# Acute Kidney Injury

Acute kidney injury requires immediate staging, cause-directed evaluation, and prevention of hyperkalemia, acidosis, volume complications, and drug toxicity. This review prioritizes KDIGO-based diagnosis, practical initial testing, hemodynamic and medication decisions, escalation, kidney replacement therapy, and post-AKI follow-up.

**Clinical question:** How should physicians diagnose, stage, evaluate, stabilize, and monitor adults with acute kidney injury?

Updated: 2026-08-20T23:19:02.640821Z

## What matters in practice
- Diagnose AKI when serum creatinine rises by at least 0.3 mg/dL within 48 hours, reaches at least 1.5 times baseline within 7 days, or urine output is below 0.5 mL/kg/h for at least 6 hours; use the higher creatinine- or urine output-derived KDIGO stage. [1][3]
- The immediate priorities are to identify sepsis or shock, assess effective circulating volume and obstruction, stop or adjust kidney-relevant medications, obtain urinalysis, and monitor creatinine, potassium, bicarbonate, and urine output. [1][3]
- Treat hypovolemia with reassessed crystalloid boluses rather than fixed-volume resuscitation; avoid continued fluids once euvolemia is reached or congestion emerges. [1][5]
- Dialysis is indicated for refractory hyperkalemia, severe refractory acidosis, refractory volume overload, uremic end-organ complications, or selected dialyzable poisonings—not for a creatinine threshold alone. [1]
- Loop diuretics do not treat intrinsic AKI or improve kidney recovery; reserve them for clinically important volume overload in a hemodynamically stable patient. [1]

## Confirm AKI and stage severity

Creatinine kinetics lag injury; urine output can establish AKI earlier but requires reliable measurement.

Use KDIGO criteria: increase in serum creatinine of at least 0.3 mg/dL within 48 hours; increase to at least 1.5 times baseline within 7 days; or urine output below 0.5 mL/kg/h for at least 6 hours. AKI may be nonoliguric. Historical creatinine is essential; when no baseline exists, repeat testing and the clinical context are central to distinguishing AKI from chronic kidney disease. [3][15]

Assign the higher stage reached by serum creatinine or urine output. Worsening stage predicts greater mortality and kidney replacement therapy requirement. Creatinine may rise approximately 24 hours after injury, whereas oliguria can be an earlier but less reliably captured signal. [3]
- Obtain or verify a baseline creatinine from prior stable measurements whenever possible. [3]
- Do not use the BUN:creatinine ratio alone to assign a prerenal versus intrinsic cause; critical illness, gastrointestinal bleeding, corticosteroids, and protein intake confound interpretation. [3]
- A new creatinine rise after trimethoprim may reflect inhibited tubular creatinine secretion rather than reduced GFR; interpret in clinical context. [3]

*KDIGO AKI staging criteria. [1][3]*

| Stage | Serum creatinine | Urine output |
| --- | --- | --- |
| 1 | Increase of at least 0.3 mg/dL within 48 hours or 1.5-1.9 times baseline | Below 0.5 mL/kg/h for at least 6 hours |
| 2 | 2.0-2.9 times baseline | Below 0.5 mL/kg/h for at least 12 hours |
| 3 | At least 3 times baseline, serum creatinine at least 4.0 mg/dL, or initiation of kidney replacement therapy | Below 0.3 mL/kg/h for at least 24 hours or anuria for at least 12 hours |

## Evaluate cause while stabilizing reversible threats

AKI is a syndrome; the cause may be multifactorial and determines definitive treatment.

