Acute Kidney Injury
Adult-Gerontology Acute Care Practice Guidelines
Definition
A.Abrupt decline in renal function associated with an increase in nitrogen waste products over the course of a short time frame (hours to days).
B.Can be defined by the RIFLE criteria (also has implied staging built into the definition).
1.Risk: Increase in serum creatinine 50% to 99% (increased SCreat ×1.5 or glomerular filtration rate [GFR] decrease >25%) OR Urine output less than 0.5 mL/kg/hr for 6 to 12 hours.
2.Injury: Increase in serum creatinine 100% to 199% (increased SCreat ×2 or GFR decrease >50%) OR Urine output less than 0.5 mL/kg/hr for 12 to 24 hours.
3.Failure—Increase in serum creatinine greater than 200% (increase SCreat ×3 GFR decrease >75% OR SCreat >4.0 mg/dL) OR increase in serum creatinine by 0.5 mg/dL to greater than 4.0 mg/dL OR urine output less than 0.3 mL/kg/hr for greater than 24 hours or anuria for greater than 12 hours OR Initiation of renal replacement therapy.
4.Loss—Persistent acute renal failure (ARF) and complete loss of kidney function; need for renal replacement therapy for greater than 4 weeks.
5.End-stage renal disease (ESRD)—End-stage kidney disease greater than 3 months; need for renal replacement therapy for greater than 3 months.
Incidence
A.The true incidence of acute kidney injury (AKI) is difficult to determine due to variation in diagnostic criteria.
B.The incidence is estimated at 1% to 25% of ICU patients.
1.This increases the odds ratio of mortality from 2.2 to 8.8, depending on the AKI stage.
2.Even small increases in serum creatinine are associated with a significant increase in mortality.
Pathogenesis
A.AKI is the reduction of renal blood flow and decrease of GFR typically from one of three main mechanisms.
1.Prerenal: Decreased renal perfusion from hypotension or hypovolemia.
2.Intrinsic: Renal failure from diseases of the kidney, with ischemic causes being the most common. May also result from medications and poorly controlled chronic kidney disease.
3.Obstructive—build up of tubular pressure caused by an obstruction of the urinary tract.
Predisposing Factors
A.Prerenal.
1.Hemorrhage.
2.Diarrhea.
3.Diuretics.
4.Heart failure.
5.Acute myocardial infarction (MI).
6.Pulmonary embolus.
7.Sepsis.
8.Anaphylaxis.
9.Medications, including nonsteroidal anti-inflammatory drugs (NSAIDs).
10.Hepatorenal syndrome.
11.Any condition that causes hypovolemia.
B.Intrinsic.
1.Renal artery or vein obstruction.
2.Severe hypertension.
3.Atherosclerosis.
4.Nephrotoxic medications (amphotericin B, NSAIDs, radiocontrast agents).
5.Goodpasture’s syndrome.
6.Glomerulonephritis from lupus.
7.Systemic diseases such as lymphoma, Sjögren’s syndrome, leukemia.
C.Postrenal.
1.Urinary stones.
2.Strictures.
3.Tumors of urinary tract.
4.Thrombosis.
Subjective Data
A.Common complaints/symptoms.
1.Usually asymptomatic.
a.However, patients may experience symptoms related to the underlying cause of AKI (see section “Differential Diagnosis“).
2.If symptomatic, patients may complain of:
a.Edema.
b.Decreased urine output.
c.Nausea.
d.Anorexia.
B.Family and social history.
1.May not be relevant; history of chronic kidney disease.
C.Review of systems.
1.Ask patient about the presence of:
a.Any new medications, especially:
i.Statins (rhabdomyolysis).
ii.Antibiotics (nephrotoxicity, intrarenal AKI).
iii.Angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs).
iv.NSAIDs.
b.Chemotherapy treatment.
c.Exposure to toxic substances such as ethyl alcohol or ethylene glycol.
d.Changes in blood pressure or blood pressure management (prerenal AKI, vasculitis intrarenal AKI).
e.Blood loss or transfusion.
f.History of liver disease (cirrhotic prerenal AKI).
g.Recent or past history of thrombus or embolisms (prerenal AKI due to renal artery thrombosis).
h.History of renal artery stenosis.
i.Recent history of infectious disease (post infectious glomerulonephritis).
j.Recent procedures or diagnostic examinations involving the use of IV radiocontrast.
i.Examples: Angiography or CT.
k.Extreme exercise or trauma (rhabdomyolysis).
l.History of myeloma.
i.Bone pain.
ii.Fractures.
iii.Weight loss.
m.History of kidney stones or gout (acute tubular necrosis [ATN]) due to intratubular crystal
deposition.
n.Rash (vasculitis).
