Acute Kidney Injury:​Diagnosis

and Management
Michael G. Mercado, MD, Naval Hospital Bremerton, Bremerton, Washington
Dustin K. Smith, DO, Branch Health Clinic, Diego Garcia, British Indian Ocean Territory
Esther L. Guard, DO, Eglin Family Medicine Residency, Eglin Air Force Base, Florida

Acute kidney injury is a clinical syndrome characterized by a rapid decline in glomerular filtration rate and resultant accu-
mulation of metabolic waste products. Acute kidney injury is associated with an increased risk of mortality, cardiovascular
events, and progression to chronic kidney disease. Severity of acute kidney injury is classified according to urine output and
elevations in creatinine level. Etiologies of acute kidney injury are categorized as prerenal, intrinsic renal, and postrenal.
Accurate diagnosis of the underlying cause is key to successful management and includes a focused history and physical
examination, serum and urine electrolyte measurements, and renal ultrasonography when risk factors for a postrenal cause
are present (e.g., older male with prostatic hypertrophy). General management principles for acute kidney injury include
determination of volume status, fluid resuscitation with isotonic crystalloid, treatment of volume overload with diuretics,
discontinuation of nephrotoxic medications, and adjustment of prescribed drugs according to renal function. Additional sup-
portive care measures may include optimizing nutritional status and glycemic control. Pharmacist-led quality-improvement
programs reduce nephrotoxic exposures and rates of acute kidney injury in the hospital setting. Acute kidney injury care
bundles are associated with improved in-hospital mortality rates and reduced risk of progression. Nephrology consultation
should be considered when there is inadequate response to supportive treatment and for acute kidney injury without a clear
cause, stage 3 or higher acute kidney injury, preexisting stage 4 or higher chronic kidney disease, renal replacement therapy,
and other situations requiring subspecialist expertise. (Am Fam Physician. 2019;100(11):687-694. Copyright © 2019 American
Academy of Family Physicians.)

Acute kidney injury is defined as the sudden loss of kid- kidney function, loss of kidney function, end-stage renal
ney function over hours to days resulting in the inability to disease) and Acute Kidney Injury Network definitions.7-9
maintain electrolyte, acid-base, and water balance. Because The KDIGO system (Table 2 7) is used in this article.
of an aging population and increasing prevalence of hyper-
tension and diabetes mellitus, from 2005 to 2014, the num- Etiology
ber of hospitalizations with a principal diagnosis of acute Acute kidney injury is a complex clinical syndrome with
kidney injury increased from 281,500 to 504,600, and the prerenal, intrinsic renal, and postrenal etiologies.10 Table 3
number of hospitalizations with a secondary diagnosis of summarizes these etiologies.10-13
acute kidney injury increased from 1 million to 2.3 mil-
lion.1 Patients with acute kidney injury requiring renal TABLE 1
dialysis and other forms of renal replacement therapy are
50 times more likely to progress to chronic kidney disease Risk Factors for Acute Kidney Injury
than those not requiring renal replacement therapy.2 Risk
Nonmodifiable Modifiable
factors for acute kidney injury are listed in Table 1.3-6 AIDS Anemia
A universal definition and staging system for acute kid- Chronic kidney disease Hypercholesterolemia
ney injury proposed by the Kidney Disease:​Improving Chronic liver disease Hypertension
Global Outcomes (KDIGO) group merges the earlier RIFLE Congestive heart failure Hypoalbuminemia
(risk of renal dysfunction, injury to the kidney, failure of Diabetes mellitus Hyponatremia
Older age (65 years or older) Mechanical ventilation
Peripheral vascular disease Nephrotoxic drug use
CME This clinical content conforms to AAFP criteria for
Prior kidney surgery Rhabdomyolysis
continuing medical education (CME). See CME Quiz on Renal artery stenosis Sepsis
page 665.
Author disclosure:​ No relevant financial affiliations. Information from references 3-6.

