Acute kidney injury: Difference between revisions
From IDWiki
(ββ) |
No edit summary Β |
||
(2 intermediate revisions by the same user not shown) | |||
Line 1: | Line 1: | ||
β | == |
+ | ==Background== |
*An inability of the kidneys to maintain body homeostasis, usually defined by an acute increase in creatinine |
*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 |
||
β | == |
+ | === KDIGO Staging === |
β | |||
{| class="wikitable" |
{| class="wikitable" |
||
!Stage |
!Stage |
||
β | !Serum |
+ | !Serum Creatinine |
+ | !Urine Output |
||
β | !Or, urine output |
||
|- |
|- |
||
|1 |
|1 |
||
β | | |
+ | |1.5 to 1.9 times baseline, or |
+ | β₯26.5 ΞΌmol/L increase |
||
β | | |
+ | |<0.5 mL/kg/h for 6-12 hours |
|- |
|- |
||
|2 |
|2 |
||
β | | |
+ | |2 to 2.9 times baseline |
β | | |
+ | |<0.5 mL/kg/h for β₯12 hours |
|- |
|- |
||
|3 |
|3 |
||
β | | |
+ | |3 times baseline, or β₯353.6 ΞΌmol/L, or started renal replacement therapy |
β | | |
+ | |<0.3 mL/kg/h for β₯24 hours, or anuria for β₯12 hours |
|} |
|} |
||
Line 26: | Line 30: | ||
*Pre-renal: decreased renal perfusion |
*Pre-renal: decreased renal perfusion |
||
β | **Hypovolemia |
+ | **[[Hypovolemia]] |
β | **Blood loss |
+ | **[[Blood loss]] |
β | **Shock |
+ | **[[Shock]] |
β | **Sepsis |
+ | **[[Sepsis]] |
β | **Heart failure |
+ | **[[Heart failure]] |
β | **Vomiting and diarrhea |
+ | **[[Vomiting]] and [[diarrhea]] |
*Renal/intrinsic |
*Renal/intrinsic |
||
β | **Glomerulonephritis (GN): glomerular damage |
+ | **[[Glomerulonephritis]] (GN): glomerular damage |
***Primary |
***Primary |
||
****Minimal change (in children) |
****Minimal change (in children) |
||
Line 40: | Line 44: | ||
***Secondary |
***Secondary |
||
****Focal sclerosing or diffuse (in diabetic patients) |
****Focal sclerosing or diffuse (in diabetic patients) |
||
β | ****Lupus, multiple myeloma, and amyloidosis |
+ | ****[[Lupus]], [[multiple myeloma]], and [[amyloidosis]] |
β | **Acute tubular necrosis (ATN): tubular damage |
+ | **[[Acute tubular necrosis]] (ATN): tubular damage |
β | ***Ischemia from prerenal disease |
+ | ***[[Ischemia]] from prerenal disease |
***Toxins |
***Toxins |
||
***Drugs |
***Drugs |
||
β | ****Aminoglycosides |
+ | ****[[Aminoglycosides]] |
β | ****Amphotericin |
+ | ****[[Amphotericin B|Amphotericin]] |
β | ****Cisplatin |
+ | ****[[Cisplatin]] |
***Pigments: hemoglobin, myoglobin |
***Pigments: hemoglobin, myoglobin |
||
β | ***Proteins: immunoglobulin light chains (e.g. multiple myeloma) |
+ | ***Proteins: immunoglobulin light chains (e.g. [[multiple myeloma]]) |
***Crystals |
***Crystals |
||
β | ****Uric acid |
+ | ****[[Gout|Uric acid]] |
β | ****Acyclovir |
+ | ****[[Acyclovir]] |
β | ****Methotrexate |
+ | ****[[Methotrexate]] |
β | ****Indinavir |
+ | ****[[Indinavir]] |
β | ****Oral |
+ | ****Oral sodium phosphate |
***Contrast-induced |
***Contrast-induced |
||
β | **Acute interstitial nephritis (AIN): interstitial damage |
+ | **[[Acute interstitial nephritis]] (AIN): interstitial damage |
***Allergic |
***Allergic |
||
β | ****Antibiotics: beta-lactams, |
+ | ****Antibiotics: [[Ξ-lactams|beta-lactams]], [[sulfonamides]] |
β | **** |
+ | ****[[NSAID]] |
β | **** |
+ | ****[[PPI]] |
***Infective |
***Infective |
||
β | ****Pyelonephritis |
+ | ****[[Pyelonephritis]] |
β | ****Legionellosis |
+ | ****[[Legionellosis]] |
***Infiltration |
***Infiltration |
||
β | ****Sarcoidosis |
+ | ****[[Sarcoidosis]] |
β | ****Lymphoma |
+ | ****[[Lymphoma]] |
β | ****Leukemia |
+ | ****[[Leukemia]] |
