Evaluation of acute kidney injury among hospitalized adult patients

Official reprint from UpToDate® www.uptodate.com

©2024 UpToDate®

Evaluation of acute kidney injury among hospitalized

adult patients
Authors: Pedram Fatehi, MD, MPH, Chi-yuan Hsu, MD, MSc
Section Editor: Paul M Palevsky, MD
Deputy Editor: John P Forman, MD, MSc

Contributor Disclosures

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: Mar 25, 2022.

INTRODUCTION

Patients with kidney disease have a variety of different clinical presentations. Some have
symptoms or signs that are directly related to the kidney (such as gross hematuria) or to
reduced renal function (edema, hypertension, signs of uremia). Many patients are
asymptomatic and are incidentally found to have an elevated serum creatinine
concentration, abnormal urine studies (such as proteinuria or microscopic hematuria), or
abnormal radiologic imaging of the kidneys.

Specific disorders generally cause acute, subacute, or chronic kidney injury. Acute kidney
injury (AKI) develops over hours to days and is usually diagnosed in the emergency
department, in hospitalized patients, or following a procedure. Occasionally, AKI is
incidentally noted on outpatient laboratory evaluation as an abrupt rise in serum
creatinine.

This topic reviews the evaluation of hospitalized patients who present with AKI. Patients
who present to the emergency department with a creatinine above the recent baseline
value may be acute or subacute. If recent baseline is not known, the kidney disease may be
chronic in nature. (Related Pathway(s): Acute kidney injury (hospital acquired): Initial
diagnostic approach in adults and Acute kidney injury (hospital acquired): Subsequent
diagnostic approach in adults.)

The evaluation of patients who present with subacute kidney injury is discussed elsewhere.

- Page 1 of 16 -
Evaluation of acute kidney injury among hospitalized adult patients

(See "Diagnostic approach to adult patients with subacute kidney injury in an outpatient
setting".)

The evaluation of patients with newly identified chronic kidney disease (CKD) is discussed
elsewhere. (See "Chronic kidney disease (newly identified): Clinical presentation and
diagnostic approach in adults".)

DEFINITION

AKI is defined by a rise in the serum creatinine concentration or a decline in urine output
that has developed within hours to days. The proposed criteria for AKI include an increase
in serum creatinine by ≥0.3 mg/dL (27 micromol/L) within 48 hours or an increase to ≥1.5
times the presumed baseline value that is known or presumed to have occurred within the
prior seven days, or a decrease in urine volume to <0.5 mL/kg/hour over six hours (Kidney
Disease: Improving Global Outcomes [KDIGO]-AKI) ( table 1) [1]. (See "Definition and
staging criteria of acute kidney injury in adults".)

CLINICAL MANIFESTATIONS

Patients with AKI may present with symptoms and signs resulting directly from diminished
kidney function. These typically include edema, hypertension, and/or decreased urine
output or, in severe AKI, anuria. However, many patients have no clinical symptoms, and an
increase in creatinine is detected by laboratory tests that are routinely obtained among
hospitalized patients.

Laboratory tests may also reveal increased urea (blood urea nitrogen [BUN]) and
hyperkalemia. Some patients, particularly those who are fluid overloaded, are
hyponatremic.

A urinalysis may show albuminuria and/or an abnormal urine sediment. (See "Diagnostic
approach to adult patients with subacute kidney injury in an outpatient setting", section on
'Urinalysis'.)

DIAGNOSIS

As noted above, AKI is occasionally accompanied by the onset of symptoms or signs

- Page 2 of 16 -
Evaluation of acute kidney injury among hospitalized adult patients

related to reduced kidney function, all which suggest the diagnosis. (See 'Clinical
manifestations' above.)

Among hospitalized patients who generally have frequent monitoring of the serum
creatinine, the diagnosis of AKI is easily established by demonstrating an increase in the
serum creatinine and/or decrease in urine output. A number of other biomarkers for
changes in kidney function are being investigated, but serum creatinine currently remains
the only lab value used in formal definitions AKI and the biomarker most commonly used
in clinical practice (see 'Estimation of glomerular filtration rate' below). All subsequent
evaluation is directed at determining the underlying cause of AKI in order to allow for
prompt management. (See 'Evaluation' below.)

