Acute kidney injury: Difference between revisions
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− | == |
+ | ==Background== |
− | * |
+ | *An inability of the kidneys to maintain body homeostasis, usually defined by an acute increase in creatinine |
+ | *Novel biomarkers are under development to complement creatinine, and are generally classified into: |
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+ | **Stress markers |
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+ | **Damage markers |
||
+ | **Functional markers, including cystatin C |
||
− | == |
+ | === KDIGO Staging === |
+ | {| class="wikitable" |
||
− | |||
⚫ | |||
− | {| |
||
+ | !Serum Creatinine |
||
⚫ | |||
+ | !Urine Output |
||
− | ! Serum creatinine |
||
− | ! Or, urine output |
||
|- |
|- |
||
− | | |
+ | |1 |
− | | |
+ | |1.5 to 1.9 times baseline, or |
+ | ≥26.5 μmol/L increase |
||
− | | |
+ | |<0.5 mL/kg/h for 6-12 hours |
|- |
|- |
||
− | | |
+ | |2 |
− | | |
+ | |2 to 2.9 times baseline |
− | | |
+ | |<0.5 mL/kg/h for ≥12 hours |
|- |
|- |
||
− | | |
+ | |3 |
− | | |
+ | |3 times baseline, or ≥353.6 μmol/L, or started renal replacement therapy |
− | | |
+ | |<0.3 mL/kg/h for ≥24 hours, or anuria for ≥12 hours |
|} |
|} |
||
− | == |
+ | ==Differential Diagnosis== |
− | * |
+ | *Pre-renal: decreased renal perfusion |
− | ** |
+ | **[[Hypovolemia]] |
− | ** |
+ | **[[Blood loss]] |
− | ** |
+ | **[[Shock]] |
− | ** |
+ | **[[Sepsis]] |
− | ** |
+ | **[[Heart failure]] |
− | ** |
+ | **[[Vomiting]] and [[diarrhea]] |
− | * |
+ | *Renal/intrinsic |
− | ** |
+ | **[[Glomerulonephritis]] (GN): glomerular damage |
− | *** |
+ | ***Primary |
− | **** |
+ | ****Minimal change (in children) |
− | **** |
+ | ****Membranous (in adults) |
− | **** |
+ | ****Focal sclerosing (in HIV patients) |
− | *** |
+ | ***Secondary |
− | **** |
+ | ****Focal sclerosing or diffuse (in diabetic patients) |
− | **** |
+ | ****[[Lupus]], [[multiple myeloma]], and [[amyloidosis]] |
− | ** |
+ | **[[Acute tubular necrosis]] (ATN): tubular damage |
− | *** |
+ | ***[[Ischemia]] from prerenal disease |
− | *** |
+ | ***Toxins |
− | *** |
+ | ***Drugs |
− | **** |
+ | ****[[Aminoglycosides]] |
− | **** Amphotericin |
+ | ****[[Amphotericin B|Amphotericin]] |
− | **** |
+ | ****[[Cisplatin]] |
− | *** |
+ | ***Pigments: hemoglobin, myoglobin |
− | *** |
+ | ***Proteins: immunoglobulin light chains (e.g. [[multiple myeloma]]) |
− | *** |
+ | ***Crystals |
− | **** |
+ | ****[[Gout|Uric acid]] |
− | **** |
+ | ****[[Acyclovir]] |
− | **** |
+ | ****[[Methotrexate]] |
− | **** |
+ | ****[[Indinavir]] |
− | **** |
+ | ****Oral sodium phosphate |
− | *** |
+ | ***Contrast-induced |
− | ** |
+ | **[[Acute interstitial nephritis]] (AIN): interstitial damage |
− | *** |
+ | ***Allergic |
− | **** |
+ | ****Antibiotics: [[Β-lactams|beta-lactams]], [[sulfonamides]] |
− | **** |
+ | ****[[NSAID]] |
− | **** |
+ | ****[[PPI]] |
− | *** |
+ | ***Infective |
− | **** |
+ | ****[[Pyelonephritis]] |
− | **** |
+ | ****[[Legionellosis]] |
− | *** |
+ | ***Infiltration |
− | **** |