Physical Examination
A.Skin.
1.Livedo reticularis (systemic vasculitis).
a.Digital ischemia.
b.Butterfly rash.
c.Palpable purpura.
2.Maculopapular rash (allergic interstitial nephritis).
3.Track marks (endocarditis).
4.Mucosal or cartilaginous lesions (Wegener’s granulomatosis).
5.Skin turgor (hypovolemic AKI).
B.Ophthalmic examination.
1.Conjunctival jaundice.
2.Band keratopathy (hypercalcemia due to multiple myeloma).
3.Symptoms of malignant hypertension.
a.Papilledema.
b.Flame-shaped hemorrhages.
4.Atheroemboli (renal ischemia due to atheroemboli or renal artery thrombosis).
5.Uveitis (interstitial nephritis/necrotizing vasculitis).
6.Ocular palsy (ethylene glycol poisoning).
C.Ears.
a.Hearing acuity (hearing loss related to aminoglycoside).
D.Cardiovascular system.
1.Assessment of volume status (intra- and extra-vascular volume).
a.Blood pressure and pulse: Sitting and standing.
b.Jugular vein distention.
c.S3 heart sounds (heart failure).
d.Peripheral/dependent edema.
e.Hourly intake and output records.
f.Daily weight.
2.Heart rate/rhythm.
a.Atrial fibrillation (thromboembolism, decreased cardiac output).
b.Murmurs (endocarditis).
c.Pericardial friction rub (endocarditis).
E.Pulmonary system.
1.Auscultation of lung sounds.
a.Pulmonary vascular congestion (congestive heart failure).
b.Rales (pulmonary-renal syndromes).
2.Hemoptysis.
3.Respiratory rate and effort (congestive heart failure).
F.Abdomen.
1.Pulsatile mass or bruit (atheroemboli).
2.Abdominal or costovertebral angle tenderness (nephrolithiasis, renal artery thrombosis, renal vein thrombosis).
3.Abdominal fluid wave (ascites, cirrhosis, or elevated intra-abdominal pressure).
4.Symptoms of urinary obstruction.
a.Pelvic/rectal masses.
b.Prostatic hypertrophy.
c.Distended bladder.
Diagnostic Tests
A.Comprehensive blood chemistry panel, with serum osmolality.
B.Complete blood count (CBC).
1.Prolonged AKI causes nephrogenic anemia (due to reduced renal erythropoietin synthesis).
C.Renal ultrasound.
1.Rule out hydronephrosis due to obstructive process.
2.Assess underlying state of kidney mass and sclerosis.
D.24-hour creatinine clearance.
1.Gives an accurate assessment of current renal clearance. Serum creatinine is a late indicator of renal dysfunction.
E.Hourly urine output.
F.Urinalysis with microscopy.
1.Granular, muddy casts in urine sediment suggest tubular necrosis.
2.Oxalate crystals also observed in ATN.
3.Eosinophils common in interstitial nephritis.
G.Urine sodium and osmolality.
H.Fractional Excretion of Sodium and Urea (FENa) helps differentiate cause of AKI in the presence of oliguria.
1.FENa = (UNa/PNa)/(UCr/PCr) x 100.
a.FENa lessthan 1% is usually prerenal azotemia.
b.FENa greater than 1% is usually ATN caused by contrast, burns, rhabdomyolysis, or acute glomerulonephritis.
I.Further testing depends on the suspected cause of AKI.
J.Renal biopsy: May be indicated if the cause cannot be determined and renal function does not return for a prolonged period of time.
Differential Diagnosis
A.Prerenal.
1.Hemorrhage.
2.Volume depletion.
3.Congestive heart failure.
4.Cirrhosis.
5.Renal artery.
6.Stenosis.
7.Thrombosis/embolism.
8.NSAIDs.
9.ACE inhibitor and ARB.
B.Intrarenal.
1.ATN.
a.Ischemic.
b.Toxic.
i.Exogenous.
1)Antibiotics.
2)Contrast.
3)Chemotherapy.
ii.Endogenous.
1)Pigment (hemoglobinuria, myoglobinuria).
2)Intratubular proteins (myeloma).
3)Intratubular crystals (uric acid, oxalate).
