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Approach to the Critical Patient
Immediate priorities
Life-threatening complications of AKI
Refractory hyperkalemia
Peaked T waves on ECG
Widened QRS or sine wave pattern
If ECG changes, IV calcium immediately
Severe metabolic acidosis
pH < 7.20
Bicarbonate < 12 mmol/l
Refractory pulmonary edema
Hypoxemia despite diuretics
If unresponsive to medical therapy, emergent dialysis
Uremic emergencies
Encephalopathy
Pericarditis
Bleeding diathesis
Hemodynamic and source threats
Ongoing shock or sepsis
SBP < 90 mmHg
Lactate >= 2 mmol/l
Sepsis as leading cause of ATN
Most common ICU cause of severe AKI
If septic, broad-spectrum antibiotics within 1 hour
Volume depletion driving ischemic injury
Hemorrhage
Vomiting or diarrhea
Early branching decision
Prerenal vs intrinsic vs postrenal
Volume status assessment first
Bladder scan for retention
If obstruction suspected, urgent renal ultrasound
Bilateral hydronephrosis
Palpable bladder
Monitoring and targets
Resuscitation targets
MAP >= 65 mmHg
Norepinephrine first-line vasopressor
Higher MAP target if chronic hypertension
Urine output trend
Oliguria < 0.5 mL/kg/h
Anuria < 0.3 mL/kg/h for >= 24 h as alarm feature
Euvolemia goal
Avoid hypovolemia worsening ischemia
Avoid fluid overload and pulmonary edema
Monitoring bundle
Continuous cardiac monitor for hyperkalemia
Telemetry for K+ 6.0 to 6.5 mmol/l
Serial ECG with treatment response
Serial chemistry
Potassium every 2 to 4 hours when treating
Bicarbonate and creatinine trend
Strict intake and output
Foley for accurate measurement when indicated
Daily weights
Immediate consults and stabilization
Nephrology activation triggers
Need for renal replacement therapy
Refractory hyperkalemia
Refractory acidosis or volume overload
Diagnostic uncertainty
Suspected glomerulonephritis or vasculitis
Unexplained intrinsic AKI
Initial stabilization actions
Discontinue all nephrotoxins immediately
NSAIDs, ACE inhibitors, ARBs
Aminoglycosides and iodinated contrast
Optimize volume status
Isotonic crystalloid for hypovolemia
If septic, address source control
History
Presentation pattern
Hallmark symptoms
Oliguria or anuria
Decreased urine output is the hallmark
Nonoliguric in 30 to 40% especially nephrotoxic ATN
Volume overload symptoms
Edema
Dyspnea or orthopnea
Uremic symptoms
Fatigue and nausea
Confusion in advanced uremia
Precipitating event context
Recent hypotensive episode
Surgery or ICU stay
Hemorrhage or shock
Nephrotoxin exposure
Contrast within 48 to 72 hours
New antibiotics or chemotherapy
Pigment nephropathy clues
Dark or cola-colored urine
Crush injury or prolonged immobilization
Timing and tempo
Onset relative to insult
Ischemic ATN
Develops 24 to 72 hours after insult
Follows sustained hypoperfusion
Aminoglycoside ATN
Appears 5 to 10 days into therapy
Nonoliguric pattern common
Contrast-induced ATN
Peaks at 48 to 72 hours
Often self-limited
Important negatives
Argue against postrenal
No hesitancy or retention
No suprapubic fullness
Argue against AIN
No rash, fever, or eosinophilia
Argue against glomerulonephritis
No gross hematuria
No heavy proteinuria
Risk factors and comorbidities
Host risk factors
Pre-existing CKD
Strongest risk factor for non-recovery
Reduced renal reserve
Advanced age
Reduced GFR baseline
Polypharmacy burden
Comorbid disease
Diabetes mellitus
Heart failure and cirrhosis
Exposure and event risk
Sepsis or septic shock
Accounts for 47% of severe AKI in ICU