Early diagnosis of AKI may allow for intervention to improve outcomes, and some studies
have suggested that early nephrologist involvement in hospital-acquired AKI confers
benefits [2]. However, a randomized, controlled trial of an electronic alert system to
promote early recognition of AKI resulted in neither reduced severity of injury nor
improved clinical outcomes [3].

EVALUATION

It is important to quickly establish the cause of AKI. In many cases, AKI is reversible if the
underlying cause is quickly identified and addressed. Our approach to evaluation of AKI is
based on our understanding of the major causes.

Major causes and classification of AKI — The causes of AKI are traditionally classified by
the portion of the renal anatomy that is most affected [4]. The traditional approach to AKI
has thus been to categorize the clinical etiology as prerenal (decreased renal perfusion
pressure), intrinsic renal (pathology of the vessels, glomeruli, or tubules-interstitium), or
postrenal (obstruction of urinary flow). However, diseases often cross these nosological
boundaries. As examples, prolonged prerenal azotemia can lead to intrinsic acute tubular
necrosis (ATN), and untreated urinary tract obstruction eventually causes fibrosis and
atrophy of the obstructed kidney(s).
● Prerenal disease - Acute prerenal injury occurs with ineffective perfusion commonly
seen in hypovolemic states, such as in acute hemorrhage, diarrhea, or unreplenished
insensible losses. Renal perfusion pressure may also be low in hypervolemic states
with low effective circulating (arterial) volume, such as severe systolic heart failure
- Page 3 of 16 -
Evaluation of acute kidney injury among hospitalized adult patients

with reduced ejection fraction (see "Cardiorenal syndrome: Definition, prevalence,

diagnosis, and pathophysiology", section on 'Pathophysiology') or acutely
decompensated liver disease with portal hypertension (see "Hepatorenal syndrome").
Alterations in renal vascular autoregulation, such as afferent arteriole
vasoconstriction caused by nonsteroidal antiinflammatory drugs (NSAIDs) or
iodinated radiocontrast media, may cause acute prerenal kidney injury (see "NSAIDs:
Acute kidney injury" and "Contrast-associated and contrast-induced acute kidney
injury: Clinical features, diagnosis, and management"). Angiotensin blockade
(angiotensin-converting enzyme inhibitor [ACEi] or angiotensin receptor blocker
[ARB] medications) also alter the kidney's ability to autoregulate blood flow during
states of decreased renal blood flow; these medications thus commonly exacerbate
prerenal AKI. (See "Major side effects of angiotensin-converting enzyme inhibitors
and angiotensin II receptor blockers".)

Low perfusion pressure to the renal parenchyma may result from low arterial
pressure, as in the etiologies mentioned above, but, since perfusion pressure to any
capillary bed is the difference between arterial and venous pressures, markedly
elevated renal venous pressures, as seen in severe heart failure with preserved
ejection fraction or in abdominal compartment syndrome, may also cause low
perfusion pressure and AKI. (See "Cardiorenal syndrome: Definition, prevalence,
diagnosis, and pathophysiology", section on 'Increased renal venous pressure' and
"Abdominal compartment syndrome in adults".)
● Intrinsic renal vascular disease - Intrinsic renal vascular diseases directly affect
both small-and large-sized blood vessels within the kidneys. Acute intrinsic diseases
that primarily involve small blood vessels include small vessel vasculitides and
diseases that cause microangiopathy and hemolytic anemia (MAHA), including
thrombotic thrombocytopenic purpura-hemolytic uremic syndrome (TTP/HUS),
scleroderma, atheroembolic disease, and malignant hypertension. (See "Clinical
presentation, evaluation, and treatment of renal atheroemboli" and "Moderate to
severe hypertensive retinopathy and hypertensive encephalopathy in adults", section
on 'Clinical manifestations and diagnosis' and "Kidney disease in systemic sclerosis
(scleroderma), including scleroderma renal crisis" and "Glomerular disease:
Evaluation and differential diagnosis in adults".)