+ | ****[[Sarcoidosis]] |
− | **** |
+ | ****[[Lymphoma]] |
− | **** |
+ | ****[[Leukemia]] |
− | *** |
+ | ***Autoimmune |
− | **** |
+ | ****[[Sjögren syndrome]] |
− | **** |
+ | ****[[TINU syndrome]] |
− | **** |
+ | ****[[IgG4 disease]] |
− | **** |
+ | ****[[Systemic lupus erythematosus]] |
− | *** |
+ | ***Small vessel disease |
− | **** |
+ | ****Cholesterol emboli |
− | **** |
+ | ****[[Thrombotic microangiopathy]] |
− | ***** |
+ | *****[[HUS]]/[[TTP]] |
− | ***** |
+ | *****[[DIC]] |
− | ***** |
+ | *****[[Preeclampsia]] |
− | ***** |
+ | *****[[Anti-phospholipid syndrome]] (APS) |
− | ***** |
+ | *****[[Malignant hypertension]] |
− | ***** |
+ | *****[[Scleroderma renal crisis]] |
− | * |
+ | *Post-renal (obstructive) |
− | ** |
+ | **Bladder neck |
− | *** |
+ | ***[[BPH]] or [[prostate cancer]] (in men) |
− | *** |
+ | ***[[Cervical cancer]] (in women) |
− | ** |
+ | **[[Neurogenic bladder]] |
− | *** |
+ | ***[[Anticholinergics]] |
− | ** |
+ | **Ureteral (bilateral) |
− | *** |
+ | ***[[Malignancy]] |
+ | ***[[Lymphadenopathy]] |
||
− | *** LAN |
||
− | *** |
+ | ***[[Retroperitoneal fibrosis]] |
− | *** |
+ | ***[[Nephrolithiasis]] |
− | == |
+ | ==Clinical Manifestations== |
− | === |
+ | ===Clinical Clues of Etiology=== |
+ | {| class="wikitable" |
||
− | {| |
||
+ | ! |
||
− | ! |
+ | !Type |
− | ! |
+ | !History |
− | ! |
+ | !Examination |
− | |- |
||
⚫ | |||
⚫ | |||
⚫ | |||
|- |
|- |
||
⚫ | |||
⚫ | |||
⚫ | |||
− | | |
||
⚫ | |||
− | | |
||
|- |
|- |
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⚫ | |||
− | | |
+ | |ATN |
− | | |
+ | |History of nephrotoxic medications, hypotension, trauma or myalgias suggestion rhabdo, CT contrast |
− | | |
+ | |Muscle tenderness, compartment syndrome, volume status |
|- |
|- |
||
− | | |
+ | |GN |
− | | |
+ | |Lupus, systemic sclerosis, rash, arthritis, uveitis, weight loss, fatigue, HCV infection, HIV infection, hematuria, foamy urine, cough, sinusitis, hemoptysis |
− | | |
+ | |Periorbital, sacral, and lower-extremity edema; rash; oral or nasal ulcers |
|- |
|- |
||
− | | |
+ | |AIN |
− | | |
+ | |Medication use (antiiotics, PPIs), rash, arthralgias, fever, infection |
− | | |
+ | |Fever, drug rash |
|- |
|- |
||
− | | |
+ | |Vascular |
− | | |
+ | |Nephrotic syndrome, trauma, flank pain, anticoagulation, vascular surgery |
− | | |
+ | |Livedo reticularis, fundoscopy showing malignant hypertension, abdominal bruits |
|- |
|- |
||
− | | Post-renal |
+ | | colspan="2" |Post-renal |
− | | |
+ | |Urinary urgency or hesitancy, gross hematuria, polyuria, stones, medications, cancer |
− | | |
+ | |Bladder distension, pelvic mass, prostate enlargement |
|} |
|} |
||
'''Source:''' Rahman M, Shad F, and Smith MC. [https://www.aafp.org/afp/2012/1001/p631.html Acute kidney injury: A guide to diagnosis and management]. ''Am Fam Physician''. 2012;86(7):631-639. |
'''Source:''' Rahman M, Shad F, and Smith MC. [https://www.aafp.org/afp/2012/1001/p631.html Acute kidney injury: A guide to diagnosis and management]. ''Am Fam Physician''. 2012;86(7):631-639. |
||
− | == |