2.Acute interstitial nephritis.
a.Drug associated.
b.Acute glomerulonephritis.
c.Post infectious.
d.Vascular.
i.Vasculitis.
ii.Malignant hypertension.
C.Postrenal.
1.Obstructive.
2.Bladder outlet obstruction.
3.Bilateral ureteral obstruction.
Evaluation and Management Plan
A.General plan.
1.Use the ABCDE-IT mnemonic to quickly determine a treatment plan (see Box 5.1, AKI ABCDE-IT Mnemonic).
2.Determine the stage of AKI using the RIFLE criteria and manage accordingly (see Figure 5.1, AKI Treatment Algorithm).
3.Monitor serum creatinine.
4.Avoid further renal insult.
5.Ensure that blood pressure is in the target range (varies depending on the patient’s age and comorbid disease status).
6.Correct fluid overload to achieve volume homeostasis.
7.Correct any acidosis or electrolyte abnormalities.
BOX 5.1
Acute Kidney Injury ABCDE-IT Mnemonic
- Assess for acute complications (high potassium, acidosis, fluid overload).
- BP check (if systolic BP <110, consider fluid challenge).
- Catheterize (to eliminate postbladder obstructive process and monitor I/O).
- Drugs; stop/avoid nephrotoxins, hold ACE inhibitors.
- Exclude obstruction (Renal US).
- Investigations; urinalysis with micro, for stage 2/3 AKI add ANCA, AntiGBM Ab, DSDNA, ANA, immunoglobulin, electrophoresis.
- Treat the cause.
ACE, angiotensin-converting enzyme; AKI, acute kidney injury; ANA, antinuclear antibody; ANCA; antineutrophil cytoplasmic antibodies; BP, blood pressure; DSDNA, double stranded deoxyribonucleic acid; US, ultrasound
B.Patient/family teaching points.
1.Signs/symptoms to monitor: Edema, headache, dizziness, or syncope.
2.Common occurrences: Hypotension or hypertension.
3.Readmission concerns.
a.Recurrent AKI due to secondary renal insult that is often due to inappropriate resumption of medications (ACE inhibitors/ARBs, NSAIDs) or hypotension/hypertension.
b.Patients should be clear about which medications to hold/restart after discharge and check home blood pressure. If the patient is able to check home blood pressure, provide high and low parameters for reporting readings.
c.These parameters will vary according to the clinical context, but generally patients should call the provider to report a systolic blood pressure less than 130 mmHg, systolic blood pressure greater than 180 mmHg, and diastolic blood pressure greater than 100 mmHg.
d.Renal vasculature is sensitive to blood pressure fluctuations in the recovery phase of AKI, and hypotension or hypertension can precipitate further renal injury.
C.Pharmacotherapy.
1.No pharmacotherapy treatment in AKI. The primary cause must be reversed.
2.Intravenous isotonic sodium chloride solution should be used to maintain euvolemia as clinically indicated.
3.Medications.
a.Hold ACE inhibitors, ARBs, NSAIDs, and any other medications associated with renal insult (e.g., nephrotoxic chemotherapy, aminoglycoside, and beta lactam antibiotics) until patient’s serum creatinine has stabilized at baseline.
b.Note that renal dose dopamine may cause some dilatation to enhance renal perfusion. However, no study has been able to demonstrate a beneficial role of vasodilator use.
D.Discharge instructions.
1.Serum creatinine has either returned to baseline OR,
2.It has significantly improved with a downward trend and resolution of AKI etiology.
Follow-Up
A.Monitor.
1.Serum creatinine and electrolytes.
2.Urine output.
3.Volume status.
B.Pursue other follow-up as indicated specific to the underlying cause of the AKI.
C.Check creatinine within 1 to 2 weeks after discharge to confirm improvement.
D.If medications are on hold due to AKI, follow to determine when medications should be restarted.
Consultation/Referral
A.Early nephrology consultation should occur after hospitalization.
FIGURE 5.1 Acute kidney injury treatment algorithm.
ACE, angiotensin-converting enzyme; AKI, acute kidney injury; ARB, angiotensin II receptor blockers; NSAIDs, nonsteroidal anti-inflammatory drugs.
Special/Geriatric Considerations
A.Geriatric considerations.
1.Elderly patients are at high risk for AKI, particularly those treated with diuretics, ACE inhibitors, ARBs, and NSAIDs.
2.Serum creatinine in elderly patients with diminished muscle mass underestimates the extent of renal impairment.
Bibliography
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