Most common cause of ATN in critically ill
Major surgery
Cardiac and vascular procedures highest risk
Multiple nephrotoxin exposure
22% of inpatient AKI meets nephrotoxic criteria
Recurrent AKI in 25% within 12 months
Collateral and medication history
Medication reconciliation
OTC NSAIDs and herbal supplements
Baseline creatinine from prior records
Social and occupational context
Cocaine use causing rhabdomyolysis
Occupational heat exposure
Physical Exam
Vitals and volume status
Vital sign patterns
Hypotension
Ischemic ATN driver
Tachycardia from hypovolemia
Hypertension with pulmonary edema
Volume overload state
Crackles and elevated JVP
Fever
Sepsis or infection precipitant
Volume status assessment as critical first step
Hypovolemia signs
Dry mucous membranes
Flat JVP and orthostatic hypotension
Hypervolemia signs
Jugular venous distension
Peripheral edema and S3 gallop
Organ-system findings
Skin findings
Livedo reticularis
Suggests atheroembolic disease
Blue toes with intact pulses
Maculopapular rash
Suggests acute interstitial nephritis
Track marks
Rhabdomyolysis from drug use
Cardiopulmonary findings
Pericardial friction rub
Uremic pericarditis
Indication for urgent dialysis
Pulmonary crackles
Volume overload
Abdominal and neurologic findings
Abdomen
Palpable bladder suggesting obstruction
Ascites suggesting cirrhosis
Neurologic
Asterixis
Altered mental status from uremic encephalopathy
Differential Diagnosis
AKI category framework
Prerenal azotemia
Most common AKI cause overall
FENa < 1%
Urine osmolality > 500 mOsm/kg
Responds to volume resuscitation
Improvement within 24 to 48 hours
ICD-10 N17.9 acute kidney failure unspecified
Intrinsic AKI
Acute tubular necrosis
Muddy brown granular casts
ICD-10 N17.0 acute kidney failure with tubular necrosis
Acute interstitial nephritis
Fever, rash, eosinophilia
WBC casts; drug-related
Glomerulonephritis
RBC casts and dysmorphic RBCs
Heavy proteinuria with FENa < 1%
Postrenal obstruction
Bilateral hydronephrosis
BPH or pelvic malignancy
ICD-10 N13.4 hydroureter
Dangerous mimics
Hepatorenal syndrome
AKI in cirrhosis
FENa < 0.1% with bland sediment
Responds to vasoconstrictors and albumin
Diagnosis of exclusion
No improvement with albumin challenge
Thrombotic microangiopathy
HUS or TTP
Schistocytes on smear
Thrombocytopenia and elevated LDH
Hematologic emergency
May require plasma exchange
Atheroembolic disease
Post-procedure timing
Livedo reticularis
Eosinophilia and blue toes
Laboratory Tests
Renal function and electrolytes
Basic metabolic panel
Rising creatinine
Diagnosis and KDIGO staging
Compare to baseline value
Elevated BUN
BUN to creatinine ratio
BUN > 112 mg/dL as nonurgent dialysis indication
Hyperkalemia
Most life-threatening complication
Drives ECG and treatment urgency
Low bicarbonate
Metabolic acidosis severity
Anion gap calculation
Additional chemistry
Phosphorus and uric acid
Hyperphosphatemia in tubular injury
Tumor lysis syndrome screen
Calcium
Hypocalcemia with hyperphosphatemia
Hypercalcemia as AKI cause
Urine studies
Urinalysis with microscopy
Muddy brown granular casts
Pathognomonic for ATN
Tubular epithelial cells
Cast differentiation
RBC casts suggest glomerulonephritis
WBC casts suggest interstitial nephritis
Fractional excretion indices
FENa
> 1% suggests ATN; > 2% highly suggestive
Unreliable on diuretics
FEUrea
> 35% suggests ATN
More reliable than FENa when on diuretics
Urine sodium and osmolality
Urine sodium > 40 mEq/L in ATN
Urine osmolality ~350 mOsm/kg isosthenuria