Diseases that affect larger vessels and cause AKI include renal infarction from aortic
dissection, systemic thromboembolism, or renal artery abnormality (such as
- Page 4 of 16 -
Evaluation of acute kidney injury among hospitalized adult patients

aneurysm) and acute renal vein thrombosis (see "Renal infarction" and "Renal vein
thrombosis in adults"). Severe AKI from renal vascular catastrophe suggests bilateral
involvement or involvement of a solitary functioning kidney.
● Intrinsic glomerular disease - Disorders that produce glomerular disease can be
classified as being primary (idiopathic, not associated with systemic disease) or
secondary (such as paraneoplastic, drug induced, or part of a systemic rheumatologic
disease). Two general patterns are observed (with considerable overlap in some
diseases):

• A nephritic pattern (proliferative glomerulonephritis) produces an active urine

sediment with dysmorphic red cells and white cells; granular, red cell, and other
cellular casts; and a variable degree of proteinuria [5,6]. Rapidly progressive
glomerulonephritis (RPGN), which causes AKI or subacute kidney injury, always
presents with a nephritic pattern. (See "Glomerular disease: Evaluation and
differential diagnosis in adults".)

• A nephrotic pattern (nonproliferative glomerulopathy) is a rare cause of AKI in the

hospitalized patient but may occur in patients with very large amounts of
proteinuria. (See "Acute kidney injury (AKI) in minimal change disease and other
primary forms of nephrotic syndrome" and "Glomerular disease: Evaluation and
differential diagnosis in adults".)

The quantification of protein excretion is discussed elsewhere. (See "Assessment

of urinary protein excretion and evaluation of isolated non-nephrotic proteinuria
in adults".)
● Intrinsic tubular and interstitial disease - Tubular and interstitial (tubulointerstitial)
diseases commonly cause AKI. The most common acute tubulointerstitial disease is
ATN from ischemia or a nephrotoxic exposure. ATN may occur following concurrent
use of ACEi/ARB medications with NSAIDs or radiocontrast media; occur following
nephrotoxin administration; be seen in the settings of cardiac or other major surgery,
sepsis, or shock (profound prerenal state); or be seen in a combination of these
etiologies. (See "Etiology and diagnosis of prerenal disease and acute tubular
necrosis in acute kidney injury in adults".)

Tubular injury in the setting of COVID-19 is discussed elsewhere. (See "COVID-19:

Issues related to acute kidney injury, glomerular disease, and hypertension", section
on 'Acute kidney injury'.)
- Page 5 of 16 -
Evaluation of acute kidney injury among hospitalized adult patients

Other tubulointerstitial diseases that cause AKI include acute interstitial nephritis
(AIN) that is often drug-induced. A large variety of drugs can produce AIN, including
checkpoint inhibitors for cancer immunotherapy, which are increasingly used. (See
"Clinical manifestations and diagnosis of acute interstitial nephritis" and "Toxicities
associated with immune checkpoint inhibitors", section on 'Kidney'.)

Less common causes of tubulointerstitial AKI that should be considered in the

appropriate setting include tumor lysis syndrome (acute urate nephropathy), which
occurs among patients with lymphomas and other cancers with high tumor burdens,
often following chemotherapy; cast nephropathy in multiple myeloma or other
monoclonal gammopathies; crystalline nephropathy associated with intravenous
acyclovir or other medications; and acute phosphate nephropathy following a
phosphate-containing bowel preparation [7]. (See "Kidney disease in multiple
myeloma and other monoclonal gammopathies: Etiology and evaluation" and
"Clinical manifestations of hypercalcemia", section on 'Kidney insufficiency' and
"Tumor lysis syndrome: Pathogenesis, clinical manifestations, definition, etiology and
risk factors" and "Acute phosphate nephropathy".)
● Postrenal disease (obstructive nephropathy) - Obstruction may occur anywhere in
the urinary tract. Among patients who do not have underlying chronic kidney disease
(CKD), a substantial reduction in the glomerular filtration rate (GFR) suggests bilateral
obstruction (or unilateral obstruction of a single functioning kidney). This is most
commonly due to prostatic disease (hyperplasia or cancer) or metastatic cancer.
Retroperitoneal fibrosis is a rare cause of progressive ureteral obstruction (see
"Clinical manifestations and diagnosis of retroperitoneal fibrosis"). If untreated,
obstructive nephropathy leads to irreversible tubulointerstitial fibrosis (ie, intrinsic
disease).

