- Adult ED approach: identify dangerous complications, assess volume status and obstruction, then determine the cause.
The Algorithm...
01 AKI?
- Compare creatinine with baseline; assess urine output and recent illness. AKI, CKD, or both?
02 Immediate Threat?
- Assess potassium / ECG, pulmonary edema, acidosis, uremic symptoms, and shock.
- Treat complications immediately; involve nephrology early when dialysis may be needed. See Emergent Complications.
03 Cause?
- Prerenal / Hemodynamic: Volume loss, impaired circulation, medication effect.
- Intrinsic: Tubular injury, nephritis, pigment injury, vascular disease.
- Postrenal: Retention or upper-tract obstruction.
- History / examination + chemistry + urine microscopy ± ultrasound direct the workup.
04 Treat
- Depleted: Crystalloid and reassessment.
- Congested: Diuresis / cardiac treatment.
- Obstructed: Drainage; antibiotics when infected.
- Intrinsic: Correct the insult, review medications, and involve nephrology when indicated.
05 Reassess / Destination
- Repeat urine output, volume assessment, creatinine, potassium, and bicarbonate.
- Discharge: Selected mild, improving injury with reliable repeat testing.
- Monitored Admission: Significant / persistent AKI or unresolved concern.
- ICU Admission: Shock, respiratory failure, or unstable metabolic complications.
Confirm AKI / Assess Severity
Acute, Chronic, Or Both?
- Obtain prior creatinine values, recent urine output, and the timing of illness / exposures. An isolated elevated creatinine does not establish acuity.
- Creatinine may lag behind injury. Preserved urine output does not exclude AKI, and calculated eGFR is unreliable while creatinine is changing rapidly. AACC — Laboratory Assessment.
KDIGO Definition
- Creatinine rise ≥0.3 mg/dL within 48 hours, or ≥1.5 × baseline within seven days.
- Alternatively, urine output <0.5 mL/kg/hour for ≥6 hours.
KDIGO Stage
| Stage | Criteria |
|---|---|
| Stage 1: | Creatinine 1.5–1.9 × baseline or rise ≥0.3 mg/dL; urine output <0.5 mL/kg/hour for 6–12 hours. |
| Stage 2: | Creatinine 2.0–2.9 × baseline; urine output <0.5 mL/kg/hour for ≥12 hours. |
| Stage 3: | Creatinine ≥3 × baseline, rise to ≥4 mg/dL meeting AKI criteria, or initiation of dialysis; urine output <0.3 mL/kg/hour for ≥24 hours or anuria ≥12 hours. |
Use the worst qualifying creatinine or urine-output criterion. Stage describes severity—not an automatic dialysis decision. KDIGO — Definition / Staging.
R/O Emergent Complications
Hyperkalemia
- Obtain an ECG / monitoring for significant AKI or suspected hyperkalemia. A normal ECG does not exclude dangerous hyperkalemia. Repeat a questionable hemolyzed sample without delaying treatment when concern is high.
- ECG Changes / Cardiotoxicity: Calcium gluconate 1 g IV; reassess the ECG and repeat after 5–10 minutes if changes persist. Calcium protects the myocardium; it does not lower potassium.
- Shift Potassium: Regular insulin 10 units IV + dextrose 25 g, adjusted to glucose and the institutional protocol; consider lower insulin dosing in patients at high hypoglycemia risk. Albuterol 10–20 mg nebulized is an adjunct.
- Remove Potassium: Arrange dialysis for severe refractory / recurrent hyperkalemia or when adequate removal cannot otherwise be achieved. Diuretics or binders are selected adjuncts—not substitutes for emergency stabilization. ACEP-Sponsored Consensus.
- Reassess: Recheck potassium around one hour after shifting treatment, then follow for rebound. Monitor glucose serially for several hours; kidney failure increases delayed hypoglycemia risk. KDIGO — Acute Hyperkalemia.
