Acute Kidney Injury: Definitions, Tests, and Imaging for a Systematic Evaluation

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Definition and staging

• KDIGO defines AKI by a serum creatinine rise ≥ 0.3 mg/dL within 48 hours, a rise to ≥ 1.5× baseline within 7 days, or urine output < 0.5 mL/kg/h for 6 hours; the definition deliberately combines creatinine and urine output criteria.
• Stage by whichever criterion is worse: stage 1 = 1.5–1.9× baseline or ≥ 0.3 mg/dL rise, or urine output < 0.5 mL/kg/h for 6–12 hours; stage 2 = 2.0–2.9× baseline, or < 0.5 mL/kg/h for ≥ 12 hours; stage 3 = ≥ 3× baseline, creatinine ≥ 4.0 mg/dL, initiation of renal replacement therapy, or < 0.3 mL/kg/h for ≥ 24 hours or anuria ≥ 12 hours.
• Confirm the true baseline creatinine, chart hourly or per-shift urine output (bladder scan, or a temporary catheter when accurate measurement matters), record daily weights, and repeat the BMP at least daily — every 12 hours if rising fast.

Localizing the lesion: prerenal, intrinsic, or postrenal

• Prerenal and hemodynamic: a focused volume exam (orthostatics, JVP, recent blood pressure trend, net fluid balance), history of vomiting, diarrhea, diuresis, sepsis, or heart failure, and a full nephrotoxin reconciliation — ACE inhibitors and ARBs, NSAIDs, iodinated contrast, vancomycin and piperacillin-tazobactam, aminoglycosides, PPIs, diuretics, SGLT2 inhibitors, and calcineurin inhibitors.
• Postrenal: a post-void residual by bladder scan and a renal and bladder ultrasound for hydronephrosis, stones, and kidney size and echogenicity (small echogenic kidneys point to underlying CKD) — especially in older men and in anyone with anuria, fluctuating urine output, or no clear prerenal or nephrotoxic explanation. NICE advises imaging when the cause is not evident, generally within 24 hours, and urgently when pyonephrosis or obstruction is suspected.
• Intrinsic: urinalysis with microscopy of fresh sediment. Bland sediment or hyaline casts → prerenal or hemodynamic; muddy-brown granular and renal tubular epithelial cell casts → acute tubular necrosis; white cell casts, pyuria, or eosinophiluria with rash, fever, or eosinophilia → acute interstitial nephritis; dysmorphic red cells, red cell casts, and proteinuria → glomerulonephritis.
• Send a urine protein-to-creatinine ratio. If glomerulonephritis is suspected, add ANA, ANCA, anti-GBM, C3 and C4, SPEP and UPEP with free light chains, and hepatitis serologies, and consult nephrology urgently. If myeloma, rhabdomyolysis, or tumor lysis fits the picture, add CK, uric acid, phosphate, LDH, and calcium.

Urine indices: FENa and FEUrea

• FENa < 1% suggests prerenal physiology and > 2% suggests tubular injury, but it is unreliable with diuretics and in CKD, and it can also be < 1% early in contrast-associated injury and in glomerulonephritis. Do not let it override the sediment and the clinical course.
• FEUrea is lower in prerenal AKI (urea reabsorption is enhanced along with sodium) and higher in intrinsic AKI, and it is less affected by diuretics than FENa — a value below about 35% favors prerenal physiology. Both indices perform imprecisely in mixed or established AKI.

Acute management while the workup runs

• Stop the insults now: discontinue NSAIDs and hold ACE inhibitors or ARBs until creatinine plateaus or improves; avoid further iodinated contrast unless essential and choose non-nephrotoxic antibiotics where alternatives exist. If contrast is required later, weigh need against risk and give isotonic crystalloid volume expansion in high-risk patients.
• Volume: assess clinically (JVP, orthostatics, passive leg raise, point-of-care ultrasound). In a patient who is hypovolemic or volume-responsive without pulmonary congestion, give isotonic crystalloid in 500–1000 mL boluses with reassessment of urine output and exam; KDIGO recommends crystalloid over colloid. Do not repeat boluses if urine output does not respond or congestion develops, and avoid indiscriminate fluid loading in a euvolemic patient. In volume overload, diurese rather than fluid-load. Low-dose dopamine is not recommended for prevention or treatment of AKI.
• Perfusion: target a MAP ≥ 65 mmHg (higher if chronically hypertensive), and hold or reduce other agents that lower GFR or renal perfusion (ARBs, SGLT2 inhibitors temporarily, high-dose diuretics, aggressive antihypertensives). Loop diuretics do not treat AKI or convert oliguria — use them only for volume overload.
• Electrolytes and acid-base: stop potassium supplements, potassium-sparing agents, and trimethoprim; a low-potassium diet; an EKG if potassium reaches 6.0 mEq/L or symptoms develop. Treat acidosis supportively and consider sodium bicarbonate if bicarbonate falls below roughly 15–18 mEq/L with worsening acidemia.
• Renally dose every medication (antibiotics, anticoagulants, gabapentinoids, metformin, opioids) to the current eGFR, check drug levels where applicable, hold metformin while creatinine is rising, and avoid phosphate-containing bowel preparations.