Immediately assess hemodynamics, volume status, infection, exposure to nephrotoxins, medication changes, surgical or vascular events, rhabdomyolysis, and symptoms of urinary retention or upper-tract obstruction. Common drivers are sepsis, hypovolemia or hypotension, and nephrotoxins; prolonged hypoperfusion can progress to acute tubular injury. [3][4]

Order serum creatinine, electrolytes including potassium, bicarbonate, urea, complete blood count, and targeted studies driven by the phenotype. Obtain an ECG promptly for substantial hyperkalemia or suspected electrical effects. If infection is possible, obtain cultures and initiate source-directed sepsis care without delaying stabilization. [1][3]

Perform urine dipstick testing for blood, protein, leukocyte esterase, nitrites, glucose, and specific gravity. Blood plus protein without urinary tract infection or catheter trauma should prompt concern for glomerular disease and early nephrology involvement; send urine culture when infection is plausible. Fresh urine microscopy can add value: granular casts support tubular injury, red-cell casts suggest glomerulonephritis or vasculitis, and oxalate crystals suggest ethylene glycol exposure. [3]
- Check creatine kinase when rhabdomyolysis is suspected. [3]
- With thrombocytopenia, obtain blood film and lactate dehydrogenase when thrombotic microangiopathy is a concern. [3]
- For suspected pulmonary-renal syndrome, nephritic urine findings, rapidly progressive dysfunction, or unexplained AKI, pursue targeted serologies and urgent nephrology consultation; biopsy may be required. [1][3]

### Imaging and obstruction

Renal ultrasonography is not required when a clear alternative cause is present, but obtain it when AKI is unexplained or obstruction, pyelonephritis, or pyonephrosis is suspected. Obtain ultrasound within 24 hours for suspected obstruction and within 6 hours for suspected pyonephrosis because infected obstruction can rapidly cause septic shock. [3]
- If bladder outlet obstruction cannot be promptly excluded clinically or by ultrasound, catheterization can be diagnostic and therapeutic. [1][3]
- Urgently involve urology or interventional radiology for pyonephrosis, bilateral upper-tract obstruction, obstruction of a solitary kidney, or obstruction-associated complications. [1]

*Cause-directed findings that change next steps. [1][3]*

| Clinical pattern | High-value findings | Immediate action |
| --- | --- | --- |
| Hypoperfusion or sepsis | Hypotension, fluid loss, infection, poor perfusion, rising lactate or oliguria | Treat source and hemodynamics; reassess fluid responsiveness and congestion after each intervention. [1][3] |
| Obstruction | Retention, palpable bladder, lower urinary tract symptoms, hydronephrosis, bilateral obstruction, solitary kidney | Bladder drainage if indicated; urgent imaging and urologic or radiologic decompression when upper-tract obstruction is present. [1][3] |
| Glomerular or vascular process | Protein plus blood without benign explanation, active sediment, edema or hypertension, rash, arthralgia, hemoptysis | Urgent nephrology evaluation; targeted immunologic testing and possible biopsy. [1][3] |
| Tubular, toxic, or pigment injury | Nephrotoxic exposure, shock, granular casts, rhabdomyolysis or hemolysis | Stop exposure, support perfusion, treat the precipitant, and monitor complications. [1][3] |

## Stabilize perfusion without causing congestion

There is no established drug that reverses typical hypoperfusion- or sepsis-associated AKI.

Supportive management is cause-directed: correct hypovolemia, treat sepsis, relieve obstruction, avoid recurrent kidney insults, and monitor volume status and electrolytes closely. Both under-resuscitation and positive fluid balance are harmful; fluid orders should be reassessed frequently rather than continued automatically. [1][5]

For clinically hypovolemic adults, crystalloid is preferred. A practical approach is an initial 500 mL bolus over 15 minutes, followed by reassessment of blood pressure, pulse, capillary refill, jugular venous pressure, pulmonary findings, and urine output; smaller boluses may be appropriate in heart failure. Balanced crystalloids are generally preferred, although normal saline may be selected when hyperkalemia is confirmed or strongly suspected. [1]

Persistent severe hypotension after adequate volume resuscitation warrants critical care escalation and vasopressor support with continuous hemodynamic monitoring. A mean arterial pressure of at least 65 mm Hg is a reasonable initial target, individualized to baseline blood pressure and clinical context; norepinephrine is the usual first vasopressor. Do not use low-dose dopamine to treat AKI. [1]
- Measure intake, output, weight, hemodynamic trajectory, and daily electrolytes at minimum for hospitalized established AKI; increase frequency with severe AKI or dynamic complications. [1][3]
- Do not place a urinary catheter solely because AKI is present; use it when precise fluid balance is crucial, obstruction is suspected, or the patient cannot reliably void into a collection device. [1][3]
- Avoid hydroxyethyl starch for resuscitation in critically ill patients because of kidney safety concerns. [5]

## Review every medication and treat volume overload selectively

Drug accumulation and iatrogenic hemodynamic injury are common, preventable contributors to morbidity.