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 TABLE 2

Staging of AKI
Stage Serum creatinine level Urine output
PRERENAL CAUSES 1 1.5-1.9 times baseline < 0.5 mL/kg/h
Prerenal acute kidney injury is associated with decreased or for 6-12 hours
renal perfusion and glomerular filtration rate (GFR) caused ≥ 0.3 mg/dL (≥ 26.5 µmol/L)
by intravascular volume depletion secondary to hypovole- increase
mia, peripheral vasodilation, decreased arterial pressures,
2 2.0-2.9 times baseline < 0.5 mL/kg/h
and impaired cardiac function resulting in decreased car-
for ≥ 12 hours
diac output.14 Sepsis is the most common cause of acute
kidney injury seen in the intensive care unit (ICU).15 3 3.0 times baseline < 0.3 mL/kg/h
for ≥ 24 hours
Angiotensin-converting enzyme inhibitors, angiotensin or
receptor blockers, and nonsteroidal anti-inflammatory drugs Increase in serum creatinine to or

are the most common medications that lower renal perfusion. ≥ 4.0 mg/dL (≥ 353.6 µmol/L) Anuria for
≥ 12 hours
The kidneys activate mechanisms to compensate for the or
reduced renal perfusion in an attempt to maintain the GFR.14 Initiation of renal replacement
therapy or, in patients < 18 years,
However, patients with impairment to these mechanisms,
decrease in eGFR to < 35 mL/min
such as those with chronic kidney disease, have an elevated per 1.73 m2
risk of acute kidney injury.3
AKI = acute kidney injury; eGFR = estimated glomerular filtration
rate.
INTRINSIC RENAL CAUSES
Reprinted with permission from Kidney Disease:​Improving Global
Intrinsic renal causes of acute kidney injury are categorized Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO clini-
by the location of the injury, most commonly the glomerulus cal practice guideline for acute kidney injury. Kidney Int Suppl. 2012;​
or tubule, and include the interstitial or vascular portions 2(suppl 1):​19.

of the kidney. Intrinsic acute kidney injury requires early

11

identification and prompt

subspecialty consultation.
Immune complexes from SORT:​KEY RECOMMENDATIONS FOR PRACTICE
systemic illness (e.g., mem-
branoproliferative glomer- Evidence
Clinical recommendation rating Comments
ulonephritis, polyarteritis
nodosa) cause acute inflam- Isotonic crystalloids are preferred over col- C Consistent evidence from RCTs show-
mation and structural loids when fluid resuscitation is indicated in ing no clear renal or mortality benefit
patients with acute kidney injury.7,27,28 of colloids over isotonic crystalloids
damage to the glomeruli.
Acute tubular necrosis, the Balanced crystalloids are preferred over B Evidence from cohort studies and
most common intrinsic 0.9% sodium chloride for fluid resusci- a limited number of RCTs showing
tation in critically ill and non–critically ill improved mortality and decreased
kidney injury, is damage
patients. 30-32 need for renal replacement therapy
to the tubular cells of the
kidney from ischemic or Pharmacist-led quality improvement ini- B Evidence from a limited number of
nephrotoxic causes. Isch- tiatives, multimodal educational programs cohort studies showing improve-
delivered to clinicians, and care bundles ments in hospital mortality and acute
emic causes include pro- may improve acute kidney injury care. 34,41,42 kidney injury progression
longed periods of severe
hypotension, hypovolemia, There is no difference in 90-day mortality B Evidence from a limited number of
between early initiation of renal replace- RCTs
or hypoperfusion to the ment therapy and delayed initiation. 38
kidneys (e.g., from hemor-
rhage, shock, sepsis, cirrho- High-dose statins lower the risk of contrast A Consistent evidence from multiple
media–induced acute kidney injury in RCTs and meta-analysis
sis, peritonitis, or infarcts) patients undergoing coronary angiography
that do not improve with or percutaneous intervention compared
rehydration.11 Nephrotoxic with low-dose statins.51
causes include endogenous RCT = randomized controlled trial.
and exogenous toxins.
A = consistent, good-quality patient-oriented evidence;​B = inconsistent or limited-quality patient-oriented
Acute interstitial nephri- evidence;​ C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For
tis, a common cause of information about the SORT evidence rating system, go to https://​w ww.aafp.org/afpsort.
acute kidney injury, is most