Relative frequency of AKI etiologies — The most detailed epidemiologic data on AKI are
in hospitalized patients in developed countries. Most of the relevant studies were
published prior to the relatively recently proposed definitions of AKI (see "Definition and
staging criteria of acute kidney injury in adults"). Nonetheless, those studies provide
important information about the causes of AKI. Among hospitalized patients, ATN and
prerenal disease are the most common causes. A report from Madrid evaluated all 748
cases of AKI at 13 tertiary hospital centers [8] and suggests the common etiologies
involved. The most frequent causes were:

- Page 6 of 16 -
Evaluation of acute kidney injury among hospitalized adult patients
● ATN – 45 percent
● Prerenal disease – 21 percent
● Acute superimposed on CKD – 13 percent (mostly due to ATN and prerenal disease)
● Urinary tract obstruction – 10 percent (most often older men with prostatic disease)
● Glomerulonephritis or vasculitis – 4 percent
● AIN – 2 percent
● Atheroemboli – 1 percent

A study from the Program to Improve Care in Acute Renal Disease (PICARD) examined the
etiology of AKI in a more acutely ill population of 618 patients in five intensive care units
(ICUs) in the United States [9]. Many patients had more than one possible cause. Over 70
percent of cases were thought to be due to ATN related to sepsis and hypotension. Other
causes included prerenal disease (eg, hypovolemia, heart failure, and hepatorenal
syndrome), contrast-induced nephropathy, and rhabdomyolysis. Some patients had two or
more causes of AKI.

Common causes of AKI differ somewhat in low- or middle-income countries compared with
high-income countries. AKI in low-income countries often occurs in younger patients with a
single disease process such as a diarrheal illness or malarial infection, among others; in
high-income countries, AKI is more frequently associated with complex surgery, sepsis,
and multi-organ diseases [10,11].

Our approach to evaluation

Overview — For all patients, we carefully review the history and particularly the timing of
onset of AKI. The timing of onset often suggests the underlying etiology. The date of onset
can very often be precisely timed if the serum creatinine concentration has been measured
frequently as part of routine blood testing or if there is accurate documentation of urine
output. As an example, suppose that a patient has had a stable serum creatinine
concentration, which then begins to rise progressively on hospital day 5. Careful study of
the patient's chart may identify the precipitating event on day 3 or 4 (eg, hypotension or
radiocontrast exposure) or identify cumulative insults prior to the increase in creatinine. An
important caveat here is that patients who receive aggressive volume resuscitation may
have the increase in serum creatinine blunted due to dilution in a larger volume of
distribution [12]. (See "Contrast-associated and contrast-induced acute kidney injury:
Clinical features, diagnosis, and management" and "Crystal-induced acute kidney injury",
section on 'Acyclovir'.)

- Page 7 of 16 -
Evaluation of acute kidney injury among hospitalized adult patients

A careful review of medications is imperative. Often, nephrotoxic medications have been

started prior to the onset of AKI, which suggests an etiology. In addition, even
longstanding medications (particularly ACEi or ARBs) render patients vulnerable to AKI
from prerenal factors or ATN.

Patients with certain underlying diseases, such as a malignancy, are often prone to specific
causes of kidney injury, and their evaluation may be tailored accordingly. (See "Overview of
kidney disease in patients with cancer".)

A physical examination may reveal the etiology. Common examples include:

● Signs of volume contraction suggest a prerenal etiology of AKI. (See "Etiology and
diagnosis of prerenal disease and acute tubular necrosis in acute kidney injury in
adults", section on 'History and physical examination'.)
● A typical "drug rash" suggests AIN. (See "Clinical manifestations and diagnosis of
acute interstitial nephritis", section on 'Clinical manifestations'.)
● Blue toes suggest cholesterol emboli. (See "Clinical presentation, evaluation, and
treatment of renal atheroemboli", section on 'History and physical examination'.)
● Significant volume overload and signs of heart failure suggest cardiorenal syndrome.
(See "Cardiorenal syndrome: Definition, prevalence, diagnosis, and
pathophysiology".)
● Ascites and jaundice suggest liver disease with portal hypertension and hepatorenal
syndrome. (See "Hepatorenal syndrome".)

