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Overview of the management of acute kidney injury (AKI) in adults
AUTHORS: Mark D Okusa, MD, Mitchell H Rosner, MD
SECTION EDITOR: Paul M Palevsky, MD
DEPUTY EDITOR: Eric N Taylor, MD, MSc, FASN
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Feb 2024.
This topic last updated: Nov 07, 2023.
INTRODUCTION
Acute kidney injury (AKI) is an abrupt and usually reversible decline in the glomerular filtration rate (GFR). This results in an elevation of
serum blood urea nitrogen (BUN), creatinine, and other metabolic waste products that are normally excreted by the kidney. In addition, if
urine output is also diminished, fluid retention and volume overload may result.
The initial assessment of patients with AKI and management of the major complications of AKI are discussed here. The incidence, causes,
pathogenesis, diagnosis, and prevention of AKI are presented separately:
● (See
"Etiology and diagnosis of prerenal disease and acute tubular necrosis in acute kidney injury in adults".)
● (See
"Diagnostic approach to adult patients with subacute kidney injury in an outpatient setting".)
● (See
"Evaluation of acute kidney injury among hospitalized adult patients".)
● (See
"Pathogenesis and etiology of ischemic acute tubular necrosis".)
● (See
"Contrast-associated and contrast-induced acute kidney injury: Clinical features, diagnosis, and management".)
● (See
"Definition and staging criteria of acute kidney injury in adults".)
● (See
"Clinical manifestations and diagnosis of urinary tract obstruction (UTO) and hydronephrosis".)
● (See
"Overview of the classification and treatment of rapidly progressive (crescentic) glomerulonephritis".)
● (See
"Clinical manifestations and diagnosis of acute interstitial nephritis".)
● (See
"Possible prevention and therapy of ischemic acute tubular necrosis".)
The diagnostic evaluation to determine the cause of AKI is discussed elsewhere. The use of urinary and serum biomarkers of kidney injury
and their evolving roles are also discussed in these sections:
● (See
"Diagnostic approach to adult patients with subacute kidney injury in an outpatient setting".)
● (See
"Etiology and diagnosis of prerenal disease and acute tubular necrosis in acute kidney injury in adults", section on 'Evaluation
and diagnosis'.)
URGENT EVALUATION AND MANAGEMENT
Patients with AKI need to be systematically evaluated for the immediate threats and complications, have an assessment of AKI severity,
and have the cause identified and treated appropriately. The Kidney Disease: Improving Global Outcomes (KDIGO) stages the severity of
AKI from stage 1 (mild) to stage 3 (severe) (
table 1). (See "Definition and staging criteria of acute kidney injury in adults".)
In general, the complications associated with AKI are more severe and life threatening with higher stages of AKI. However, all patients
with AKI are at risk for complications and for the possibility of milder AKI progressing to more severe AKI. The initial steps of urgent
management depend upon whether the patient is in the hospital or in an outpatient setting.
Triage of outpatients with acute kidney injury — In the outpatient setting, the initial evaluation of the patient with AKI is directed at
triaging the patient to the appropriate setting, such as the emergency department for more severe disease or life-threatening electrolyte
abnormalities. (See 'Identifying patients for emergency department referral' below.)
Identifying patients for emergency department referral — We refer the following patients to the emergency department:
● Patients
with stage 2 or 3 AKI as per the KDIGO criteria. (See "Definition and staging criteria of acute kidney injury in adults".)
● Patients
with stage 1 AKI who have an unclear etiology, patients who have an unknown duration or trajectory of elevated creatinine,
or if there is concern that the condition may not be rapidly reversible with simple interventions (such as volume expansion or
removal of a potential nephrotoxin). In addition, patients with stage 1 AKI should be referred to the emergency department if they
have a concomitant, uncontrolled comorbid condition (eg, acute or chronic exacerbation of heart failure, diabetic ketoacidosis) or if
there is concern for sepsis or multiorgan dysfunction.
● Patients
with AKI of any stage seen in a resource-limited outpatient setting where the initial diagnostic evaluation (eg, kidney
ultrasound to rule out urinary tract obstruction) or interventions (eg, intravenous fluid administration) require an emergency
department referral.
Patients who do not need referral to the emergency department
Initial assessment following diagnosis — The diagnostic approach to outpatients with kidney injury is discussed elsewhere. (See
"Diagnostic approach to adult patients with subacute kidney injury in an outpatient setting".)
Indications for urgent nephrology referral — Patients who do not need an emergency department referral and who are managed
as an outpatient should be referred for outpatient nephrology consultation if:
● Initial
interventions fail to substantially improve the kidney injury.
● Glomerulonephritis
● AKI
(GN) is strongly suspected (such as in a patient with AKI, hematuria, and proteinuria).
occurs as a complication of treatment of an unrelated condition and future treatment depends upon nephrology input (such as
AKI occurring as a complication of chemotherapy).
The time frame of obtaining an outpatient nephrology consult may be variable. A patient suspected of having GN should be seen by a
nephrologist within one to two days. However, if the AKI is thought to be due to other etiologies, an initial evaluation within one week is
reasonable. If expedited nephrology follow-up cannot be obtained, then the patient should be referred to the emergency department.
In addition, patients who have a history of recent admission to the hospital for evaluation and management of AKI should also be seen by
a nephrologist in the outpatient setting for longitudinal follow-up and secondary prevention of AKI. These patients are at risk for recurrent
AKI, which is discussed at length elsewhere. (See "Kidney and patient outcomes after acute kidney injury in adults", section on 'Recurrent
AKI'.)
Evaluate need for urgent kidney replacement therapy — Patients needing management of life-threatening fluid and electrolyte
abnormalities due to AKI should be started on kidney replacement therapy (KRT) immediately. Complications of AKI that might require
emergency KRT include the following:
● Hypervolemia
● Severe
with pulmonary edema
hyperkalemia (ie, serum potassium >6.5 mEq/L), hyperkalemia associated with symptoms or signs (ie, cardiac conduction
abnormalities, muscle weakness), or hyperkalemia >5.5 mEq/L if there is ongoing tissue breakdown (eg, rhabdomyolysis) or ongoing
potassium absorption (eg, significant gastrointestinal bleeding) (
algorithm 1) (see "Treatment and prevention of hyperkalemia in
adults", section on 'Hemodialysis in patients with severe kidney dysfunction')
● Signs
of uremia, such as pericarditis, or an otherwise unexplained decline in mental status
● Severe
metabolic acidosis (pH <7.1) and hypervolemia, unless acidosis can be rapidly resolved by quickly correcting the underlying
etiology (eg, diabetic ketoacidosis)
● Acute
poisoning
Patients with any of these complications despite appropriate medical therapy generally require urgent KRT. However, since KRT often
cannot be immediately provided, such patients usually require medical treatment during the period prior to the initiation of KRT.
Appropriate measures are discussed in sections below or in other topic reviews, to which links are provided.