Adjunctive and pigment labs
Pigment nephropathy workup
Creatine kinase and myoglobin
Elevated in rhabdomyolysis
CK often > 5000 with renal risk
Hemolysis panel
LDH, haptoglobin, peripheral smear
Rule out TMA
Hematologic and infection labs
Complete blood count
Anemia possible
Thrombocytopenia suggests TMA
Lactate and cultures when septic
Lactate >= 2 mmol/l as hypoperfusion marker
Blood cultures before antibiotics
Diagnostic Tests
Scoring Systems
KDIGO AKI staging
Stage 1
Creatinine rise >= 0.3 mg/dL or 1.5 to 1.9x baseline
Urine output < 0.5 mL/kg/h for 6 to 12 h
Stage 2
Creatinine 2.0 to 2.9x baseline
Urine output < 0.5 mL/kg/h for >= 12 h
Stage 3
Creatinine >= 3x baseline or >= 4 mg/dL
Need for renal replacement therapy
Urine sediment scoring
Sediment score >= 3
Muddy brown casts and tubular cells
High specificity for ATN
Limitations
Operator-dependent microscopy
Clinical context required
Novel biomarkers
NGAL
Predicts severe AKI
May distinguish ATN from HRS
TIMP-2 x IGFBP-7
FDA-approved for AKI prediction
Limited clinical availability
MRI
MR role in AKI
Limited acute utility
Availability constraints
Time-intensive in unstable patients
Problem-solving indications
Renal vein thrombosis evaluation
Mass characterization without contrast
Gadolinium caution
Nephrogenic systemic fibrosis risk in severe AKI
Avoid group I agents when GFR very low
CT
Non-contrast CT abdomen and pelvis
Indications
Obstruction suspected but ultrasound equivocal
Nephrolithiasis evaluation
Findings
Hydronephrosis and obstructing stone
Perinephric stranding
Contrast considerations
Iodinated contrast risk
Avoid in established ATN when possible
Weigh diagnostic benefit against nephrotoxicity
Mitigation
Pre-hydration with isotonic fluids
Minimize contrast volume
Ultrasound
Renal ultrasound as first-line imaging
Rule out obstruction
Hydronephrosis identifies postrenal cause
Bladder volume for retention
Parenchymal assessment
Normal-sized kidneys with increased cortical echogenicity in ATN
Small kidneys suggest underlying CKD
When imaging may be deferred
Clear ATN picture post-shock with muddy brown casts
No risk factors for obstruction
Point-of-care ultrasound adjuncts
IVC and volume assessment
Fluid responsiveness estimation
Integrate with clinical exam
Bladder scan
Post-void residual for retention
Guides catheterization decision
Disposition
Level of care
Admission indications
All new ATN
Requires inpatient management
Trend creatinine and electrolytes
ICU indications
Hemodynamic instability
Need for renal replacement therapy
Severe hyperkalemia with ECG changes
Telemetry
Moderate hyperkalemia K+ 6.0 to 6.5 mmol/l
Pending treatment response
Observation candidates
Mild Stage 1 AKI
Clear reversible cause such as NSAID use
Creatinine trending down with stable electrolytes
Close outpatient follow-up arranged
Recheck within 1 to 2 weeks
Consultation and follow-up
Nephrology consultation triggers
Stage 3 AKI or unclear etiology
Need for RRT
Pre-existing CKD stage 4 or higher
Inadequate response to supportive care
Suspected glomerulonephritis or vasculitis
Follow-up plan
Recheck labs
Creatinine and electrolytes within 1 to 2 weeks
Nephrology within 1 to 3 months for Stage 2 to 3
Long-term surveillance
Creatinine, proteinuria, blood pressure at 3 months then annually
Counsel on recurrent AKI risk
Treatment
Initial stabilization
Volume optimization
Isotonic crystalloid for hypovolemia
Balanced solution or normal saline
Reassess after each bolus to avoid overload