Initial testing should include reagent strip urinalysis (dipstick) with automated urine
microscopy and the quantification of urine protein or albumin (by random or "spot"
protein-to-creatinine ratio or albumin-to-creatinine ratio) (see "Assessment of urinary
protein excretion and evaluation of isolated non-nephrotic proteinuria in adults"). Manual
urine microscopy for the assessment of urine sediment is best performed by an
experienced operator ( algorithm 1).

Among patients who are considered at higher risk for multiple myeloma based on key
clinical features, we obtain a serum protein electrophoresis (SPEP), urine protein
electrophoresis (UPEP) with immunofixation, and a serum light chain assay at the time of
the initial evaluation. Patients who are considered at higher risk for myeloma include all
patients who are >40 years of age who have no other obvious cause for increased
creatinine, such as NSAID use, contrast exposure, or sepsis. Other features, such as
- Page 8 of 16 -
Evaluation of acute kidney injury among hospitalized adult patients

hypercalcemia, unexplained anemia, and increased globulin gap (the difference between
total protein and albumin in the serum), may increase suspicion of monoclonal
gammopathy. Another important clue to the presence of abnormal immunoglobulins in
kidney disease is a discrepancy between undetectable urinary protein by dipstick reagent
and concurrently high random urine protein-to-creatinine ratio. (See "Kidney disease in
multiple myeloma and other monoclonal gammopathies: Etiology and evaluation", section
on 'Patients with acute or subacute kidney injury'.)

Patients who have hematuria without recent urinary tract instrumentation and/or an
abnormally increased albumin-to-creatinine ratio should be evaluated for glomerular
disease or vasculitis. (See "Glomerular disease: Evaluation and differential diagnosis in
adults".)

Patients who have sterile pyuria should be evaluated for interstitial nephritis. (See "Clinical
manifestations and diagnosis of acute interstitial nephritis".)

Radiographic imaging is generally performed in patients with AKI when the underlying
cause is not immediately apparent. The major reason for performing imaging is to assess
for urinary tract obstruction.

Patients who have an obvious cause of AKI do not require imaging, at least initially. As an
example, we do not initially perform imaging when the history and physical examination
reveal an obvious cause of ATN (such septic shock) and/or urine microscopy is consistent
with ATN. Some clinicians will perform an ultrasound if renal function does not improve
after a few days, but the diagnostic yield is low.

The most commonly used radiographic technique in patients with AKI is renal ultrasound.
Ultrasound is safe, easy to perform, and sensitive for obstruction. Helical computed
tomography (CT) scan without contrast is generally preferred among patients with possible
urolithiasis. Such patients usually, though not always, present with flank pain and
hematuria. (See "Radiologic assessment of kidney disease" and "Kidney stones in adults:
Diagnosis and acute management of suspected nephrolithiasis", section on 'Diagnostic
imaging'.)

Magnetic resonance imaging (MRI) with gadolinium should be avoided, if possible, among
patients with AKI. Among patients with AKI or advanced CKD with estimated glomerular
filtration rate (eGFR) <30 mL/min, the administration of gadolinium (particularly older and
unstable group I gadolinium agents) has been associated with the potentially severe
syndrome of nephrogenic systemic fibrosis (NSF). (See "Nephrogenic systemic
- Page 9 of 16 -
Evaluation of acute kidney injury among hospitalized adult patients

fibrosis/nephrogenic fibrosing dermopathy in advanced kidney disease".)

Bladder outlet obstruction can be assessed by measuring post-void bladder volume by

ultrasound or by placement of a bladder catheter, which may, in some situations, be both
diagnostic and therapeutic. (See "Clinical manifestations and diagnosis of urinary tract
obstruction (UTO) and hydronephrosis".)

The results of the urinalysis and ultrasound generally direct the remainder of the
diagnostic evaluation. Patients who have newly developed hydronephrosis or hydroureter
usually require prompt intervention to relieve or bypass the obstruction and further
urologic investigation to determine the cause. (See "Clinical manifestations and diagnosis
of urinary tract obstruction (UTO) and hydronephrosis".)