Hypervolemia with pulmonary edema — Patients who present with AKI and who have severe hypoxia due to pulmonary edema often
need KRT urgently. Some patients may respond quickly to loop diuretics and may therefore avoid the need for KRT. For patients who are
oliguric and hemodynamically stable, we use 80 to 200 mg of intravenous (IV) furosemide or equivalent and monitor for an increase in
urine output (
table 2). We consider a urine output of greater than 200 mL within two hours of the furosemide dose as adequate.
Accurate urine output monitoring is therefore important, and in some patients, bladder catheter placement may be necessary.
If a lower dose (eg, 80 mg) is given and does not induce an adequate response, then a higher dose (eg, 200 mg) should be given without
delay. Hypervolemic patients with pulmonary edema who do not respond adequately to diuretics should be prepared for KRT without
delay.
Dosing strategies for diuretics in the setting of AKI have not been formally developed and therefore require a cautious consideration of
side effects such as ototoxicity. In addition, the purpose of the diuretics in this setting is to relieve hypervolemia. There is no evidence that
use of diuretics reduces the incidence or severity of AKI. In addition, diuretics may help categorize the severity of the kidney injury. In a
study of 326 patients with AKI, the need for diuretics was associated with a higher risk of death or nonrecovery of kidney function (odds
ratio [OR] 1.77, 95% CI 1.14-2.76) [1]. Nonresponsiveness to diuretics was defined as the furosemide dose equivalent of 1 mg per mL of
daily urine output (eg, 200 mL urine output in response to 200 mg of furosemide equates to dose equivalent ratio of 1 mg per mL).
Patients with a ratio of 1 or higher on the day of nephrology consultation had higher odds of death or nonrecovery compared with
nonusers of diuretics (OR 2.94, 95% CI 1.61-5.36). By contrast, patients with a dose equivalent ratio of less than 1 experienced no
significant increase in risk (OR 1.15, 95% CI 0.79-1.68). These data suggest that continued use of loop diuretics is not warranted in patients
with no increase in urine output and that diuretic unresponsiveness may be a marker for increased severity of AKI. Other studies have
reported similar findings [2-5].
Many patients with AKI have hypervolemia that is not severe enough to warrant emergency KRT. Management of hypervolemia in such
patients is discussed below. (See 'Hypervolemic patients' below.)
Severe hyperkalemia — Patients with AKI who have a serum potassium >6.5 mEq/L or those with symptoms or signs of hyperkalemia
(ie, cardiac conduction abnormalities, muscle weakness) should be dialyzed urgently (preferably with hemodialysis), in addition to
receiving rapidly acting therapies (ie, insulin and glucose, intravenous calcium) and gastrointestinal potassium binders (
algorithm 1). In
addition, patients with AKI and hyperkalemia >5.5 mEq/L should be dialyzed urgently if there is ongoing tissue breakdown (eg,
rhabdomyolysis) or ongoing potassium absorption (eg, significant gastrointestinal bleeding). The use of potassium-binding resins to treat
acute hyperkalemia in the setting of AKI to avoid the need for KRT has not been well studied and cannot be recommended. (See
"Treatment and prevention of hyperkalemia in adults", section on 'Treatment approach to hyperkalemic emergencies'.)
Management of less severe hyperkalemia in patients with AKI is presented elsewhere. (See "Treatment and prevention of hyperkalemia in
adults", section on 'Patients without a hyperkalemic emergency'.)
Life-threatening uremic symptoms — Uremic symptoms may occur in patients with AKI. Patients with AKI who have seizures or severe
pericardial effusion that are attributed to uremia should undergo urgent KRT.
Patients who have less severe uremic findings, such as altered mental status, are also frequently treated with KRT unless resolution of AKI
is judged to be imminent. (See 'Assessing for uremia' below.)
Toxin exposure — Dialysis for toxic exposures that may require extracorporeal removal is discussed elsewhere:
● (See
"Methanol and ethylene glycol poisoning: Management", section on 'Extracorporeal removal (hemodialysis)'.)
● (See
"Lithium poisoning", section on 'Candidates for hemodialysis'.)
● (See
"Metformin poisoning", section on 'Extracorporeal removal'.)
SUBSEQUENT MANAGEMENT
Subsequent management of AKI includes:
● Identifying
the etiology of AKI (see "Evaluation of acute kidney injury among hospitalized adult patients" and "Diagnostic approach
to adult patients with subacute kidney injury in an outpatient setting" and "Etiology and diagnosis of prerenal disease and acute
tubular necrosis in acute kidney injury in adults")
● Treating
reversible causes, such as hypotension, volume depletion, or urinary tract obstruction (see 'Elimination and avoidance of
potential insults' below and 'Volume assessment and management' below and "Clinical manifestations and diagnosis of urinary tract
obstruction (UTO) and hydronephrosis")
● Removing
any active insults to minimize new injury (see 'Elimination and avoidance of potential insults' below)
● Identifying
and treating the complications that may eventually require kidney replacement therapy (KRT) at a later period of time (if
AKI does not resolve) (see 'Volume assessment and management' below and 'Managing electrolyte imbalances' below and
'Managing acid-base disturbances' below and 'Assessing for uremia' below)
Elimination and avoidance of potential insults
Medications — In patients with AKI, we stop medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), angiotensinconverting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), and nephrotoxins (eg, aminoglycoside antibiotics, piperacillintazobactam, amphotericin, tenofovir, nephrotoxic chemotherapy), at least in the acute phase of AKI. However, there may be clinical
situations in which medications implicated in causing AKI cannot be discontinued (eg, those that are being used to treat life-threatening
conditions).
Drugs that are renally cleared and that can produce serious adverse effects with accumulation in the setting of AKI should also be
discontinued or undergo dose adjustment, even though they may not directly impact kidney function (eg, metformin, gabapentin,
cefepime, morphine). If available, the patient should be switched to alternative agents that are not renally cleared. Where applicable,
therapeutic drug level monitoring and assistance from a pharmacist in dosing medications should be sought.
Dosing — In patients with AKI, all medications should be carefully reviewed for appropriate dose adjustments, as needed, according
to the presumed glomerular filtration rate (GFR). However, patients with AKI are usually not in steady state and the estimated GFR (eGFR;
calculated from the serum creatinine) should typically not be used to dose medications. Instead, we examine the trend in serum
creatinine over multiple measurements (if available) to judge the degree of decline in GFR. It is important to remember that medication
doses may be changed multiple times during the course of AKI depending on the eGFR:
● If
the serum creatinine is rising briskly (or if only a single initial value is available), then the GFR should be presumed to be 0 mL/min,
and drugs should be dosed accordingly.
● If
the serum creatinine is falling, the eGFR based on the serum creatinine likely underestimates the true GFR. In such cases, the
medications should be dosed according to a GFR greater than the calculated eGFR, with re-evaluation of dosing on a daily basis
depending upon the trajectory of improvement.
● If
the creatinine has reached a plateau and is stable for several days or more, the serum creatinine may be used to estimate GFR
(using an estimating equation).