688  American Family Physician www.aafp.org/afp Volume 100, Number 11 ◆ December 1, 2019
 ACUTE KIDNEY INJURY
TABLE 3

Etiologies of Acute Kidney Injury

Etiology Examples

Prerenal often due to a hypersensitiv-

Increased intra-abdominal Abdominal compartment syndrome ity reaction to medications,
pressure usually an antibiotic or non-
steroidal anti-inflammatory
Intravascular volume Hemorrhage, gastrointestinal losses, renal losses, skin and mucous
depletion membrane losses, nephrotic syndrome, cirrhosis, capillary leak drug.16 Acute interstitial
nephritis related to proton
Peripheral vasodilation Sepsis, cirrhosis, anaphylaxis, pharmacologic adverse effects
pump inhibitors is increas-
Reduced cardiac output Cardiogenic shock, pericardial diseases, congestive heart failure, ingly common, especially in
valvular diseases, pulmonary diseases, sepsis older people.17,18 Infections
Renal vasoconstriction Early sepsis, hepatorenal syndrome, acute hypercalcemia, phar- cause 5% to 10% of acute
macologic adverse effects, iodinated contrast media interstitial nephritis cases.16
Intrinsic renal
Vascular causes of acute
Glomerular injury Pharmacologic adverse effects
kidney injury include large
Hematologic disorders:​hemolytic uremic syndrome, thrombotic
vessel diseases, such as renal
thrombocytopenic purpura artery thrombosis;​embo-
Inflammation:​anti–glomerular basement membrane disease, lism;​stenosis;​and operative
antineutrophil cytoplasmic antibody disease, infection, cryo- renal arterial clamping.11
globulinemia, membranoproliferative glomerulonephritis,
immunoglobulin A nephropathy, systemic lupus erythematosus,
POSTRENAL CAUSES
Henoch-Schönlein purpura, polyarteritis nodosa
Postrenal acute kidney
Renal microvasculature Malignant hypertension, toxemia of pregnancy, hypercalcemia, injury is due to extrarenal
radiocontrast media, scleroderma, pharmacologic adverse effects
obstruction of urinary flow.
Tubular injury Endogenous toxins:​myoglobin, hemoglobin, paraproteinemia, Causes include neurogenic
uric acid bladder;​ retroperitoneal
Exogenous toxins:​antibiotics, chemotherapy agents, radiocon- fibrosis;​and the tumor bur-
trast media, phosphate preparations
den of bladder, prostate, or
Ischemia due to hypoperfusion
cervical cancer. Prostatic
Tubulointerstitial injury Acute allergic interstitial nephritis hypertrophy is the most
Infections:​ Legionella, Leptospira, Rickettsia, Hantavirus, Candida, common cause in older
Plasmodium, tuberculosis men.11
Infiltration

Vascular causes (e.g., large Arterial thrombosis, vasculitis, dissection, thromboembolism,

Diagnosis
vessel diseases, such as renal venous thrombosis, compression, trauma The history and physical
artery thrombosis;​embo- examination are important
lism;​stenosis;​and operative
renal arterial clamping)
in determining the etiology
of acute kidney injury. The
Postrenal history can identify nephro-
Lower urinary tract causes Bladder:​neck obstruction, calculi, carcinoma, infection toxic medications or a sys-
(schistosomiasis)
temic illness contributing
Functional:​neurogenic bladder, diabetes, multiple sclerosis, stroke,
to impaired renal function.
pharmacologic adverse effects (anticholinergics, antidepressants)
The physical examination
Prostate:​benign prostatic hypertrophy, carcinoma, infection
should focus on evaluating
Urethral:​posterior urethral valves, strictures, trauma, infections,
tuberculosis, tumors intravascular volume status.
Skin rashes may indicate an
Upper urinary tract extrinsic Retroperitoneal space tumors, pelvic or intra-abdominal tumors, underlying condition (e.g.,
causes retroperitoneal fibrosis, ureteral ligation or surgical trauma, gran-
ulomatous disease, hematoma systemic lupus erythemato-
sus, atheroembolism/vascu-
Upper urinary tract intrinsic Nephrolithiasis, strictures, edema, debris, blood clots, sloughed
litis) or exposure (e.g., drug
causes papillae, fungal ball, malignancy
rash suggesting acute inter-
Information from references 10-13. stitial necrosis) leading to
acute kidney injury.11