Stop avoidable nephrotoxins and reassess all medications for renal clearance, current kidney function, and evolving volume status. NSAIDs, aminoglycosides, and iodinated contrast are common nephrotoxic exposures. In hypotension or dehydration, ACE inhibitors, angiotensin receptor blockers, diuretics, and other antihypertensives may worsen reduced filtration reserve and often require temporary withholding. [1][3]

Dose adjustment is required for drugs cleared by the kidneys; clinically important examples include insulin, opioids, digoxin, and gabapentin. Medication reconciliation should include over-the-counter agents, supplements, and recent antimicrobials. At discharge, document which chronic therapies were withheld, a plan for reintroduction, and follow-up creatinine and potassium testing. [1]

Use loop diuretics only to manage clear volume overload, including pulmonary edema, and not to convert oliguric AKI to nonoliguric AKI or accelerate recovery. Stop if there is no response and do not allow diuretic trials to delay definitive kidney support when overload is refractory. [1]
- Avoid diuretics in hypovolemia or hypotension. [1]
- Fluid restriction and sodium restriction may be necessary with congestion; escalate early if pulmonary edema is refractory. [1]
- Restart disease-modifying heart failure therapy when clinically appropriate after stabilization, with a documented laboratory monitoring plan. [1]

## Recognize complications requiring urgent kidney support

Treat immediately reversible complications while arranging nephrology or critical care support.

Hyperkalemia requires ECG assessment and cardiac monitoring when clinically significant. Immediate intravenous calcium provides membrane stabilization when severe hyperkalemia or ECG changes are present; insulin with glucose shifts potassium intracellularly, and nebulized beta-agonist can be adjunctive. These measures do not remove potassium; identify and reverse the cause, stop potassium-raising drugs, and arrange dialysis when hyperkalemia is refractory. [1]

Consider intravenous sodium bicarbonate for severe metabolic acidosis only with expert supervision because sodium load, volume overload, hypernatremia, and ionized hypocalcemia can complicate therapy. Refractory acidosis, especially with volume overload, should prompt kidney replacement therapy rather than repeated bicarbonate administration. [1]

Do not initiate kidney replacement therapy from an isolated creatinine, urea, or potassium value. The decision integrates biochemical trajectory, urine output, catabolic burden, fluid needs, reversible cause, organ dysfunction, and patient-centered goals. [1]
- Urgently seek kidney replacement therapy for refractory hyperkalemia, particularly potassium above 6.5 mmol/L; refractory acidosis, particularly pH below 7.15; refractory volume overload with or without pulmonary edema; uremic pericarditis, encephalopathy, or bleeding; and selected poisonings such as lithium or ethylene glycol. [1]
- Intermittent hemodialysis is generally used for hemodynamically stable patients; continuous kidney replacement therapy is often selected when hemodynamic instability limits rapid solute or fluid shifts. Trials have not shown a consistent mortality advantage of one modality over the other. [1]

*Complications that require action beyond routine monitoring. [1]*

| Complication | Immediate management | Escalate to kidney replacement therapy when |
| --- | --- | --- |
| Hyperkalemia | ECG and cardiac monitoring; intravenous calcium for electrical instability; insulin with glucose and adjunctive beta-agonist as appropriate; stop contributory drugs. [1] | Severe or persistent hyperkalemia does not respond promptly to medical therapy. [1] |
| Metabolic acidosis | Treat the underlying cause; consider expert-supervised bicarbonate in selected severe acidosis without volume overload. [1] | Acidosis is refractory, especially at pH below 7.15 or when bicarbonate is unsafe because of overload. [1] |
| Pulmonary edema or volume overload | Stop unnecessary fluids; provide oxygen and pharmacologic decongestion when hemodynamically appropriate. [1] | Hypoxemia or overload persists despite medical treatment. [1] |
| Uremic syndrome or poisoning | Assess for encephalopathy, pericarditis, bleeding, neuropathy, and dialyzable toxins. [1] | End-organ uremic manifestations or a dialyzable toxic exposure is present. [1] |

## Use nephrology consultation selectively and plan post-AKI surveillance

Stage, uncertainty, treatment response, and recovery trajectory determine consultation urgency.