● For
medications that have a clear physiologic response (eg, vasopressors), the dose should be titrated to the desired clinical
endpoint.
The serum creatinine may not accurately reflect the true GFR in patients who are not in steady state. If the serum creatinine is actively
increasing, the eGFR based upon the serum creatinine will overestimate the true GFR. Conversely, if the serum creatinine is decreasing,
the eGFR will underestimate the true GFR. In order to address this non-steady state phenomenon of serum creatinine, a kinetic GFR
evaluation formula can be utilized [6,7].
Hypotension — Low systolic and/or diastolic blood pressure due to any cause can precipitate or complicate AKI. Rapid identification,
evaluation, and correction of hypotension largely depends upon the cause of hypotension and is critical to ameliorate the extent of kidney
injury. Initial evaluation of a patient with hypotension and its role in kidney injury is discussed elsewhere. (See "Evaluation of and initial
approach to the adult patient with undifferentiated hypotension and shock" and "Etiology and diagnosis of prerenal disease and acute
tubular necrosis in acute kidney injury in adults".)
Iodinated contrast agents — After AKI has already occurred, intravascular iodinated contrast should not be given unless it is required
for an emergency or life-saving procedure, such as for treatment of ST-elevation myocardial infarction (STEMI), or for a critical diagnostic
test, such as identification of aortic dissection. In these cases, the lowest possible dose of contrast agent should be used, and standard
prophylactic measures should be administered. (See "Prevention of contrast-associated acute kidney injury related to angiography",
section on 'Prevention'.)
Dialysis should not be routinely performed to mitigate the risk of further kidney injury (ie, for "contrast removal") following iodinated
contrast-based procedures in the setting of acutely impaired GFR. However, KRT may become necessary if the kidney function worsens
due to concomitant iodinated contrast-induced nephropathy. In that case, indications for KRT are no different than in the patient who did
not receive iodinated contrast.
Patient evaluation for iodinated contrast, clinical features, and prevention of iodinated contrast-induced nephropathy are discussed in
detail elsewhere:
● (See
"Contrast-associated and contrast-induced acute kidney injury: Clinical features, diagnosis, and management".)
● (See
"Prevention of contrast-associated acute kidney injury related to angiography".)
● (See
"Prevention of contrast-induced acute kidney injury associated with computed tomography".)
● (See
"Patient evaluation prior to oral or iodinated intravenous contrast for computed tomography".)
Volume assessment and management — Volume status should be assessed in all patients with AKI by physical examination. In addition,
inferior vena cava ultrasound (if available) may be helpful in the assessment of volume status. Correction of volume depletion or volume
overload (especially when associated with worsening cardiac output) should be a primary aim of therapy. Small degrees of fluid overload
are associated with a higher risk of mortality and other poor outcomes, and, therefore, fluid therapy should be used with careful attention
to net fluid balance and avoiding overload [8]. (See "Cardiorenal syndrome: Definition, prevalence, diagnosis, and pathophysiology" and
"Cardiorenal syndrome: Prognosis and treatment".)
Hypovolemic patients — Intravenous fluid therapy should be administered to patients with a clinical history consistent with fluid loss
(such as vomiting and diarrhea), a physical examination consistent with hypovolemia (hypotension and tachycardia), or oliguria. However,
fluid therapy should be avoided in patients with pulmonary edema or clear evidence of anuria.
● Goals
of resuscitation – The overall goal of fluid therapy is to increase cardiac output and improve tissue oxygenation in patients
who are preload dependent or volume responsive. Administering fluids in patients who are non-volume responsive is detrimental
and should be avoided. Fluids should be targeted to physiologic endpoints such as mean arterial pressure, or among patients in
whom invasive monitoring is utilized, to dynamic changes in cardiac output. (See "Treatment of severe hypovolemia or hypovolemic
shock in adults", section on 'Initial rate of fluid repletion' and "Treatment of severe hypovolemia or hypovolemic shock in adults",
section on 'Monitoring the response'.)
Prompt reversal of volume depletion in patients with a prerenal state may improve kidney perfusion and prevent progression to
acute tubular necrosis (ATN). With certain causes of AKI, maintenance of tubular flow rate and urine output may increase excretion of
nephrotoxins and protect against tubular injury. This is especially true for certain etiologies such as rhabdomyolysis. (See "Crushrelated acute kidney injury" and "Prevention and treatment of heme pigment-induced acute kidney injury (including
rhabdomyolysis)".)
In certain patients, such as those with cirrhosis or the nephrotic syndrome, patients may appear to be volume overloaded but have
low effective circulating volume (due to intravascular volume depletion) and may respond with increased urine output, improved
GFR, and improved hemodynamics after fluid therapy. In unclear cases, central hemodynamic measurements that assess volume
responsiveness may be helpful.
● Choice
and quantity of fluid – Our approach to the choice and quantity of fluid depends upon the presence of other underlying
conditions, the clinical assessment, and the patient's response to initial fluid therapy:
• If hypovolemia is confirmed by clinical assessment, we administer 1 to 3 liters of crystalloid (preferably buffered crystalloid) with
assessment of clinical response. For volume responsive patients with a robust response in urine output and improvement in GFR,
and with persistent evidence of hypovolemia or inability to maintain fluid balance, we continue maintenance isotonic fluids at 75
mL/hour or greater depending upon the ongoing losses. Additional details regarding fluid resuscitation are covered elsewhere.
(See "Maintenance and replacement fluid therapy in adults" and "Treatment of severe hypovolemia or hypovolemic shock in
adults".)
• Among patients with AKI who have a volume status that is difficult to interpret, such as in older adult patients or patients with
reduced effective arterial blood volume, we administer a smaller volume trial (up to 1 liter) of an isotonic fluid. Based upon the
response, a decision regarding continuation of fluid therapy may be made.
• Patients who do not respond to administered volume with an increase in urine output or a decrease in the serum creatinine are
unlikely to have prerenal disease and are more likely to have established ATN or another form of intrinsic AKI such as rapidly
progressive glomerulonephritis (GN) or acute interstitial nephritis. Continued volume expansion in these patients after a fixed
initial trial is discouraged.
• Patients with conditions such as acute pancreatitis, rhabdomyolysis, or tumor lysis syndrome may require more liberal fluid
resuscitation regimens. The management of these disorders is presented separately. (See "Prevention and treatment of heme
pigment-induced acute kidney injury (including rhabdomyolysis)" and "Tumor lysis syndrome: Prevention and treatment", section
on 'Treatment of established tumor lysis syndrome' and "Uric acid kidney diseases", section on 'Prevention and treatment' and
"Management of acute pancreatitis", section on 'Fluid replacement'.)
In all patients, careful and repeated evaluation and monitoring are essential to modify treatment, to maximize benefit, and to minimize
harm while receiving intravenous fluids.
We do not use colloid solutions for treatment of hypovolemia in patients with AKI. A discussion of crystalloid and colloid solutions for this
purpose is presented elsewhere. (See "Treatment of severe hypovolemia or hypovolemic shock in adults", section on 'Normal saline
(crystalloid)'.)