Diuretics for overload only
Furosemide does not prevent or reverse ATN
Used to manage volume, not improve renal outcome
Remove the insult
Discontinue nephrotoxins
NSAIDs, ACE inhibitors, ARBs
Aminoglycosides and contrast
Treat underlying cause
Antibiotics for sepsis
Relieve obstruction
Hyperkalemia management
Membrane stabilization
Calcium gluconate IV
1 to 2 g (10 to 20 mL of 10%) over 2 to 3 minutes
Repeat if ECG changes persist
Onset within minutes, short duration
Intracellular potassium shift
Insulin with dextrose
Regular insulin 10 units IV
Dextrose 25 g IV if glucose < 14 mmol/l
Monitor for hypoglycemia
Nebulized albuterol
10 to 20 mg nebulized
Additive to insulin
Potassium elimination
Loop diuretic if making urine
Furosemide IV
Potassium binders
Patiromer or sodium zirconium cyclosilicate
Slower onset, not for emergencies
If refractory, emergent dialysis
Definitive potassium removal
Acidosis and volume overload
Metabolic acidosis
Sodium bicarbonate IV
Indicated if pH < 7.20
Caution with sodium and volume load
If refractory acidosis, dialysis
Persistent pH < 7.20 despite therapy
Pulmonary edema and overload
Furosemide
IV bolus 40 to 80 mg, higher in CKD
Continuous infusion if poor bolus response
If diuretic-refractory, ultrafiltration or dialysis
Refractory hypoxemia
Inability to make urine
Renal replacement therapy
Urgent indications
Refractory hyperkalemia
ECG changes despite medical therapy
Persistent K+ rise
Refractory acidosis or pulmonary edema
Unresponsive to medical management
Uremic complications
Pericarditis, encephalopathy, bleeding
Nonurgent indications and timing
Markers favoring initiation
BUN > 112 mg/dL
Oliguria or anuria > 72 hours
Watchful waiting supported by trials
STARRT-AKI, AKIKI, IDEAL-ICU
Early initiation does not improve mortality
40 to 50% of deferred patients never need RRT
Modality selection
CRRT
Preferred in hemodynamic instability
Intermittent hemodialysis
For hemodynamically stable patients
Supportive measures
Medication and nutrition
Renal dose adjustment
Antibiotics, anticoagulants, opioids, digoxin
Avoid further nephrotoxins
Nutritional support
Enteral preferred over parenteral
Protein 0.8 to 1.0 g/kg/day, higher on CRRT
Infection prevention
Minimize invasive devices
Avoid unnecessary lines and catheters
Sepsis causes 30 to 70% of ATN deaths
Therapies of limited or no benefit
Low-dose dopamine not recommended
Fenoldopam not proven to improve outcomes
Special Populations
Pregnancy
Pregnancy-specific considerations
Causes unique to pregnancy
Preeclampsia and HELLP
Pregnancy-related TMA
Physiologic baseline
GFR increased; normal creatinine is lower
Creatinine > 0.8 mg/dL may be abnormal
Medication safety
Avoid ACE inhibitors and ARBs
Avoid NSAIDs especially third trimester
Dialysis approach
More frequent dialysis with lower BUN targets
Maternal-fetal monitoring
Geriatric
Older adult features
Reduced renal reserve
Lower baseline GFR
Creatinine underestimates dysfunction with low muscle mass
Polypharmacy risk
Multiple nephrotoxins
Careful medication reconciliation
Volume sensitivity
Prone to both depletion and overload
Cautious fluid titration
Atypical presentation
Delirium as presenting sign
Higher mortality and non-recovery risk
Pediatrics
Pediatric differences
Common etiologies
Hemolytic uremic syndrome
Sepsis and hypovolemia from gastroenteritis
Staging
pRIFLE and KDIGO pediatric criteria
Estimated GFR by height-based formula
Weight-based therapy
Fluid bolus 10 to 20 mL/kg isotonic crystalloid