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 ACUTE KIDNEY INJURY

SERUM CREATININE LEVEL

The serum creatinine level, which is part of the diagnostic TABLE 4
criteria for acute kidney injury, is easily obtained. However,
it is not an ideal marker, because creatinine concentration Urinalysis and Urine Microscopy Findings
is influenced by age, sex, race, muscle mass, and protein Associated with Acute Kidney Injury
catabolic rate. Additionally, serum creatinine is a slow Etiologies
changing surrogate for decreased GFR and may take 24 to Etiology Findings
72 hours to reach a new steady state following acute kid- Acute or chronic tubu- Leukocyturia, renal tubular epi-
ney injury.6 lointerstitial injury thelial cells, white blood cell casts,
and granular casts
URINE OUTPUT
Drug-induced or Urinary crystal casts
Urine output can be difficult to accurately assess because endogenous crystalline
of collection and documentation errors. Serum creatinine nephropathy
or urine output can be used for diagnosis of acute kidney
Glomerular injury Urinary acanthocytes and red
injury, although patients who meet diagnostic criteria for blood cell casts
both are at increased risk of mortality from renal replace-
ment therapy and hospitalization.7,19 Ischemic or nephro- Renal tubular epithelial cells, renal
toxic tubular injury tubular epithelial cell casts, and
muddy brown casts
CREATININE CLEARANCE
Creatinine clearance is a direct measure of GFR, and serial Information from reference 21.

creatinine clearance testing provides a more efficient and

accurate assessment of renal function than serum creatinine
testing.20 Creatinine clearance can be performed in collec- value greater than 50% suggests an intrinsic cause. Inter-
tion periods of one to 24 hours, although longer collection pretation of urine electrolytes is limited because it is a single
times increase the likelihood of errors related to inaccurate measure in time, and the results are confounded by acute
time recording and incomplete collection.6 A cohort study volume changes. Fractional excretion of urea is more sensi-
of 484 patients in the ICU found that four-hour creatinine tive in patients with increased sodium excretion caused by
clearance testing is a valid measurement of acute kidney diuretic therapy.22
injury (defined as an increase in serum creatinine greater
than 50% in the control group or a decrease in creatinine OTHER TESTS
clearance greater than 33% in the intervention group). A Renal ultrasonography may show evidence of a postrenal
decrease of greater than 33% in the first 12 hours conferred cause of acute kidney injury but should be performed only
a twofold elevated risk of dialysis or death.20 when the history suggests the presence of urinary tract
obstruction.23 Renal biopsy is reserved for patients with
URINALYSIS AND URINE MICROSCOPY intrinsic acute kidney injury of unclear etiology or when
Urinalysis in combination with urine microscopy provides diagnostic confirmation is necessary before initiating
insight into the location and cause of acute kidney injury. disease-specific therapy.
Table 4 summarizes common findings and associated diag-
noses based on urine evaluation.21 Management
Management of acute kidney injury is primarily supportive,
URINE ELECTROLYTES with the goals of preventing further damage and promoting
The fractional excretion of sodium and the fractional recovery of renal function.7 Figure 1 is a suggested approach
excretion of urea are used to identify prerenal azote- to the management of acute kidney injury based primarily
mia. Online tools for calculating fractional excretion of on expert opinion.11,24 The prompt diagnosis and treatment
sodium and urea are available at https://​w ww.mdcalc.com/ of the underlying cause is critical.12
fractional-excretion-sodium-fena and https://​w ww.mdcalc.
com/fractional-excretion-urea-feurea. FLUID RESUSCITATION
A fractional excretion of sodium less than 1% suggests a An assessment of volume status and hemodynamic stabil-
prerenal cause of acute kidney injury, whereas a value greater ity is a key component in the management of patients with
than 2% suggests an intrinsic cause. A fractional excretion acute kidney injury because fluid overload is associated
of urea less than 35% suggests a prerenal cause, whereas a with increased mortality.25 Consequently, a delicate balance