For patients who have normal renal imaging, minimal proteinuria, benign urine sediment
on urinalysis/microscopy (no red cells or cellular casts), and no clear explanation for AKI,
further evaluation is determined by the severity of disease and rate of further decline.
● If the creatinine is markedly elevated or if an initially mild increase in the creatinine
worsens over the course of days, then a kidney biopsy should be performed. A biopsy
usually provides a more definitive tissue diagnosis and may allow a therapeutic
intervention to prevent end-stage kidney disease (ESKD).

In some cases, even without kidney biopsy, the etiology of kidney disease can be
ascertained with reasonable certainty with tissue diagnosis from other sites. As an
example, a bone marrow biopsy among patients with multiple myeloma or a fat pad
biopsy among patients with amyloidosis may avert the need for a kidney biopsy. The
indications for renal biopsy are discussed in more detail elsewhere. (See "The kidney
biopsy".)
● Among patients who have signs and symptoms of rapidly progressive or unexplained
systemic disease, a renal biopsy is warranted, even if the eGFR remains stable after
initial increase.
● Among patients who have a mild decrease in eGFR (eg, down to 45 to 60 mL/min/1.73
m2) that subsequently remains stable, we often just follow the serum creatinine. If
the creatinine remains stable, we generally continue to follow creatinine, urine
studies (urinalysis/microscopic studies, urine protein/creatinine), and blood pressure
until a clear temporal pattern is established.

Estimation of glomerular filtration rate — The most common methods utilized to

- Page 10 of 16 -
Evaluation of acute kidney injury among hospitalized adult patients

estimate the GFR in adults are the serum creatinine concentration, the creatinine
clearance, and equations based upon the serum creatinine concentration, age, and sex.
(See "Assessment of kidney function".)

The equations that use serum creatinine concentration to estimate GFR were derived in
nonhospitalized patients with stable kidney function [13]. Although more complex
formulas have been proposed to estimate GFR from the change in creatinine values
among patients with AKI [14,15], any equation that uses creatinine may lead to errors
among patients who are not in steady state. As an example, early in the course of AKI, the
serum creatinine could be low because there has not yet been adequate time for it to
accumulate; in such cases, equations that use creatinine will overestimate kidney function.
The serum creatinine may also be falsely low immediately after cardiopulmonary bypass
surgery due to the administration of large volumes of intravenous fluid during surgery,
which expands the extracellular fluid volume and the volume of distribution for creatinine.

Urinalysis — The urinalysis involves both use of a urine dipstick and microscopic
examination of the urine sediment. The dipstick can test for protein (albumin), pH, glucose,
hemoglobin (or myoglobin), leukocyte esterase (reflecting pyuria), and specific gravity.
Microscopic examination of the urine sediment by an experienced operator is an important
component of the diagnostic evaluation since characteristic findings strongly suggest
certain diagnoses ( table 2). (See "Urinalysis in the diagnosis of kidney disease", section
on 'Urine dipstick analysis'.)

Urine sodium excretion — The urine sodium may be measured with calculation of
fractional urine excretion (FENa) in patients with AKI. In an oliguric patient whose effective
circulating volume is difficult to assess, the FENa may help to distinguish prerenal AKI from
ATN. However, there are many instances where the FENa is not helpful, and we believe that
the evaluation of AKI is better guided by history, physical, and other lab findings. The
fractional excretion of urea may also provide information in some patients. (See "Fractional
excretion of sodium, urea, and other molecules in acute kidney injury" and "Etiology and
diagnosis of prerenal disease and acute tubular necrosis in acute kidney injury in adults",
section on 'Fractional excretion of sodium and urine sodium concentration'.)

Urine volume — Trending and comparing volume of fluid going in and coming out of a
patient (including urine output) are helpful physiologic parameters in patients with AKI.

Oliguria (typically defined as <0.3 mL/kg per hour or <500 mL/day of urine output) may or
may not occur in AKI with rising creatinine. Normal urine output can be maintained even
- Page 11 of 16 -
Evaluation of acute kidney injury among hospitalized adult patients

with an abnormally low GFR in patients with nonoliguric ATN. The prognosis of nonoliguric
AKI is generally better than oliguric or anuric disease [16-19].