Inpatient course, consultation, and biopsy

• Reassess daily for recovery versus progression. Most hemodynamic, NSAID-related, and contrast-associated injury improves within 3–7 days once the insults are removed; persistent or worsening AKI beyond 5–7 days without an explanation should prompt nephrology input and reconsideration of interstitial nephritis, glomerulonephritis, or obstruction.
• Consult nephrology when creatinine keeps rising despite nephrotoxin withdrawal and volume optimization or fails to improve within about 48–72 hours, the etiology remains unclear after urinalysis, urine indices, and ultrasound, the sediment is active (red cell casts, heavy proteinuria), vasculitis, myeloma, or thrombotic microangiopathy is suspected, or renal replacement therapy may be needed. NICE also advises referral for AKI with no clear cause, stage 3 AKI, and AKI complicating CKD stage 4–5 or a kidney transplant.
• Kidney biopsy is reserved for suspected glomerulonephritis or vasculitis, steroid-candidate interstitial nephritis, and unexplained non-recovering AKI. For suspected drug-induced interstitial nephritis, stopping the culprit drug is the key step; corticosteroids follow nephrology input, generally with biopsy confirmation.
• Rechallenge: once creatinine returns toward baseline and the patient is euvolemic and normotensive, restart the ACE inhibitor or ARB when there is a strong indication (HFrEF, proteinuric CKD, post-MI) with a BMP in 5–7 days; NSAIDs should be avoided permanently.
• Document the episode and peak stage. AKI raises the risk of CKD and recurrent AKI, so arrange outpatient creatinine, electrolytes, blood pressure, and urine protein within 1–2 weeks of discharge, and teach sick-day rules (hold ACE inhibitor or ARB, diuretics, NSAIDs, metformin, and SGLT2 inhibitors during vomiting, diarrhea, or poor intake).

Monitoring and disposition

• Daily (twice daily if unstable) BMP with potassium, bicarbonate, BUN and creatinine, magnesium, and phosphorus; strict intake and output, hourly urine output if oliguric, and daily weights.
• Telemetry if potassium is ≥ 6.0 mEq/L, rising rapidly, or EKG changes are present; otherwise ward-level care is appropriate for a hemodynamically stable patient.
• Discharge when creatinine is stable or improving, urine output is adequate, potassium and acid-base status are stable off nephrotoxins, and the culprit exposures and medication plan are documented. Repeat a BMP within 48–72 hours if creatinine is not yet at baseline, and arrange nephrology follow-up if it fails to return near baseline.

Escalate care if

• A refractory indication for renal replacement therapy appears — refractory hyperkalemia, refractory metabolic acidosis, diuretic-refractory volume overload with hypoxemia, uremic pericarditis, encephalopathy, or bleeding, or a dialyzable toxin — urgent nephrology and ICU involvement. The decision rests on the overall clinical trajectory, not a single BUN or creatinine value; without these indications there is no benefit to starting dialysis on numbers alone.
• Ultrasound shows hydronephrosis or the post-void residual is elevated — immediate bladder catheter and urgent urology for decompression, with monitoring for post-obstructive diuresis.
• Sediment shows dysmorphic red cells or red cell casts, significant proteinuria, hemoptysis, or systemic features — urgent nephrology consult for serologies and likely biopsy.
• Blood pressure falls, lactate rises, or hypoperfusion develops — treat as shock with crystalloid resuscitation and vasopressors and escalate the level of care.

Duration

Withdraw nephrotoxins immediately and reassess renal function daily. Expect improvement over 3–7 days for hemodynamic or contrast-associated tubular injury, and escalate the evaluation if there is no recovery by day 5–7.

Caveats

• This approach assumes no indwelling catheter obstruction, no advanced baseline CKD, and no sepsis — reassess if any is present.
• A fluid challenge is contraindicated with pulmonary congestion or decompensated heart failure; treat with diuresis rather than volume expansion in that setting.
• Loop diuretics should not be used to prevent or treat AKI itself or to convert oliguric to non-oliguric AKI, only for volume overload; low-dose dopamine is not recommended for AKI.
• Avoid further iodinated contrast, NSAIDs, and nephrotoxic antibiotics while creatinine is rising; hold metformin and SGLT2 inhibitors during the acute episode.
• Do not delay renal replacement therapy when a life-threatening indication emerges.

References

1. Reading between the (guide)lines — the KDIGO practice guideline on acute kidney injury in the individual patient. (2013) · Guideline-derived“AKI is defined as any of the following: Increase in SCr by ≥0.3 mg/dl within 48 h; or increase in SCr to ≥1.5 times baseline, which is known or presumed to have occurred within the prior 7 days; or Urine volume of 0.5 ml/kg/h for 6 h.”
2. Assessing the utility of fractional excretion of urea in distinguishing intrinsic and prerenal acute kidney injury in hospitalised patients: a systematic review and meta-analysis. BMJ Open. (2026) · Systematic review“In prerenal AKI, where there is a physiological response to conserve sodium, urea reabsorption is also enhanced, leading to a lower FEUN. Conversely, in intrinsic AKI, the renal tubules' capacity to reabsorb urea is impaired, resulting in a higher FEUN level.”