690  American Family Physician www.aafp.org/afp Volume 100, Number 11 ◆ December 1, 2019
 ACUTE KIDNEY INJURY

exists between optimizing renal perfusion and avoiding be associated with worsening renal function and acid-base
fluid overload.26 disturbances.29 A prospective study of patients in the ICU
If fluid resuscitation is indicated, isotonic crystal- found that a chloride-restrictive strategy for resuscitation
loids (e.g., 0.9% normal saline, lactated Ringer solution, was associated with a lower incidence of acute kidney injury
Plasma-Lyte A) are recommended over colloids (e.g., albu- and need for renal replacement therapy.30 Subsequently, two
min, dextran) as the initial therapy.7,27,28 Excess chloride may trials comparing balanced crystalloids with 0.9% sodium
chloride demonstrated improved composite renal
outcomes (mortality, need for renal replacement
FIGURE 1 therapy, and persistent renal dysfunction) in the
balanced crystalloid group for both critically ill
Confirmed diagnosis of acute kidney injury
patients (absolute risk reduction [ARR] = 1.1%;​
number needed to treat [NNT] = 91) and non–
critically ill patients (ARR = 0.9%;​NNT = 111).31,32
Focused history and physical examination A mean arterial pressure goal of 65 mm Hg
Assess volume status or greater is acceptable, and vasopressors may
Monitor blood urea nitrogen, creatinine, and
electrolyte levels; assess hemodynamic stability
be required if this is not achieved through fluid
Urine testing (dipstick, microscopy, chemistries)
resuscitation. An online calculator to determine
mean arterial pressure is available at https://​
www.mdcalc.com/mean-arterial-pressure-map.
Discontinue potential nephrotoxins Protocol-based strategies are recommended
Review medications and order adjustments as indicated
to prevent and improve acute kidney injury in
Use guideline-based care bundles when available
high-risk patients (e.g., those who are postop-
Determine cause
erative or in septic shock).7 A randomized con-
trolled trial (RCT) of 776 patients with septic
shock compared outcomes with a mean arte-
Prerenal disease Intrinsic renal disease Postrenal disease rial pressure goal of 65 to 70 mm Hg vs. a goal
of 80 to 85 mm Hg. No mortality difference was
observed between the groups, but in a subset of
Fluid resuscitation with Consider Consider renal ultrasonog-
isotonic crystalloid renal biopsy raphy when urinary tract
patients with chronic hypertension, the higher
Administer diuretics Nephrology obstruction is suspected goal group had lower rates of acute kidney injury
if volume overload is consultation (ARR = 13%;​NNT = 8) and renal replacement
present therapy (ARR = 11%;​NNT = 10).33
Consider vasopressor Relieve obstruction
support Urology consultation
AVOIDANCE OF NEPHROTOXICITY
A review of medications requiring discontinua-
tion, dose adjustment, or monitoring is critical to
Treat the underlying cause the management of acute kidney injury (Tables
Provide supportive management 5 and 6).12 In addition, the implementation of
pharmacist-led quality-improvement programs
is associated with reductions in nephrotoxic
Monitor volume status, acid-base
status, and electrolyte levels
exposures and rates of acute kidney injury in the
hospital setting.34

ADDITIONAL MANAGEMENT
Clinical improvement Consider renal replacement CONSIDERATIONS
in renal function therapy, if indicated (Table 7) Because of a lack of benefit, diuretics are not rec-
ommended for the treatment or prevention of
An approach to the diagnosis and management of acute kidney acute kidney injury, except to alleviate volume
injury. overload.7 For ICU patients, a plasma glucose tar-
Information from references 11 and 24. get of 110 to 149 mg per dL (6.1 to 8.3 mmol per L)
is recommended, although this target has not