Pulmonary Edema / Severe Acidosis
- Pulmonary Edema: Oxygen / NIV as needed; IV loop diuretic for congestion. Persistent respiratory compromise despite treatment requires urgent dialysis assessment.
- Acidosis: Obtain a blood gas and treat the cause. Consider bicarbonate for selected severe metabolic acidemia, particularly pH ≤7.2 with moderate–severe AKI; assess ventilation and sodium / volume load.
- BICARICU-2: Bicarbonate reduced dialysis use but did not reduce 90-day mortality. This does not establish benefit for every low bicarbonate result. Jung 2025.
Urgent Dialysis? — AEIOU
- Acidosis: Severe and refractory to appropriate treatment.
- Electrolytes: Dangerous / recurrent hyperkalemia without adequate control or elimination.
- Intoxications: Selected dialyzable toxins; coordinate with toxicology / nephrology.
- Overload: Pulmonary edema / respiratory compromise refractory to treatment.
- Uremia: Encephalopathy, pericarditis, or clinically significant uremic bleeding.
- A creatinine of 7 mg/dL alone does not mandate dialysis. The complication, clinical course, and ability to maintain safe fluid / electrolyte balance determine urgency. KDIGO — Dialysis Indications.
- STARRT-AKI: Accelerated dialysis without conventional urgent indications did not improve 90-day survival. STARRT-AKI 2020.
Determine The Cause
History / Examination
- Perfusion / Volume: Vomiting, diarrhea, poor intake, bleeding, sepsis, hypotension; assess BP, perfusion, JVP, edema, and lungs.
- Obstruction: Retention, weak stream, stones, pelvic malignancy, solitary kidney, or catheter dysfunction.
- Intrinsic Disease: Rash / arthritis, hematuria, pulmonary symptoms, muscle injury, or a recent medication / toxin exposure.
- Medications: Review NSAIDs, ACE inhibitors / ARBs, diuretics, antibiotics, PPIs, supplements, and recent contrast. Identify timing, dose, and combinations. KDIGO — Evaluation.
Prerenal / Hemodynamic
- Volume Depletion: Vomiting / diarrhea, poor intake, hemorrhage, or excessive diuresis → reduced circulating volume and kidney perfusion. Correct the deficit and ongoing losses.
- Volume Overload / Impaired Circulation: CHF may impair filtration through reduced forward flow, elevated renal venous pressure, or both—even with edema and a preserved BP.
- Congestion: Increased venous / interstitial pressure can impair kidney blood flow and filtration. Diuresis may improve kidney function by relieving congestion while maintaining perfusion; it does not directly repair tubular injury. AHA — Cardiorenal Syndrome.
- Other Hemodynamic Causes: Shock, cirrhosis with reduced effective arterial circulation, and medication-related changes in renal autoregulation. Ascites / edema alone does not establish the right fluid strategy.
- Bland urine sediment and improvement after correcting the hemodynamic problem support the mechanism; hemodynamic and structural injury may coexist. KDIGO — AKI Conference.
- Assess Both Congestion And Perfusion: Depleted → fluid replacement; congested and perfusing → decongestion; congested with hypoperfusion → circulatory support and individualized fluid removal. See Treatment. AHA/ACC/HFSA — HF Management.
Intrinsic Renal
- Tubular Injury / ATN: Ischemia, sepsis, nephrotoxins, or pigments; tubular epithelial cells / muddy brown casts support the diagnosis.
- Glomerulonephritis: Hematuria + proteinuria, dysmorphic RBCs / RBC casts, hypertension, edema, or rapidly rising creatinine.
- Interstitial Nephritis: Recent medication exposure, pyuria / WBC casts; rash, fever, and eosinophilia may be absent.
- Pigment Injury: Elevated CK with muscle injury; dipstick blood with few RBCs suggests myoglobin or hemoglobin rather than true hematuria.
- Vascular / TMA: AKI with thrombocytopenia and hemolysis requires urgent evaluation.