Hypervolemic patients — Hypervolemia may be present upon initial evaluation or occur due to excessive fluid administration in the
setting of impaired ability to excrete sodium and water. This is especially true for patients with sepsis who commonly receive aggressive
intravenous fluid resuscitation. (See "Evaluation and management of suspected sepsis and septic shock in adults", section on 'Intravenous
fluids (first three hours)'.)
Daily fluid balance is commonly positive in critically ill patients with ATN as a result of obligate fluid intake due to the administration of
antibiotics, blood products, other intravenous medications, and nutritional support. This may result in progressive volume expansion and
pulmonary edema, which may be poorly tolerated in patients with acute lung injury and which is associated with poor outcomes [9]. (See
"Acute respiratory distress syndrome: Fluid management, pharmacotherapy, and supportive care in adults", section on 'Conservative fluid
management'.)
Less commonly, volume overload may result from primary left or right ventricular dysfunction and lead to AKI (type 1 cardiorenal
syndrome). The diagnosis and treatment of cardiorenal syndrome are discussed elsewhere. (See "Cardiorenal syndrome: Definition,
prevalence, diagnosis, and pathophysiology" and "Cardiorenal syndrome: Prognosis and treatment".)
Role of diuretics — Diuretics may be used to relieve hypervolemia among patients with AKI who are not anuric. Loop diuretics are
the preferred agents as they provide a greater natriuretic effect than thiazide diuretics. Dosing of loop diuretics varies inversely with GFR.
Hence, high (or maximum) doses of diuretics may be needed for patients with impaired GFR (
table 2). Among hospitalized patients,
diuretics are generally given intravenously rather than orally since the absorption of oral agents is variable in patients with decreased
intestinal perfusion and motility and in those with mucosal edema:
● In
diuretic-naïve patients, we start with 80 mg of intravenous (IV) furosemide, or equivalent, and assess for response. Patients who
were on diuretics prior to the onset of AKI should receive a dose that is at least double their prior (home) dose.
● If
there is no definite augmentation in the urine output within two hours of an IV diuretic dose, then we administer double the initial
dose (maximum of 200 mg in a single dose of IV furosemide or equivalent). Addition of a thiazide diuretic such as chlorothiazide (500
to 1000 mg IV) is sometimes given in conjunction with furosemide to augment urine output. Lack of response to a 200 mg dose of IV
furosemide or equivalent, with or without a thiazide diuretic, may suggest the need for extracorporeal removal of excess volume.
● Among
patients who respond to diuretics, we continue to give repeated doses to avoid hypervolemia if kidney function is improving
or improvement is thought to be imminent. However, even among those patients who respond to diuretics, the urine output may be
too meager to avoid worsening hypervolemia if the obligate intake is high. In such situations, or if improvement is not imminent, we
generally avoid using diuretics to postpone the initiation of KRT, since dialysis and ultrafiltration offer the most efficient method of
volume removal in patients with AKI from any cause.
The optimal diuretic dose and regimen are discussed in greater detail elsewhere. (See "Causes and treatment of refractory edema in
adults".)
Role of kidney replacement therapy — We typically initiate KRT for volume overload in patients who have anuria for more than 24
hours, who fail to respond to diuretics, or whose response to diuretics is insufficient to avoid worsening hypervolemia due to high
obligate intake. In addition to relieving volume overload, KRT may allow clinicians to optimize nutritional support and the use of
intravenous medications without concern for inducing volume overload. However, the benefit of early initiation of KRT for volume
management remains uncertain, despite an association between the severity of volume overload at KRT initiation and mortality [10-12].
(See "Kidney replacement therapy (dialysis) in acute kidney injury in adults: Indications, timing, and dialysis dose".)
Managing electrolyte imbalances
Hyperkalemia — Management of hyperkalemia depends on its severity, etiology of the AKI (readily reversible or likely to be prolonged),
clinical manifestations (cardiac conduction abnormalities), and effect of medical management. All patients with hyperkalemia should be
on a potassium-restricted diet (less than 2 g per day). In addition, all potassium-containing infusions and medications should be avoided
in these patients. Emergency management of severe and symptomatic hyperkalemia is discussed elsewhere. (See 'Severe hyperkalemia'
above.)
Specific treatment of hyperkalemia is directed at antagonizing the membrane effects of potassium, driving extracellular potassium into
the cells, or removing excess potassium from the body. The indications for specific medical therapies are discussed at length elsewhere
(
algorithm 1). (See "Treatment and prevention of hyperkalemia in adults".)
● We
do not dialyze, at least initially, patients with mild hyperkalemia and AKI that is from a known, reversible cause (such as volume
depletion or an ACE inhibitor/ARB). We treat such patients with discontinuation of the ACE inhibitor or ARB, a low-potassium diet,
volume administration with or without diuretics (among euvolemic or hypovolemic patients), or diuretics alone (among
hypervolemia patients). A repeat potassium level should be obtained within 24 to 48 hours depending upon the degree of
hyperkalemia and anticipated response to therapy.
● We
also do not dialyze, at least initially, patients who have AKI from a cause that is not readily reversible, such as ATN, and who have
hyperkalemia that is adequately treated with medical therapy.
However, depending upon other variables (such as the time of day and available medical staff), preparations for KRT, such as
placement of a dialysis catheter, are often initiated for such patients, since hyperkalemia is likely to recur unless kidney function
recovers. This is especially true for patients who are oliguric or anuric, but the approach must be individualized for each patient. In
addition, certain patient populations who have hyperkalemia that is due to continued release of intracellular potassium
(rhabdomyolysis, compartment syndrome, tumor lysis syndrome) should undergo earlier initiation of KRT to gain sustained control
of potassium.
Hyperphosphatemia — We restrict dietary phosphorous to <2 g per day in all patients with AKI, except those with hypophosphatemia.
Although studies are lacking to support our approach, we typically prescribe phosphate binders in patients with AKI who meet the
following requirements:
● Have
● Are
a phosphate concentration >5.5 mg/dL (1.8 mmol/L)
receiving enteral feeding (eating or receiving tube feeds)
● Have
a likely prolonged course of AKI (ie, cause of AKI is not readily reversible)
In addition, other patients who should start phosphate binder therapy include:
● Hyperphosphatemic
patients with AKI who have severe hypocalcemia, even if the phosphate concentration is <6 mg/dL or if KRT
initiation is imminent
● Hyperphosphatemic
patients with continued release of intracellular phosphate such as rhabdomyolysis and tumor lysis syndrome
The selection of phosphate binder depends on the level of serum ionized calcium concentration. If the serum ionized calcium
concentration is low, calcium-containing phosphate binders such as calcium acetate or calcium carbonate may be given to control serum
phosphate levels, providing patients can take oral medications. If the serum ionized calcium concentration is high, non-calcium phosphate
binders, such as lanthanum carbonate, sevelamer, or aluminum hydroxide (Al(OH)3), should be given. Among such patients, non-calcium
binders are preferred in order to prevent increases in the calcium/phosphate product. However, there are no data that have compared
outcomes among patients treated with different agents in the setting of AKI. The use of Al(OH)3 should be limited to several days to
minimize accumulation of aluminum.
