kidney affliction.

Prevention

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

Because of the morbidity and mortality associated with astute kidney injury, it is of import for primary intendance physicians to identify patients who are at loftier chance 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 illness; 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 can be tailored to the clinical circumstances of the private patient (Tabular array five).xix–21,27,29–31

Table 5.

Preventive Strategies for Patients at High Risk of Acute Kidney Injury

Risk factors Preventive strategies

Cancer chemotherapy with risk of tumor lysis syndrome27

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

Exposure to nephrotoxic medications

Avoid nephrotoxic medications if possible

Measure out and follow drug levels if available

Utilise appropriate dosing, intervals, and duration of therapy

Exposure to radiographic contrast agents29

Avoid use of intravenous contrast media when risks outweigh benefits

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

Optimize volume status before administration of dissimilarity media; use of isotonic normal saline or sodium bicarbonate may be considered in high-risk patients who are non at take a chance of volume overload

Apply of N-acetylcysteine may be considered

Hemodynamic instability

Optimal fluid resuscitation; although at that place is no consensus, a hateful arterial force per unit area goal of > 65 mm Hg is widely used; isotonic solutions (e.g., normal saline) are preferred over hyperoncotic solutions (e.one thousand., albumin)19

Vasopressors are recommended for persistent hypotension (mean arterial pressure level < 65 mm Hg) despite fluid resuscitation; pick of vasoactive agent should exist tailored to patients' needs20

Dopamine is non recommended21

Hepatic failure30

Avoid hypotension and gastrointestinal bleeding

Early recognition and treatment of spontaneous bacterial peritonitis; employ albumin, ane.5 g per kg at diagnosis and 1 g per kg at 48 hours

Early on recognition and management of ascites

Albumin infusion during large volume paracentesis

Avoid nephrotoxic medications

Rhabdomyolysis20

Maintain adequate hydration

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

Undergoing surgery

Adequate book 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 key words AKI, acute kidney injury, and acute renal failure. Search engagement: February 2012.

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The Authors

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

FARIHA SHAD, Md, is a nephrologist at Kaiser Permanente in Cleveland. At the time the article was written, Dr. Shad was a fellow at Case Western Reserve Academy School of Medicine.

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

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

Author disclosure: No relevant fiscal affiliations to disclose.

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