Calcium gluconate 60 mg/kg IV for hyperkalemia with ECG changes
Nephrotoxin caution
Aminoglycoside and vancomycin dosing by levels
Avoid NSAIDs in volume depletion
Background
Epidemiology
Burden and causes
ATN is most common intrinsic AKI cause
Ischemic or nephrotoxic tubular injury
Frequently diagnosed presumptively
Sepsis predominates in ICU
47% of severe AKI cases
Major contributor to mortality
Nephrotoxic exposure
22% of inpatient AKI meets nephrotoxic criteria
Recurrent AKI in 25% within 12 months
Outcomes
Recovery
Over 85% with previously normal kidneys recover within 6 to 12 months
Oliguric ATN has worse prognosis than nonoliguric
Mortality
In-hospital mortality ~50% in severe cases needing RRT
Driven largely by underlying illness
Pathophysiology
Mechanisms of tubular injury
Ischemic injury
Sustained hypoperfusion
Tubular epithelial cell death and sloughing
Nephrotoxic injury
Direct tubular toxicity
Aminoglycosides, contrast, cisplatin
Pigment nephropathy
Myoglobin or hemoglobin tubular obstruction
Rhabdomyolysis and hemolysis
Resulting physiology
Tubular dysfunction
Impaired sodium reabsorption raises FENa
Loss of concentrating ability causes isosthenuria
Cast formation
Sloughed cells form muddy brown granular casts
Tubular obstruction reduces GFR
Therapeutic Considerations
Core management principles
Supportive, not curative
No therapy reverses established ATN
Remove insult and support until recovery
Maintain euvolemia
Avoid hypovolemia and overload
Correct electrolytes and acidosis
Evidence on adjuncts
Diuretics
Manage volume but do not improve renal recovery
Cochrane review shows no mortality benefit
Unproven agents
Low-dose dopamine not recommended
Fenoldopam without proven outcome benefit
Dialysis timing
Watchful waiting non-inferior to early initiation
Reserve for urgent indications
Patient Discharge Instructions
copy discharge instructions
Acute kidney injury home care
Take only medications approved by your kidney team
Avoid ibuprofen, naproxen, and other anti-inflammatory drugs
Stay hydrated unless told to limit fluids
Follow any low-potassium and low-salt diet instructions
Warning signs to return to ER
Little or no urine output
Swelling of legs or face or sudden weight gain
Shortness of breath
Confusion or excessive drowsiness
Nausea or vomiting preventing you from drinking
Chest pain or palpitations
Follow-up
Blood test to recheck kidney function within 1 to 2 weeks
Kidney specialist appointment as arranged
Bring an updated list of all medications
Long-term kidney protection
Tell every provider about your AKI history
Ask about hydration before any contrast scan
Keep blood pressure and diabetes well controlled
References
Guidelines and key sources
Major guidelines
KDIGO Clinical Practice Guideline for Acute Kidney Injury
ACR Manual on Contrast Media 2025
VA DoD Primary Care Management of CKD 2025
Landmark trials on dialysis timing
STARRT-AKI trial NEJM 2020
AKIKI and IDEAL-ICU trials
Watchful waiting non-inferior to early RRT
Key reviews and evidence
Ostermann et al, Acute Kidney Injury, Lancet 2025
Abdelhafez et al, FENa diagnostic performance meta-analysis CJASN 2022
Cochrane reviews on diuretics and fenoldopam for AKI
Coding standards
ICD-10 N17.0 acute kidney failure with tubular necrosis
SNOMED CT acute tubular necrosis disorder concept
SymptomDx is an educational tool for medical professionals. It does not replace clinical judgment. Verify all clinical data and drug dosages with authoritative sources.