Although studies are lacking to support our approach, our goal of phosphate binder therapy is to keep phosphate concentrations in the
normal range, with titration on an individual basis to meet this goal. Further details regarding individual phosphate binders and their
dosing are discussed elsewhere. (See "Management of hyperphosphatemia in adults with chronic kidney disease", section on 'Specific
treatment'.)
There are no published data that have shown that the treatment of acute hyperphosphatemia related to AKI improves outcomes. We do
not treat patients with mild hyperphosphatemia (ie, 4.5 to 5.5 mg/dL) that is due to AKI.
Hypocalcemia — The treatment of hypocalcemia depends on the acuity, severity, and presence of symptoms. The management of
acute, severe, or symptomatic hypocalcemia is presented elsewhere. (See "Treatment of hypocalcemia", section on 'Therapeutic
approach'.)
Hyperphosphatemia should also be corrected in patients with hypocalcemia. The reduction of serum phosphate as a result of treatment
with oral phosphate binders is often sufficient to improve the serum calcium. In the setting of hyperphosphatemia-induced hypocalcemia,
the dose of calcium supplementation should be limited to ameliorate symptoms and not necessarily to target normal serum calcium
levels, which can raise the calcium-phosphate product to levels that can promote precipitation. (See 'Hyperphosphatemia' above.)
For diagnosis of hypocalcemia as well as monitoring, serum ionized calcium should be measured in addition to the total serum calcium if
a laboratory known to reliably measure ionized calcium is available. The total serum calcium concentration does not accurately reflect the
ionized calcium concentration among patients with low or high serum albumin levels, since calcium is bound to albumin. In addition, since
the binding of calcium to albumin is pH dependent, the amount of free calcium may be altered by acid-base disorders or by the rapid
correction of such disorders. (See "Diagnostic approach to hypocalcemia" and "Relation between total and ionized serum calcium
concentrations".)
Hypomagnesemia and hypermagnesemia — Patients with hypomagnesemia and kidney function impairment should be treated
cautiously with small doses and frequent monitoring. Details regarding management of hypomagnesemia in patients with kidney
function impairment are discussed elsewhere. (See "Hypomagnesemia: Evaluation and treatment".)
Hypermagnesemia may be seen in patients with AKI due to the central role played by the kidneys in elimination of magnesium. Severe,
symptomatic hypermagnesemia is rare except in patients treated with high doses of intravenous magnesium, such as women with severe
preeclampsia.
The treatment of hypermagnesemia is presented elsewhere. (See "Hypermagnesemia: Causes, symptoms, and treatment", section on
'Treatment'.)
Hyperuricemia — Patients with tumor lysis syndrome can develop AKI as a result of severe elevations of uric acid and acute urate
nephropathy. The management of such patients is discussed elsewhere. (See "Tumor lysis syndrome: Prevention and treatment" and "Uric
acid kidney diseases", section on 'Acute uric acid nephropathy'.)
Less severe hyperuricemia occurring in patients without tumor lysis is frequently present in patients with AKI due to impaired renal
excretion of uric acid. However, the role of urate-lowering therapy in this scenario is unclear.
Managing acid-base disturbances — Acid-base disturbances are often noted in patients with AKI as a complication of it or as a direct
result of the underlying cause. Metabolic acidosis is far more common, although metabolic alkalosis may also be noted.
Metabolic acidosis — We initiate KRT in patients with oliguric or anuric AKI who are volume overloaded and have severe metabolic
acidosis (a pH <7.1), unless the acidosis can be rapidly resolved by quickly correcting the underlying etiology (eg, diabetic ketoacidosis).
However, among patients with AKI and severe metabolic acidosis who are not volume overloaded and have no other indication for acute
KRT, bicarbonate may be administered instead of KRT; diuretics can be used in nonoliguric patients to prevent hypervolemia and to
enhance excretion of acid. The goal serum bicarbonate level is 20 to 22 mEq/L and the goal pH is >7.2 [13].
Among nondialyzed patients, the total amount of bicarbonate that will be needed can be estimated from the calculated bicarbonate
deficit (see "Approach to the adult with metabolic acidosis", section on 'Dosing of alkali therapy (when given)'). The rate of bicarbonate
administration is dependent upon severity of acidosis and upon the volume status of the patient. A reasonable strategy is to administer 3
ampules (or 150 mEq) of sodium bicarbonate in 1L of 5 percent dextrose at a rate that is determined by the severity of acidosis and the
ability of the patient to tolerate the volume load. Oral sodium bicarbonate tablets or sodium citrate solution can also be used in patients
who are able to tolerate oral administration of medications and who have mild acidosis (bicarbonate >18 mEq/L). We calculate the
bicarbonate deficit as a guide to therapy and aim for 50 percent replacement of the deficit in the first 24 hours.
KRT is preferred to the administration of bicarbonate among hypervolemic patients with reduced urine output because bicarbonate
administration results in a large sodium load that may worsen volume overload. Among patients who are not hypervolemic but who have
oliguria or anuria, bicarbonate therapy may produce volume overload and should therefore be used cautiously.
Among patients with AKI, bicarbonate administration may be associated with serious side effects due to hypocalcemia and hypokalemia.
Bicarbonate administration may cause a decrease in the level of ionized or free calcium because of a pH-dependent increase in the
binding of calcium to albumin. This could cause or worsen the symptoms of hypocalcemia (eg, tetany) since symptoms of hypocalcemia
reflect from the ionized, not total, calcium. (See 'Hypocalcemia' above.)
As in patients without AKI, bicarbonate administration could cause hypernatremia, an increase in the partial pressure of carbon dioxide
(pCO2) among patients with circulatory or ventilatory compromise, and increased intracranial pressure in patients with diabetic
ketoacidosis [14]. (See "Bicarbonate therapy in lactic acidosis".)
Physiologic studies have suggested that, at a pH of <7.1, acidemia may produce hemodynamic instability related to reduced left
ventricular contractility, arrhythmias, arterial vasodilation and venoconstriction, and impaired responsiveness to catecholamine
vasopressors [15-22]. (See "Approach to the adult with metabolic acidosis", section on 'Overview of therapy'.)
A low GFR is the major cause of metabolic acidosis in patients with AKI, although other factors may contribute, including increased
production of organic acid such as in lactic acidosis associated with compromised perfusion. Much of the acid that is normally excreted by
the kidney is the product of daily metabolism. (See "Approach to the adult with metabolic acidosis", section on 'Pathogenesis'.)