- Pulmonary–Renal Pattern: Active urine sediment + hypoxemia / infiltrates ± hemoptysis warrants urgent nephrology / pulmonary assessment. AACC — Urine Microscopy.
Postrenal
- Assess bladder outlet obstruction, bilateral ureteral obstruction, or obstruction of a solitary functioning kidney.
- Bladder Scan / Catheter Check: Retention versus reduced urine production.
- Renal Ultrasound: Hydronephrosis / upper-tract obstruction; persistent suspicion despite a negative study may require CT or urologic evaluation. Early obstruction may not yet be dilated. AUA — Urologic Emergencies.
Laboratory Testing / Imaging
- BMP / CMP: Creatinine / BUN, potassium, bicarbonate, sodium; consider calcium, magnesium, and phosphate with significant injury.
- UA / Microscopy: Blood, protein, casts, infection, and pigment clues; quantify urine protein when glomerular disease is suspected.
- CBC: Anemia, infection, or thrombocytopenia. Add blood gas, lactate, CK, cultures, and pregnancy testing according to the presentation.
- Suspected GN / TMA: Discuss focused serologies or hemolysis studies with nephrology / hematology; do not delay consultation for results.
- Imaging: Bladder / renal ultrasound for obstruction; lung / cardiac POCUS or CXR for congestion; additional imaging follows the suspected cause. KDIGO — Evaluation.
Urine Indices — Supporting Evidence
- FeNa <1%: May support prerenal physiology, particularly without CKD or recent diuretics. It does not prove fluid responsiveness.
- FeUrea / BUN:Creatinine: Consider selectively; neither reliably settles the cause. Interpret with medications, urine sediment, and the clinical course. FeNa 2022 · FeUrea 2024.
Treat The Cause
Volume Depletion / Shock
- Hypovolemia: Isotonic crystalloid, often a balanced solution; a 250–500 mL challenge is a practical starting option when volume tolerance is uncertain. Substantial depletion / shock may require more rapid resuscitation.
- Reassess perfusion, BP, urine output, lungs, and ongoing losses. AKI does not prohibit necessary fluid; persistent oliguria does not justify unlimited fluid. KDIGO — Fluid Assessment.
- Septic Shock: Antibiotics / source control, individualized crystalloid resuscitation, and norepinephrine when indicated. Follow the sepsis pathway rather than a universal AKI fluid prescription. SSC 2026.
Congestion / Cardiorenal
- Treat heart failure and impaired perfusion; use IV loop diuretics for clinically important overload.
- Diuretics relieve congestion; increasing urine output does not itself repair tubular injury. Assess dialysis if overload remains refractory. KDIGO — Diuretics.
Obstruction
- Retention: Decompress the bladder; confirm drainage and monitor output.
- Infected Upper-Tract Obstruction: Antibiotics + urgent urologic drainage, usually stent or nephrostomy—not antibiotics alone. AUA — Stone Guidance.
- After decompression, monitor brisk diuresis, BP, and electrolyte losses; substantial ongoing output may require admission.
Intrinsic Injury
- ATN: Correct the initial insult and support perfusion. Creatinine may remain elevated after circulation improves; repeated fluid will not reverse established injury in a euvolemic / overloaded patient.
- GN / Vasculitis / TMA: Urgent nephrology ± hematology; coordinate serologies, biopsy, and disease-specific treatment.
- Suspected AIN: Stop the likely offending drug when feasible; nephrology for significant or persistent injury.
- Rhabdomyolysis: Goal-directed crystalloid and electrolyte monitoring. Preventive benefit from bicarbonate / mannitol is unproven; reserve these for a separate indication. AAST 2022.
Medications / Contrast
- Stop avoidable nephrotoxins and adjust renally cleared medications. Review NSAIDs, antibiotics, supplements, and potentially accumulating sedatives / analgesics.
- Consider temporary medication holds according to perfusion, potassium, and illness. Distinguish ACE inhibitor / ARB hemodynamic effects from direct toxicity; do not automatically stop needed diuresis in congestion.