Anuria (<50 mL/day) reflects severe AKI, which will likely require dialytic therapy unless
there is prompt recovery. Anuria generally occurs as a result of severe prolonged shock,
bilateral urinary tract obstruction, pregnancy-related cortical necrosis, or bilateral renal
artery obstruction.

Although the administration of diuretics in AKI has not been shown to improve renal
function or creatinine trajectory, the increase of urine output (ie, the conversion of anuric
or oliguric AKI to nonoliguric AKI) spontaneously or with the use of diuretics often reflects
renal recovery or less severe injury [20]. Furthermore, increasing urine output will mitigate
the risk of volume overload and pulmonary edema, thus potentially allowing the patient to
be managed without dialysis. (See "Residual kidney function in kidney failure" and
"Nonoliguric versus oliguric acute kidney injury".)

Abrupt decline in urine volume may suggest new obstruction (such as an obstructed
bladder catheter) or another new, superimposed cause of AKI.

Serologic testing and role of renal biopsy — Depending on the history, physical,
radiographic, and urine findings, particularly those that suggest nephritic glomerular
disease, serologic testing is ordered to further characterize the etiology of kidney disease.
(See "Glomerular disease: Evaluation and differential diagnosis in adults".)

A native (nontransplanted) kidney biopsy is most commonly obtained when noninvasive

evaluation has been unable to establish the correct diagnosis [21,22].

Biopsy may be deferred if other findings and serologic testing strongly support diagnostic
and therapeutic decision making or if the risk of biopsy outweighs the expected benefit.
Issues related to renal biopsy, including indications, when biopsy may not be necessary,
prebiopsy evaluation, technique, and complications, are discussed separately. (See "The
kidney biopsy".)

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".)

- Page 12 of 16 -
Evaluation of acute kidney injury among hospitalized adult patients

INFORMATION FOR PATIENTS

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the
Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th
grade reading level, and they answer the four or five key questions a patient might have
about a given condition. These articles are best for patients who want a general overview
and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces
are longer, more sophisticated, and more detailed. These articles are written at the 10th to
12th grade reading level and are best for patients who want in-depth information and are
comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to
print or e-mail these topics to your patients. (You can also locate patient education articles
on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
● Basics topics (see "Patient education: Chronic kidney disease (The Basics)" and
"Patient education: Acute kidney injury (The Basics)")
● Beyond the Basics topics (see "Patient education: Chronic kidney disease (Beyond the
Basics)" and "Patient education: Dialysis or kidney transplantation — which is right for
me? (Beyond the Basics)" and "Patient education: Hemodialysis (Beyond the Basics)"
and "Patient education: Peritoneal dialysis (Beyond the Basics)" and "Patient
education: Protein in the urine (proteinuria) (Beyond the Basics)" and "Patient
education: Split urine collection for orthostatic proteinuria (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

● Acute kidney injury (AKI) is defined by a rise in the serum creatinine concentration or
a decline in urine output that has developed within hours to days. The proposed
criteria for AKI include an increase in serum creatinine by ≥0.3 mg/dL (27 micromol/L)
within 48 hours or an increase to ≥1.5 times the presumed baseline value that is
known or presumed to have occurred within the prior seven days or a decrease in
urine volume to <3 mL/kg over six hours. (See 'Definition' above.)
● Patients with AKI may present with symptoms and signs resulting directly from
diminished kidney function. These include edema, hypertension, and/or decreased
urine output. However, many patients have no clinical symptoms, and an increase in
- Page 13 of 16 -
Evaluation of acute kidney injury among hospitalized adult patients

serum creatinine is detected by routine laboratory tests. (See 'Clinical manifestations'

above.)
● Among hospitalized patients who generally have frequent monitoring of the serum
creatinine and/or urine output, the diagnosis of AKI is easily established based on
increases in serum creatinine or the development of oliguria. All subsequent
evaluation is directed at determining the underlying cause of AKI in order to allow for
prompt treatment. (See 'Diagnosis' above.)
● The major components to the evaluation of patients with an elevated creatinine
include a careful history and physical examination, examination of the urine by both
qualitative chemical tests and microscopic examination, radiographic imaging of the
kidneys, serologic testing in the setting of possible glomerulonephritis, and tissue
diagnosis with renal biopsy if noninvasive evaluation is not sufficient for diagnosis (
algorithm 1). (See 'Evaluation' above.)