+ | ==Investigations== |
− | * |
+ | *Laboratory |
− | ** |
+ | **Urinalysis and microscopy |
− | *** |
+ | ***Granular casts (from heme), suggesting ATN |
− | *** |
+ | ***Red blood cell casts, suggesting GN |
− | ** |
+ | **Urine sodium |
− | *** |
+ | ***<10mmol/L suggests pre-renal, unless diuresed |
− | ** |
+ | **Urea to creatinine ratio |
− | *** |
+ | ***Increased ratio suggests pre-renal cause |
− | ** |
+ | **Extended electrolytes |
− | * |
+ | *Renal ultrasound, for possible obstruction |
− | === |
+ | ===Fractional excretion of sodium (FENa)=== |
− | $FENa = \frac{U_{Na} \div U_{Cr}}{S_{Na} \div S_{Cr}} = \frac{U_{Na} \times S_{Cr}}{S_{Na} \times U_{Cr}}$ |
+ | <nowiki>$FENa = \frac{U_{Na} \div U_{Cr}}{S_{Na} \div S_{Cr}} = \frac{U_{Na} \times S_{Cr}}{S_{Na} \times U_{Cr}}$</nowiki> |
+ | {| class="wikitable" |
||
− | {| |
||
− | ! |
+ | !FENa |
− | ! |
+ | !Etiology |
|- |
|- |
||
− | | |
+ | |<1% |
− | | |
+ | |Pre-renal |
|- |
|- |
||
− | | |
+ | |1 to 4%<br /> >2% |
− | | |
+ | |Intrinsic renal<br /> Acute tubular necrosis (ATN) |
|- |
|- |
||
− | | |
+ | |>4% |
− | | |
+ | |Post-obstructive |
|} |
|} |
||
− | == |
+ | ==Management== |
− | * |
+ | *Treatment depends on etiology |
− | ** |
+ | **Prerenal: Fluid challenge |
− | ** |
+ | **Renal: Stop nephrotoxic medications |
− | ** |
+ | **Post-renal: Nephrostomy tubes |
− | * |
+ | *Dialysis if |
− | ** |
+ | **Acidosis |
− | ** |
+ | **Electrolyte imbalance (K+) |
− | ** |
+ | **Intoxication (drugs, alcohols) |
− | ** |
+ | **Overloaded fluid (heart failure) |
− | ** |
+ | **Uremia (pericarditis, neurological symptoms) |
− | == |
+ | ==Prognosis== |
− | * |
+ | *Increased risk of developing CKD with |
− | ** |
+ | **Increasing age |
− | ** |
+ | **Female sex |
− | ** |
+ | **AKIN stage |
− | ** |
+ | **Absolute increase in serum creatinine |
− | ** |
+ | **Albuminuria |
[[Category:Nephrology]] |
[[Category:Nephrology]] |
Latest revision as of 22:04, 9 October 2022
Background
- An inability of the kidneys to maintain body homeostasis, usually defined by an acute increase in creatinine
- Novel biomarkers are under development to complement creatinine, and are generally classified into:
- Stress markers
- Damage markers
- Functional markers, including cystatin C
KDIGO Staging
Stage | Serum Creatinine | Urine Output |
---|---|---|
1 | 1.5 to 1.9 times baseline, or
≥26.5 μmol/L increase |
<0.5 mL/kg/h for 6-12 hours |
2 | 2 to 2.9 times baseline | <0.5 mL/kg/h for ≥12 hours |
3 | 3 times baseline, or ≥353.6 μmol/L, or started renal replacement therapy | <0.3 mL/kg/h for ≥24 hours, or anuria for ≥12 hours |
Differential Diagnosis
- Pre-renal: decreased renal perfusion
- Renal/intrinsic
- Glomerulonephritis (GN): glomerular damage
- Primary
- Minimal change (in children)
- Membranous (in adults)
- Focal sclerosing (in HIV patients)
- Secondary
- Focal sclerosing or diffuse (in diabetic patients)
- Lupus, multiple myeloma, and amyloidosis
- Primary
- Acute tubular necrosis (ATN): tubular damage
- Ischemia from prerenal disease
- Toxins
- Drugs
- Pigments: hemoglobin, myoglobin