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 TABLE 5 TABLE 6

Medications Commonly Associated Key Medications Requiring Dose Adjustment

with Acute Tubular Necrosis (or Cessation) in AKI
Medications and agents associated with acute tubular Analgesics (morphine, meperidine, gabapentin, pregabalin)
necrosis
Antiepileptics (lamotrigine)
Aminoglycosides (tobramycin, gentamycin)
Antivirals (acyclovir, ganciclovir, valganciclovir)
NSAIDs (ibuprofen, naproxen, ketorolac, celecoxib)
Antifungals (fluconazole)
ACEi (captopril, lisinopril, benazepril, ramipril)
Antimicrobials (almost all antimicrobials need dose adjustment
ARB (losartan, valsartan, candesartan, irbesartan) in AKI, with important exceptions of azithromycin, ceftriaxone,
doxycycline, linezolid, moxifloxacin, nafcillin, rifampin)
Amphotericin
Diabetic agents (sulfonylureas, metformin)
Cisplatin
Allopurinol
Foscarnet
Baclofen
Iodinated contrast
Colchicine
Pentamidine
Digoxin
Tenofovir
Lithium
Zoledronic acid
Low-molecular-weight heparin
Note: Although not a classic cause of acute tubular necrosis, vol-
ume depletion caused by diuretics can exacerbate the effects of NOACs
some of these other medications. This table does not include com-
Note: Medications that are associated with acute tubular necrosis
mon causes of pigment or crystal nephropathy or medications
(Table 5) should be withheld, if possible.
associated with osmotic injury.
AKI = acute kidney injury; NOAC = novel anticoagulants.
ACEi = angiotensin-converting enzyme inhibitor; ARB = angiotensin
receptor blocker; NSAIDs = nonsteroidal anti-inflammatory drugs. Reprinted with permission from Moore PK, Hsu RK, Liu KD. Man-
agement of acute kidney injury: core curriculum 2018. Am J Kidney
Reprinted with permission from Moore PK, Hsu RK, Liu KD. Man-
Dis. 2018;72(1):139.
agement of acute kidney injury: core curriculum 2018. Am J Kidney
Dis. 2018;72(1):139.

of the time.40 Multimodal educational programs deliv-

been studied in RCTs. Nutritional status should be evalu-
7
ered to clinicians have shown improvements in clinician
ated, and dietary recommendations should be based on the self-assessment of acute kidney injury care.41 Acute kidney
underlying cause and severity of the acute kidney injury.7,12 injury care bundles, a specific set of guideline-based diag-
If metabolic derangements from acute kidney injury nostic and therapeutic interventions, are associated with
do not respond to conservative treatment, renal replace- improved in-hospital mortality rates and reduced risk of
ment therapy, in consultation with a nephrologist, may be progression in observational studies.42
required. Table 7 includes indications for initiat-
ing renal replacement therapy.7,35-37 A multicenter
RCT of 488 patients with acute kidney injury TABLE 7
and septic shock compared early initiation of
renal replacement therapy (within 12 hours) with Life-threatening Indications for Renal Replacement
delayed initiation (48 hours) and found no differ- Therapy in Patients with Acute Kidney Injury
ence in 90-day mortality. 38 Condition Signs or symptoms
Early nephrology consultation (within 48 hours) Anuria Negligible urine output for six hours
appears to be beneficial for patients with acute kid- Hyperkalemia Potassium level > 6.5 mEq per L (6.5 mmol per L)
ney injury.39 In addition to when initiating renal Poisoning or Ethylene glycol or lithium ingestion
replacement therapy, nephrology consultation intoxication
should be considered when there is inadequate Pronounced azotemia Urea nitrogen concentrations > 84 mg per dL
response to supportive treatment and for acute kid- (30 mmol per L)
ney injury without a clear cause, stage 3 or higher Severe metabolic pH < 7.2 despite normal or low partial pressure
acidosis of carbon dioxide in arterial blood
acute kidney injury, stage 4 or higher chronic
Severe oliguria Urine output < 200 mL over 12 hours
kidney disease, and other situations requiring
Uremic complications Encephalopathy, neuropathy, pericarditis
specialist expertise (e.g., renal transplant, glomer-
Volume overload Pulmonary edema unresponsive to diuretics
ulonephritis, multiple myeloma). 36