REFERENCES

1. Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group.
KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Int Suppl 2012; 2:1.
2. Balasubramanian G, Al-Aly Z, Moiz A, et al. Early nephrologist involvement in hospital-
acquired acute kidney injury: a pilot study. Am J Kidney Dis 2011; 57:228.
3. Wilson FP, Shashaty M, Testani J, et al. Automated, electronic alerts for acute kidney
injury: a single-blind, parallel-group, randomised controlled trial. Lancet 2015;
385:1966.
4. Rose BD. Pathophysiology of Renal Disease, 2nd ed., McGraw-Hill, New York 1987. p.4
1.
5. Kitamoto Y, Tomita M, Akamine M, et al. Differentiation of hematuria using a uniquely
shaped red cell. Nephron 1993; 64:32.
6. Köhler H, Wandel E, Brunck B. Acanthocyturia--a characteristic marker for glomerular
bleeding. Kidney Int 1991; 40:115.
7. Esson ML, Schrier RW. Diagnosis and treatment of acute tubular necrosis. Ann Intern
Med 2002; 137:744.
8. Liaño F, Pascual J. Epidemiology of acute renal failure: a prospective, multicenter,
community-based study. Madrid Acute Renal Failure Study Group. Kidney Int 1996;

- Page 14 of 16 -
Evaluation of acute kidney injury among hospitalized adult patients

50:811.

9. Mehta RL, Pascual MT, Soroko S, et al. Spectrum of acute renal failure in the intensive
care unit: the PICARD experience. Kidney Int 2004; 66:1613.

10. Mehta RL, Cerdá J, Burdmann EA, et al. International Society of Nephrology's 0by25
initiative for acute kidney injury (zero preventable deaths by 2025): a human rights
case for nephrology. Lancet 2015; 385:2616.

11. Ojo B, Campbell CH. Perioperative acute kidney injury: impact and recent update. Curr
Opin Anaesthesiol 2022; 35:215.

12. Liu KD, Thompson BT, Ancukiewicz M, et al. Acute kidney injury in patients with acute
lung injury: impact of fluid accumulation on classification of acute kidney injury and
associated outcomes. Crit Care Med 2011; 39:2665.

13. Inker LA, Eneanya ND, Coresh J, et al. New Creatinine- and Cystatin C-Based Equations
to Estimate GFR without Race. N Engl J Med 2021; 385:1737.

14. Moran SM, Myers BD. Course of acute renal failure studied by a model of creatinine
kinetics. Kidney Int 1985; 27:928.

15. Chen S. Retooling the creatinine clearance equation to estimate kinetic GFR when the
plasma creatinine is changing acutely. J Am Soc Nephrol 2013; 24:877.

16. Anderson RJ, Linas SL, Berns AS, et al. Nonoliguric acute renal failure. N Engl J Med
1977; 296:1134.

17. Parker RA, Himmelfarb J, Tolkoff-Rubin N, et al. Prognosis of patients with acute renal
failure requiring dialysis: results of a multicenter study. Am J Kidney Dis 1998; 32:432.

18. Morgan DJ, Ho KM. A comparison of nonoliguric and oliguric severe acute kidney
injury according to the risk injury failure loss end-stage (RIFLE) criteria. Nephron Clin
Pract 2010; 115:c59.

19. Oh HJ, Shin DH, Lee MJ, et al. Urine output is associated with prognosis in patients
with acute kidney injury requiring continuous renal replacement therapy. J Crit Care
2013; 28:379.

20. Koyner JL, Davison DL, Brasha-Mitchell E, et al. Furosemide Stress Test and Biomarkers
for the Prediction of AKI Severity. J Am Soc Nephrol 2015; 26:2023.

21. Madaio MP. Renal biopsy. Kidney Int 1990; 38:529.

22. Appel GB. Renal biopsy: How effective, what technique, and how safe. J Nephrol 1993;

- Page 15 of 16 -
Evaluation of acute kidney injury among hospitalized adult patients

6:4.

Topic 102834 Version 22.0

© 2024 UpToDate, Inc. All rights reserved.

- Page 16 of 16 -