Metabolic alkalosis — Metabolic alkalosis with AKI may be seen in a minority of cases such as in patients with milk-alkali syndrome,
severe vomiting, or nasogastric tube suction. Most such patients are hypovolemic and the alkalosis typically responds to IV sodium
chloride infusion. Compensatory metabolic alkalosis without alkalemia may also be seen in patients with underlying lung disease who
develop AKI. Management of metabolic alkalosis is discussed elsewhere. (See "Treatment of metabolic alkalosis".)
Managing nutrition — The goals of nutritional support for critically ill patients with AKI are to provide adequate amounts of energy,
protein, and nutrients [23]. Restrictions on potassium, phosphorous, and sodium intake are applicable to most patients with AKI. Given
the complexities of nutritional support in these patients and the individual needs of a given patient, we obtain a nutrition consult in
hospitalized patients with stage 3 AKI to best tailor therapy. For patients with lesser stages of AKI, the need for consultation should be
based upon an individual needs assessment. In the absence of volume depletion, patients with AKI on KRT or with impending KRT are also
placed on a fluid restriction of 1 to 1.5 L/day.
Nutritional requirements are dependent upon the severity of the underlying disease, preexisting nutritional status, and comorbidities
[23]. (See "Nutrition support in intubated critically ill adult patients: Initial evaluation and prescription", section on 'Calculating calorie and
protein requirements in adequately nourished patients'.)
Although requirements vary based upon the underlying catabolic state, some investigators feel that patients need approximately 25 to 30
kcal/kg per day. Others, however, feel that permissive underfeeding may actually be a preferred approach [24], despite the lack of specific
data on underfeeding in AKI [25]. (See "Nutrition support in intubated critically ill adult patients: Initial evaluation and prescription",
section on 'Calorie prescription'.)
Protein energy wasting is common among critically ill patients with AKI and contributes to mortality [26]. Protein requirement increases
with the severity of the underlying illness and with initiation of KRT. Whereas nondialysis patients with only mild to moderate illness
require only 0.8 to 1.2 g/kg per day, critically ill patients or patients who are on KRT generally require 1.2 to 1.5 g/kg per day or more [27].
(See "Nutrition support in intubated critically ill adult patients: Initial evaluation and prescription", section on 'Protein prescription'.)
Providing adequate nutrition to patients with AKI who require KRT may necessitate parenteral or enteral nutrition. Among critically ill
patients without AKI, most clinicians feel that enteral nutrition should be employed in preference to parenteral nutrition whenever
possible because of its lower cost, less frequent and severe complications, less mucosal permeability, greater wound healing, and lower
rates of infection. (See "Nutrition support in intubated critically ill adult patients: Initial evaluation and prescription".)
Among patients with AKI, there are limited data concerning the efficacy and safety of enteral nutrition. In one study, enteral nutritionrelated outcomes were compared among 247 consecutive patients fed enterally: 114 required dialysis, 68 had AKI but did not require
dialysis, and 65 had normal kidney function [28]. Other than an increased incidence of nasogastric tube obstruction and high gastric
residual volumes among dialyzed patients, there was no difference in gastrointestinal and mechanical complications in the three groups.
The mean amounts of nonprotein calories and protein intake for dialyzed patients were 23.4 kcal/kg and 0.92 g/kg, respectively, with the
amount of delivered protein calories being slightly less than planned. This can be overcome by administering parenteral amino acids
during daily KRT.
There are few good studies that have evaluated the safety and efficacy of parenteral nutrition among patients with AKI. A Cochrane review
was unable to show an overall benefit of parenteral nutrition on survival but was limited by poor quality of available studies [29].
Assessing for uremia — Nonemergency dialysis may also be indicated for patients with prolonged AKI who develop uremic symptoms,
even in the absence of the indications listed above. (See "Kidney replacement therapy (dialysis) in acute kidney injury in adults: Indications,
timing, and dialysis dose".)
Uremic signs and symptoms include anorexia, nausea, vomiting, metallic taste, and altered mental status, among others. Physical
examination findings such as asterixis and pericardial rub, among others, may be noted. Given the nonspecific nature of the uremic
symptoms and signs, elimination of other causes is essential before KRT is initiated, especially in the absence of another indication.
However, a pericardial rub or effusion is a strong indication to start KRT, as noted above. (See 'Life-threatening uremic symptoms' above.)
Daily assessment for uremia is necessary until AKI improves or the patient is on KRT. The decision to start KRT based upon one of these
symptoms is usually difficult. This is especially true for critically ill patients in whom neurologic dysfunction may be attributable to many
causes. Thus, KRT initiation should be approached with a clear goal of monitoring whether or not putative uremic symptoms improve with
therapy. Typically, several dialysis sessions are required to empirically determine if symptoms resolve with KRT.
Prevention and management of uremic bleeding — AKI can cause qualitative platelet dysfunction, which can result in a hemorrhagic
diathesis. The major clinical manifestation of this is cutaneous bleeding, but gastrointestinal bleeding can also occur. The clinical
manifestations, indications for treatment, and modes of therapy are discussed elsewhere. (See "Uremic platelet dysfunction".)
MONITORING AND FOLLOW-UP
Serum creatinine, electrolytes, ionized calcium, total serum calcium, and phosphate should be measured daily in stable patients. The
serum calcium and ionized calcium should be measured more frequently (twice daily) in patients who require calcium or bicarbonate.
Serum potassium should be checked more frequently in patients who have an elevated serum potassium on presentation or who are
oliguric or hemodynamically unstable.
It is important to carefully monitor daily weights, fluid intake, and urine output in order to assess daily fluid balance [30]. In critically ill
patients who are incontinent or otherwise unable to monitor urine output due to compromised mental status, an indwelling catheter may
be necessary to ensure accurate measurement of urine output. The risks of an indwelling catheter primarily include infection and must be
weighed against the potential benefit in each patient. This is discussed elsewhere. (See "Catheter-associated urinary tract infection in
adults".)
Patients with moderate to severe AKI should be closely monitored after discharge from the hospital regardless of the extent of their
recovery, in order to guard against recurrent AKI, development of chronic kidney disease, end-stage kidney disease, and cardiovascular
events [31]. Such patients should also have at least a single nephrology outpatient evaluation, if available, to ensure optimal management
following discharge. If nephrology follow-up is not available, patients should be seen by their primary care clinicians. Simple interventions
at the follow-up appointment include monitoring for kidney recovery, medication adjustments, volume assessment, blood pressure
evaluation, dietary counseling, and patient education. (See "Kidney and patient outcomes after acute kidney injury in adults", section on
'Recurrent AKI'.)
SOCIETY GUIDELINE LINKS
Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately.
(See "Society guideline links: Acute kidney injury in adults".)
SUMMARY AND RECOMMENDATIONS
● Triage
– Among outpatients identified as having AKI, we refer to the emergency department those who have any of the following:
Kidney Disease: Improving Global Outcomes (KDIGO) stage 2 or 3 AKI (
table 1); stage 1 AKI with an unclear etiology, or one that
cannot be rapidly reversed with simple interventions, or in the presence of a concomitant, uncontrolled comorbid condition; or stage
1 AKI if the initial diagnostic evaluation and management cannot be performed in the outpatient setting. (See 'Identifying patients
for emergency department referral' above.)