- Proteins: immunoglobulin light chains (e.g. multiple myeloma)
- Crystals
- Uric acid
- Acyclovir
- Methotrexate
- Indinavir
- Oral sodium phosphate
- Contrast-induced
- Acute interstitial nephritis (AIN): interstitial damage
- Allergic
- Antibiotics: beta-lactams, sulfonamides
- NSAID
- PPI
- Infective
- Infiltration
- Autoimmune
- Small vessel disease
- Cholesterol emboli
- Thrombotic microangiopathy
- Allergic
- Glomerulonephritis (GN): glomerular damage
- Post-renal (obstructive)
- Bladder neck
- BPH or prostate cancer (in men)
- Cervical cancer (in women)
- Neurogenic bladder
- Ureteral (bilateral)
- Bladder neck
Clinical Manifestations
Clinical Clues of Etiology
Type | History | Examination | |
---|---|---|---|
Prerenal | Volume loss (e.g. vomiting, diarrhea, diuretics, hemorrhage, burns) Thirst and reduced fluid intake Heart failure or cirrhosis |
Weight loss, orthostatic hypotension and tachycardiac, poor skin turgor, signs of heart failure or liver failure | |
Intrinsic renal | ATN | History of nephrotoxic medications, hypotension, trauma or myalgias suggestion rhabdo, CT contrast | Muscle tenderness, compartment syndrome, volume status |
GN | Lupus, systemic sclerosis, rash, arthritis, uveitis, weight loss, fatigue, HCV infection, HIV infection, hematuria, foamy urine, cough, sinusitis, hemoptysis | Periorbital, sacral, and lower-extremity edema; rash; oral or nasal ulcers | |
AIN | Medication use (antiiotics, PPIs), rash, arthralgias, fever, infection | Fever, drug rash | |
Vascular | Nephrotic syndrome, trauma, flank pain, anticoagulation, vascular surgery | Livedo reticularis, fundoscopy showing malignant hypertension, abdominal bruits | |
Post-renal | Urinary urgency or hesitancy, gross hematuria, polyuria, stones, medications, cancer | Bladder distension, pelvic mass, prostate enlargement |
Source: Rahman M, Shad F, and Smith MC. Acute kidney injury: A guide to diagnosis and management. Am Fam Physician. 2012;86(7):631-639.
Investigations
- Laboratory
- Urinalysis and microscopy
- Granular casts (from heme), suggesting ATN
- Red blood cell casts, suggesting GN
- Urine sodium
- <10mmol/L suggests pre-renal, unless diuresed
- Urea to creatinine ratio
- Increased ratio suggests pre-renal cause
- Extended electrolytes
- Urinalysis and microscopy
- Renal ultrasound, for possible obstruction
Fractional excretion of sodium (FENa)
$FENa = \frac{U_{Na} \div U_{Cr}}{S_{Na} \div S_{Cr}} = \frac{U_{Na} \times S_{Cr}}{S_{Na} \times U_{Cr}}$
FENa | Etiology |
---|---|
<1% | Pre-renal |
1 to 4% >2% |
Intrinsic renal Acute tubular necrosis (ATN) |
>4% | Post-obstructive |
Management
- Treatment depends on etiology
- Prerenal: Fluid challenge
- Renal: Stop nephrotoxic medications
- Post-renal: Nephrostomy tubes
- Dialysis if
- Acidosis
- Electrolyte imbalance (K+)
- Intoxication (drugs, alcohols)
- Overloaded fluid (heart failure)
- Uremia (pericarditis, neurological symptoms)
Prognosis
- Increased risk of developing CKD with
- Increasing age
- Female sex
- AKIN stage
- Absolute increase in serum creatinine
- Albuminuria