Urgently involve nephrology for stage 3 AKI, uncertain cause, suspected glomerulonephritis, vasculitis, tubulointerstitial nephritis, myeloma, transplant recipients, advanced pre-existing CKD, refractory complications, or anticipated kidney replacement therapy. Immediate critical care and nephrology involvement is appropriate for severe metabolic complications, hemodynamic instability, or multiorgan failure. [1]

Recovery should not be assumed from hospital discharge creatinine alone. AKI is associated with later CKD and cardiovascular morbidity; intensity of follow-up should reflect baseline kidney function, AKI severity, duration, recovery, proteinuria, and dialysis exposure. Health systems should measure whether indicated patients receive laboratory and clinical follow-up after hospitalization. [12][18]

At discharge, communicate the AKI episode, likely cause, peak stage, discharge creatinine, medication changes, and a plan for kidney function and potassium reassessment. Current guidance supports kidney-function monitoring within 3 months after AKI, with longer surveillance for CKD risk. [20]
- Refer or discuss with nephrology after recovery when eGFR is 30 mL/min/1.73 m² or lower, or when proteinuria or hypertension persists. [1]
- Include urine protein assessment and cardiovascular risk management in follow-up when kidney dysfunction or proteinuria persists. [18][20]

## Use biomarker-guided prevention after major surgery selectively

Evidence supports a postoperative care bundle in biomarker-positive, high-risk surgical patients, not universal testing.

In BigpAK-2, adults undergoing major surgery with clinical AKI risk factors and postoperative urinary TIMP-2 × IGFBP7 of at least 0.3 (ng/mL)²/1000 were randomized to usual care or a KDIGO-based prevention bundle. The bundle included advanced hemodynamic monitoring, individualized fluid responsiveness assessment, MAP target of at least 65 mm Hg, nephrotoxin and contrast avoidance, temporary ACE inhibitor or ARB interruption, and hyperglycemia prevention. [8]

Moderate or severe AKI within 72 hours occurred in 14.4% with the bundle versus 22.3% with usual care, with an odds ratio of 0.57 and number needed to treat of 12. The trial did not show differences in 90-day major adverse kidney events, dialysis, or mortality, and its population excluded advanced CKD and pre-existing AKI. This strategy is therefore best viewed as targeted perioperative risk management in settings with assay availability and implementation capacity. [8]
- Do not extrapolate the TIMP-2 × IGFBP7 threshold or bundle outcome to unselected medical inpatients. [8]
- The trial found prevention of hypotension and ACE inhibitor or ARB interruption most strongly associated with the primary outcome in multivariable analysis; component-level causal effects remain uncertain. [8]

## Common questions

### When should renal ultrasound be ordered in AKI?

Order renal tract ultrasound when AKI has no clear cause or obstruction, pyelonephritis, or pyonephrosis is suspected. Obtain it within 24 hours for suspected obstruction and within 6 hours for suspected pyonephrosis. [3]

### Should fractional excretion of sodium be used to diagnose prerenal AKI?

FENa below 1% can support sodium retention but is not definitive and is confounded by diuretics, glomerular disease, hepatorenal physiology, obstruction, and early tubular injury. Fractional excretion of urea may be less affected by loop diuretics but remains imperfect. [3]

### Do loop diuretics improve kidney recovery in AKI?

No. Loop diuretics have no routine role in treating AKI or improving recovery and should be reserved for volume overload in a hemodynamically stable patient. [1]

### When should AKI survivors have kidney follow-up?

Monitor kidney function within 3 months after AKI for all patients, then individualize longer surveillance according to kidney recovery, CKD, proteinuria, AKI severity, and comorbid risk. [20]

## References
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## Editorial note

Prepared from cited clinical literature using Astra's research workflow. Verify recommendations against current guidance and patient-specific factors.