Those who are managed as an outpatient should be referred for outpatient nephrology consultation if the cause of AKI is not
immediately apparent, if initial interventions fail to improve the kidney injury, if glomerulonephritis (GN) is strongly suspected, or
when AKI occurs as a complication of treatment of an unrelated condition and future treatment depends upon nephrology input.
(See 'Indications for urgent nephrology referral' above.)
● Indications
for emergency kidney replacement therapy (KRT) – Emergency KRT should be performed in patients with AKI who
have one or more of the following (see 'Evaluate need for urgent kidney replacement therapy' above):
• Hypervolemia with pulmonary edema that does not promptly respond to diuretics (see 'Hypervolemia with pulmonary edema'
above)
• Severe hyperkalemia (serum potassium >6.5 mEq/L or those with symptoms or signs of hyperkalemia) (see 'Severe hyperkalemia'
above)
• Life-threatening uremic symptoms, such as seizures or severe pericardial effusion (see 'Life-threatening uremic symptoms' above)
• Exposure to certain toxins (see 'Toxin exposure' above)
● Initial
management
• Eliminate potential insults – Additional management entails elimination of potential insults, including hypotension, iodinated
contrast agents, or medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), angiotensin-converting enzyme (ACE)
inhibitors, angiotensin receptor blockers (ARBs), and nephrotoxins. (See 'Elimination and avoidance of potential insults' above.)
• Treat hypovolemic (if present) – Intravenous fluid therapy with 1 to 3 liters of crystalloid should be administered to patients with a
clinical history consistent with fluid loss (such as vomiting and diarrhea), a physical examination consistent with hypovolemia
(hypotension and tachycardia), or oliguria. However, fluid therapy should be avoided in patients with pulmonary edema or clear
evidence of anuria. Additional fluid management depends upon the clinical condition and response to initial fluid therapy. (See
'Hypovolemic patients' above.)
Among patients with AKI and hypervolemia who are hemodynamically stable and not anuric, we start intravenous (IV) furosemide
at 80 mg up to a single dose of 200 mg, or equivalent, to augment the urine output and relieve symptoms. Additional therapy
depends upon the response to initial therapy. We typically initiate KRT for volume overload in patients who have anuria for more
than 24 hours, who fail to respond to diuretics, or whose response to diuretics is insufficient to avoid worsening hypervolemia
due to high obligate intake. (See 'Hypervolemic patients' above and 'Role of diuretics' above and 'Role of kidney replacement
therapy' above.)
• Treat electrolyte imbalances (if present) – Electrolyte imbalances such as the following can complicate AKI and need specific
management:
-
Hyperkalemia (see 'Hyperkalemia' above)
Hyperphosphatemia (see 'Hyperphosphatemia' above)
Hypocalcemia (see 'Hypocalcemia' above)
Hypomagnesemia and hypermagnesemia (see 'Hypomagnesemia and hypermagnesemia' above)
Hyperuricemia (see 'Hyperuricemia' above)
• Treat metabolic acidosis (if present) – We initiate KRT in patients with oliguric or anuric AKI who are volume overloaded and have
severe metabolic acidosis (a pH <7.1), unless the acidosis can be rapidly resolved by quickly correcting the underlying etiology (eg,
diabetic ketoacidosis). However, in other patients who have no indications for acute KRT, bicarbonate may be administered
instead of KRT to treat acidosis. Diuretics can be used in nonoliguric patients to prevent hypervolemia and to enhance excretion
of acid. The goal serum bicarbonate level is 20 to 22 mEq/L and the goal pH is >7.2. Metabolic alkalosis with AKI is usually seen in
volume depleted patients and responds to IV sodium chloride infusion. (See 'Managing acid-base disturbances' above.)
● Subsequent
management
• Nutrition management – Patients with AKI generally benefit from dietary restrictions on potassium, phosphorous, sodium and
fluid intake (1 to 1.5 L per day, except if volume depleted). Given the complexities of nutritional support in these patients and the
individual needs of a given patient, we obtain a nutrition consult to best tailor therapy in hospitalized patients with severe stage 3
AKI. For patients with lesser stages of AKI, the need for consultation should be based upon an individual needs assessment. (See
'Managing nutrition' above.)
• Assess for uremia – We perform daily assessment of uremic signs and symptoms (such as anorexia, nausea, vomiting, metallic
taste, altered mental status) to determine if KRT may be indicated. KRT initiation in such patients should be approached with a
clear goal of monitoring whether or not putative uremic symptoms improve with therapy. Typically, several KRT sessions are
required to determine if symptoms resolve with KRT. (See 'Assessing for uremia' above.)
• Assess for fluid and electrolyte imbalances – We monitor serum creatinine, electrolytes, albumin, and measures of fluid balance
(weight, fluid intake, and urine output) daily in most patients, although more frequent monitoring may be warranted. (See
'Monitoring and follow-up' above.)
● Follow-up
– We advise that patients hospitalized for moderate to severe AKI have an outpatient nephrology evaluation (or primary
care if nephrology is unavailable) shortly after discharge. (See 'Monitoring and follow-up' above.)
Use of UpToDate is subject to the Terms of Use.
Topic 14035 Version 40.0
GRAPHICS
Criteria for acute kidney injury
RIFLE [1]
AKIN [2]
KDIGO [3]
Increase in serum creatinine of ≥0.3
mg/dL or ≥50% within 48 hours
Increase in serum creatinine of ≥0.3
mg/dL within 48 hours or ≥50%
Diagnostic criteria*
OR
Urine output of <0.5 mL/kg/hour for
>6 hours
within 7 days
OR
Urine output of <0.5 mL/kg/hour for
>6 hours
Staging criteria
Risk (RIFLE) or stage 1
(AKIN/KDIGO)
Injury (RIFLE) or stage 2
(AKIN/KDIGO)
Failure (RIFLE) or stage 3
(AKIN/KDIGO)
Loss (RIFLE)
Increase in serum creatinine to 1.5
times baseline
Increase in serum creatinine of ≥0.3
mg/dL or to 150 to 200% baseline
Increase in serum creatinine of ≥0.3
mg/dL or 1.5 to 1.9 times baseline
OR
OR
OR
Urine output of <0.5 mL/kg/hour for
6 to 12 hours
Urine output of <0.5 mL/kg/hour for
6 to 12 hours
Urine output of <0.5 mL/kg/hour for
6 to 12 hours
Increase in serum creatinine to 2
times baseline
Increase in serum creatinine to 200
to 300% baseline
Increase in serum creatinine to 2 to
2.9 times baseline
OR
OR
OR
Urine output of <0.5 mL/kg/hour for
12 to 24 hours
Urine output of <0.5 mL/kg/hour for
12 to 24 hours
Urine output of <0.5 mL/kg/hour for
12 to 24 hours
Increase in serum creatinine to 3
times baseline
Increase in serum creatinine to
>300% baseline
Increase in serum creatinine to ≥3
times baseline
OR
OR
OR
Increase in serum creatinine by >0.5
mg/dL to >4 mg/dL
Increase in serum creatinine by >0.5
mg/dL to ≥4 mg/dL
Increase in serum creatinine of ≥0.3
mg/dL to ≥4 mg/dL ¶
OR
OR
OR
Urine output of <0.3 mL/kg/hour for
>24 hours or anuria for >12 hours
Urine output of <0.3 mL/kg/hour for
>24 hours or anuria for >12 hours
Urine output of <0.3 mL/kg/hour for
≥24 hours or anuria for ≥12 hours
OR
OR
OR
Initiation of kidney replacement
therapy
Initiation of kidney replacement
therapy
Initiation of kidney replacement
therapy
Need for kidney replacement
therapy for >4 weeks
End stage (RIFLE)
Need for kidney replacement
therapy for >3 months
RIFLE: risk, injury, failure, loss, ESKD; AKIN: Acute Kidney Injury Network; KDIGO: Kidney Disease: Improving Global Outcomes; ESKD: end-stage kidney
disease.