Inpatient data from a health care system found Information from references 7 and 35-37.
acute kidney injury care to be optimal only 50%

692  American Family Physician www.aafp.org/afp Volume 100, Number 11 ◆ December 1, 2019
 ACUTE KIDNEY INJURY

FOLLOW-UP This article updates previous articles on this topic by Rahman, et

al.13;​ Needham53;​and Agrawal and Swartz.54
The transition from the hospital to the outpatient setting
presents an opportunity to improve the care of patients with Data Sources:​ This manuscript was based on literature identified
in Essential Evidence Plus, PubMed Clinical Queries, the Agency
acute kidney injury. Follow-up three months after hospital- for Healthcare Research and Quality, the Cochrane Database of
ization is reasonable if renal function is recovered (90% or Systematic Reviews, and Google Scholar using the search terms
greater from baseline), with earlier follow-up intervals (at acute kidney injury and acute renal failure. References from
three weeks and then again at three months) for patients with those sources were also searched. Search dates:​October 2018,​
a slower recovery.43 Blood pressure, weight, serum creatinine January 2019, April 2019, and August 2019.
level, and GFR should be measured at each visit. Nephrology The opinions and assertions contained herein are the private
views of the authors and are not to be construed as official or as
consultation is recommended if the estimated GFR remains
reflecting the views of the U.S. Navy, U.S. Air Force, Department
less than 60 mL per minute per 1.73 m2.43 The optimal dura- of Defense, or the U.S. government.
tion of monitoring after acute kidney injury is unclear.

Prognosis The Authors

Stage 3 acute kidney injury requiring renal replacement MICHAEL G. MERCADO, MD, FAAFP, is director of medical
therapy is associated with mortality rates between 44% and services at the Naval Hospital in Bremerton, Wash., and is an
assistant professor in the Department of Family Medicine at
52%.44,45 Observational studies have shown an increased the Uniformed Services University of the Health Sciences,
risk of developing chronic kidney disease following acute Bethesda, Md.
kidney injury.3 In a cohort study that followed hospitalized
Medicare beneficiaries for two years after discharge, acute DUSTIN K. SMITH, DO, FAAFP, is senior medical officer for
the U.S. Naval Hospital in Yokosuka, Japan, stationed at
kidney injury was associated with a 13-fold increased risk
Branch Health Clinic, Diego Garcia, British Indian Ocean
of end-stage renal disease in patients without preexisting Territory. He is an assistant professor in the Department of
chronic kidney disease and a 40-fold increase in patients Family Medicine at the Uniformed Services University of the
with both acute kidney injury and chronic kidney disease.5 Health Sciences.
Acute kidney injury is also associated with an increased risk
ESTHER L. GUARD, DO, FAAFP, is a faculty member at the
of cardiovascular mortality, acute myocardial infarction, Eglin Family Medicine Residency, Eglin Air Force Base, Fla., and
and heart failure.46,47 A retrospective cohort study of 2,451 an assistant professor in the Department of Family Medicine at
hospitalized patients with acute kidney injury found that the Uniformed Services University of the Health Sciences.
they had a 22% increased risk of developing hypertension
Address correspondence to Michael G. Mercado, MD, FAAFP,
within six months.48
Naval Hospital Bremerton, 1 Boone Rd., Bremerton, WA 98312
(email:​michael.mercado.md@​gmail.com). Reprints are not
Prevention available from the authors.
An individualized approach to implementing preventive
strategies is based on the presence of clinical situations that
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8. Bellomo R, Ronco C, Kellum JA, et al. Acute renal failure - definition, out- 32. Self WH, Semler MW, Wanderer JP, et al. Balanced crystalloids versus
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694  American Family Physician www.aafp.org/afp Volume 100, Number 11 ◆ December 1, 2019