- Review metformin and SGLT2 inhibitors during significant acute illness; specify a reassessment / restart plan for held medications. KDIGO 2024 — Medication Management.
- Essential Contrast CT: AKI requires risk–benefit assessment, not automatic cancellation. Do not delay imaging needed for a life-threatening diagnosis solely because creatinine is elevated; consider hydration when appropriate and tolerated. ACR–NKF 2020.
Reassessment / Disposition
- Recheck creatinine, potassium / bicarbonate, urine output, perfusion, and congestion according to severity. Confirm that obstruction and medication risks have been addressed.
- Involve nephrology early for significant / worsening AKI, persistent oliguria, suspected GN / TMA, or possible dialysis need.
Discharge
- Selected mild, improving AKI with stable physiology, adequate urine output / oral intake, a plausible reversible cause, and no unresolved dangerous findings.
- Arrange repeat creatinine / electrolytes and a clinician responsible for reviewing them. 24–72 hours is a practical interval for selected low-risk patients—not a universal discharge rule; higher-risk patients need earlier reassessment or admission.
- Provide medication instructions and return precautions for reduced urine, dyspnea, weakness, confusion, or worsening illness. Reassess kidney recovery / CKD risk by approximately three months. KDIGO — Follow-Up.
Monitored Admission
- Significant / progressive AKI, persistent oliguria, electrolyte disturbance, unresolved obstruction, active urine sediment, or important systemic illness.
- Serial testing, IV treatment, nephrology evaluation, or reliable follow-up cannot be arranged safely outside the hospital.
ICU Admission
- Shock, unstable hyperkalemia / dysrhythmia, refractory acidemia, respiratory failure from overload, or severe uremic neurologic complications.
- Arrange urgent dialysis where indicated; the care setting follows instability, support requirements, and local capabilities—not creatinine alone.
In The Pit
- Immediate Threat: Potassium / ECG, pulmonary edema, severe acidosis, and uremic symptoms first.
- Obstruction: Check the bladder; infected obstruction needs antibiotics and drainage.
- Volume: Depleted → fluid; congested → decongestion. Reassess either way.
- Intrinsic Disease: Active sediment / proteinuria, hemolysis, or pulmonary–renal findings → early nephrology.
- ATN: Restore perfusion; do not chase persistent oliguria with repeated fluid once adequately resuscitated.
- Disposition: Complications, urine output, trajectory, and follow-up—not one creatinine value.
Must-Read References
View Full References
- KDIGO 2012 — AKI Guideline — Definition, staging, complication management, and follow-up. The 2026 update remains in preparation.
- Rafique 2021 — ACEP-Sponsored Hyperkalemia Consensus — ED stabilization, potassium removal, and reassessment. ACEP Algorithm.
- STARRT-AKI 2020 — Dialysis timing when emergency indications are absent.
- ACR–NKF 2020 — Iodinated Contrast — Necessary imaging in patients with kidney disease.
- AUA — Urologic Emergencies / Stone Guideline — Retention, obstruction, and drainage priorities.
Additional Cited Guidance
- AHA 2019 — Cardiorenal Syndrome — Forward flow, venous congestion, and heart–kidney interactions.
- AHA/ACC/HFSA 2022 — HF Management — Decongestion, perfusion support, and interpretation of mild renal-function changes during treatment.
- AACC 2021 — Creatinine, urine microscopy, and diagnostic limitations.
- KDIGO Conference 2020 — Volume assessment and AKI management.
- KDIGO 2024 — Medication Management — Medication review and restart planning in CKD / acute illness.
- KDIGO Hyperkalemia 2020 — Potassium rebound and glucose monitoring.
- BICARICU-2 2025 — Bicarbonate in severe metabolic acidemia with AKI.
- FeNa 2022 · FeUrea 2024 — Limits of fractional-excretion testing.
- AAST 2022 — Rhabdomyolysis — Goal-directed fluid and complication management.
- SSC 2026 — Sepsis-specific resuscitation and kidney-support guidance.