* AKIN and KDIGO provided both diagnostic and staging criteria. RIFLE provided a graded definition of AKI that is implicit in the staging criteria.
¶ In patients <18 years, stage 3 AKI is also defined by KDIGO as a decrease in estimated glomerular filtration rate (eGFR) to <35 mL/min/1.73 m 2 .
References:
1. Bellomo R, Ronco C, Kellum JA, et al. Acute renal failure-definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International
Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Crit Care 2004; 8:B204. Copyright © 2004 BioMed Central Ltd.
2. Mehta RL, Kellum JA, Shah SV, et al. Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury. Crit Care 2007; 11:R31. Copyright © 2007 BioMed
Central Ltd.
3. Kidney Disease: Improving Global Outcomes (KDIGO). Acute Kidney Injury Work Group. KDIGO clinical practice guidelines for acute kidney injury. Kidney Int Suppl 2012; 2:1.
Graphic 83168 Version 14.0
Treatment of hyperkalemia in adults
ESKD: end-stage kidney disease; ACE: angiotensin-converting enzyme; CKD: chronic kidney disease; RAS: renin-angiotensin system; NSAIDs:
nonsteroidal antiinflammatory drugs; IV: intravenous; ECG: electrocardiogram.
* Cardiac manifestations of hyperkalemia are discussed in detail in the topic on clinical manifestations of hyperkalemia.
¶ Some experts given IV calcium only to patients with ECG changes. Details are presented in the topic on treatment of hyperkalemia.
Graphic 109740 Version 3.0
Loop diuretic doses for adult patients with common causes of edema
¶
Starting dose
(oral or intravenous*)
Maximum effective dose
(higher individual doses or more
frequent dosing intervals are
unlikely to produce substantial
additional diuresis) Δ
¶
Maximal recommended daily dose
(greater daily total doses are
associated with a risk for toxicity)
Furosemide
Bumetanide
Torsemide
Furosemide
Bumetanide
Torsemide
Furosemide
Bumetanide
Torsemide
Heart
failure ◊
20 mg once
or twice daily
0.5 mg once
or twice daily
5 mg once
daily
80 mg 3
times daily
3 mg 3 times
daily
50 mg twice
daily
600 mg
10 mg
200 mg
Cirrhotic
40 mg once
1 mg once or
10 mg once
40 mg 3
1 mg 3 times
20 mg twice
160 mg
4 mg
40 mg
ascites §
or twice daily
twice daily
daily
times daily
daily
daily
Nephrotic
40 mg once
1 mg once or
10 mg once
120 mg 3
3 mg 3 times
50 mg twice
600 mg
10 mg
200 mg
syndrome
or twice daily
twice daily
daily
times daily
daily
daily
Chronic
kidney
‡
‡
‡
200 mg 3
times daily
10 mg 3 times
daily
100 mg
twice daily
600 mg
10 mg
200 mg
80 mg once
or twice daily
2 mg once or
twice daily
20 mg once
daily
500 † mg
once
Not reported
Not
reported
600 mg
Not reported
Not
reported
disease ¥
Acute
kidney
injury
* Refer to UpToDate topics on the maximum effective dose and major side effects of loop diuretics for details.
¶ Dose is delivered intravenously.
Δ More aggressive regimens have been shown to be safe and effective for acute decompensated heart failure. Refer to UpToDate topics on the use of
diuretics in patients with heart failure for details.
◊ Guidelines from American College of Cardiology/American Heart Association [1] recommend furosemide and bumetanide starting daily or twice daily
and torsemide starting daily. Similar guidelines are available from the European Society of Cardiology [2] . Note that higher doses may be useful in acute
decompensated heart failure.
§ In most patients with cirrhosis, furosemide (or equivalent) should be combined with spironolactone at a ratio of 40 mg furosemide to 100 mg of
spironolactone; the dosing ratio should be adjusted based upon the plasma potassium concentration. Refer to UpToDate topics on initial therapy of
ascites for details.
¥ Chronic kidney disease alone typically does not cause edema but complicates the treatment of other edematous syndromes. In this situation, the
presence of chronic kidney disease should guide dosing. Refer to UpToDate topics on the maximum effective dose and major side effects of loop
diuretics for details.
‡ Initial diuretic doses for patients with chronic kidney disease depend on its stage but are generally higher than those given for patients with heart
failure or cirrhosis.
† High doses of furosemide (500 mg) may be effective, but most authorities now avoid such high doses and, instead, recommend a single trial with a
lower starting dose.
References:
1. Writing Committee Members, Yancy CW, Jessup M, et al. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology
Foundation/American Heart Association Task Force on practice guidelines. Circulation 2013; 128:e240.
2. Mullens W, Damman K, Harjola VP, et al. The use of diuretics in heart failure with congestion - a position statement from the Heart Failure Association of the European Society of
Cardiology. Eur J Heart Fail 2019; 21:137.
Courtesy of David H Ellison, MD, FASN, FAHA.
Graphic 120718 Version 2.0
Contributor Disclosures
Mark D Okusa, MD Grant/Research/Clinical Trial Support: NIH [Acute kidney injury]. Consultant/Advisory Boards: GentiBio [Regulatory T cells in acute
kidney injury]. All of the relevant financial relationships listed have been mitigated. Mitchell H Rosner, MD No relevant financial relationship(s) with
ineligible companies to disclose. Paul M Palevsky, MD Consultant/Advisory Boards: Chiesi [AKI, Kidney Function Assessment]; Janssen Research &
Development [AKI trial design]. All of the relevant financial relationships listed have been mitigated. Eric N Taylor, MD, MSc, FASN No relevant financial
relationship(s) with ineligible companies to disclose.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multi-level
review process, and through requirements for references to be provided to support the content. Appropriately referenced content is required of all
authors and must conform to UpToDate standards of evidence.
Conflict of interest policy
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