***Autoimmune |
***Autoimmune |
||
β | ****SjΓΆgren |
+ | ****[[SjΓΆgren syndrome]] |
β | ****TINU syndrome |
+ | ****[[TINU syndrome]] |
β | ****IgG4 disease |
+ | ****[[IgG4 disease]] |
β | ****Systemic lupus |
+ | ****[[Systemic lupus erythematosus]] |
***Small vessel disease |
***Small vessel disease |
||
****Cholesterol emboli |
****Cholesterol emboli |
||
β | ****Thrombotic microangiopathy |
+ | ****[[Thrombotic microangiopathy]] |
β | *****HUS/TTP |
+ | *****[[HUS]]/[[TTP]] |
β | *****DIC |
+ | *****[[DIC]] |
β | *****Preeclampsia |
+ | *****[[Preeclampsia]] |
β | *****Anti-phospholipid syndrome (APS) |
+ | *****[[Anti-phospholipid syndrome]] (APS) |
β | *****Malignant hypertension |
+ | *****[[Malignant hypertension]] |
β | *****Scleroderma renal crisis |
+ | *****[[Scleroderma renal crisis]] |
*Post-renal (obstructive) |
*Post-renal (obstructive) |
||
**Bladder neck |
**Bladder neck |
||
β | ***BPH or prostate cancer (in men) |
+ | ***[[BPH]] or [[prostate cancer]] (in men) |
β | ***Cervical cancer (in women) |
+ | ***[[Cervical cancer]] (in women) |
β | **Neurogenic bladder |
+ | **[[Neurogenic bladder]] |
β | ***Anticholinergics |
+ | ***[[Anticholinergics]] |
**Ureteral (bilateral) |
**Ureteral (bilateral) |
||
β | ***Malignancy |
+ | ***[[Malignancy]] |
+ | ***[[Lymphadenopathy]] |
||
β | ***LAN |
||
β | ***Retroperitoneal fibrosis |
+ | ***[[Retroperitoneal fibrosis]] |
β | ***Nephrolithiasis |
+ | ***[[Nephrolithiasis]] |
==Clinical Manifestations== |
==Clinical Manifestations== |
||
β | ===Clinical |
+ | ===Clinical Clues of Etiology=== |
{| class="wikitable" |
{| class="wikitable" |
||
+ | ! |
||
!Type |
!Type |
||
!History |
!History |
||
!Examination |
!Examination |
||
|- |
|- |
||
β | |Prerenal |
+ | | colspan="2" |Prerenal |
|Volume loss (e.g. vomiting, diarrhea, diuretics, hemorrhage, burns)<br />Thirst and reduced fluid intake<br />Heart failure or cirrhosis |
|Volume loss (e.g. vomiting, diarrhea, diuretics, hemorrhage, burns)<br />Thirst and reduced fluid intake<br />Heart failure or cirrhosis |
||
|Weight loss, orthostatic hypotension and tachycardiac, poor skin turgor, signs of heart failure or liver failure |
|Weight loss, orthostatic hypotension and tachycardiac, poor skin turgor, signs of heart failure or liver failure |
||
|- |
|- |
||
β | |Intrinsic renal |
+ | | rowspan="4" |Intrinsic renal |
β | | |
||
β | | |
||
β | |- |
||
|ATN |
|ATN |
||
|History of nephrotoxic medications, hypotension, trauma or myalgias suggestion rhabdo, CT contrast |
|History of nephrotoxic medications, hypotension, trauma or myalgias suggestion rhabdo, CT contrast |
||
Line 128: | Line 130: | ||
|Livedo reticularis, fundoscopy showing malignant hypertension, abdominal bruits |
|Livedo reticularis, fundoscopy showing malignant hypertension, abdominal bruits |
||
|- |
|- |
||
β | |Post-renal |
+ | | colspan="2" |Post-renal |
|Urinary urgency or hesitancy, gross hematuria, polyuria, stones, medications, cancer |
|Urinary urgency or hesitancy, gross hematuria, polyuria, stones, medications, cancer |
||
|Bladder distension, pelvic mass, prostate enlargement |
|Bladder distension, pelvic mass, prostate enlargement |
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
β₯26.5 ΞΌmol/L increase |
<0.5 mL/kg/h for 6-12 hours |
2 | 2 to 2.9 times baseline | <0.5 mL/kg/h for β₯12 hours |
3 | 3 times baseline, or β₯353.6 ΞΌmol/L, or started renal replacement therapy | <0.3 mL/kg/h for β₯24 hours, or anuria for β₯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