Diagnostic Assessment and KDIGO Classification of Acute Kidney Injury
Learning Objective
Apply diagnostic and classification criteria to assess patients with AKI and guide management.
Key Learning Points:
- Recognize AKI clinical signs: oliguria, fluid overload, electrolyte disturbances, rising serum creatinine.
- Interpret laboratory (SCr, BUN, FENa, FEUrea), urine output, urinalysis, and imaging to confirm and classify AKI.
- Utilize RIFLE and KDIGO staging to stratify severity, guide interventions, and predict outcomes.
I. Introduction and Clinical Impact
Early detection of Acute Kidney Injury (AKI) is critical to reducing morbidity, mortality, and ICU length of stay. Even small changes in serum creatinine (SCr) and urine output (UO) are linked to adverse outcomes. Prompt recognition informs crucial management decisions, including hemodynamic optimization and nephrotoxin stewardship.
- AKI incidence in the ICU ranges from 10% to 60%, depending on the patient population and definitions used.
- Each 0.3 mg/dL rise in SCr significantly increases the risk of requiring renal replacement therapy (RRT) and death.
- Delayed diagnosis can allow AKI to progress to irreversible injury, leading to higher healthcare costs and poorer patient outcomes.
Clinical Pearl
Monitor both SCr trends and hourly UO in at-risk patients for the earliest possible detection of AKI. These two parameters are cornerstones of AKI diagnosis and staging.
II. Clinical Presentation of AKI
AKI manifests with a constellation of signs and symptoms, primarily decreased urine output, fluid accumulation, electrolyte imbalances, and a rise in serum creatinine. Accurate measurement and differentiation of these signs are essential to guide further evaluation and management.
A. Oliguria and Anuria
- Oliguria: Urine output <0.5 mL/kg/h for ≥6 hours.
- Anuria: Urine output <0.3 mL/kg/h for ≥12 hours, or often practically defined as <50-100 mL total urine output in 24 hours.
- Accurate assessment requires an indwelling urinary (Foley) catheter and hourly documentation in critically ill patients.
B. Fluid Overload
Fluid accumulation is a common consequence of impaired renal excretion.
- Signs: Peripheral edema (pitting edema in dependent areas), pulmonary crackles on auscultation, jugular venous distension (JVD), weight gain, and positive fluid balance.
- Impact: Can impair gas exchange, delay ventilator weaning, and contribute to organ dysfunction.
C. Electrolyte Abnormalities
Kidney dysfunction leads to disturbances in electrolyte and acid-base balance.
| Abnormality | Key Findings / Monitoring | Management Considerations |
|---|---|---|
| Hyperkalemia | Serum K+ >5.5 mEq/L. Monitor ECG for peaked T waves, widened QRS, sine wave. | Calcium gluconate/chloride (stabilize myocardium), insulin/glucose, beta-agonists, sodium bicarbonate (shift K+ intracellularly), loop diuretics, potassium binders (e.g., patiromer, sodium zirconium cyclosilicate), RRT. |
| Metabolic Acidosis | Low serum bicarbonate (HCO3-), low pH (<7.35). Assess anion gap (often elevated). | Address underlying cause. Consider sodium bicarbonate if pH <7.1-7.2 or severe acidemia, though controversial. RRT may be needed. |
| Hyperphosphatemia / Hypocalcemia | Elevated phosphate, low total and ionized calcium. | Dietary phosphate restriction, phosphate binders (e.g., sevelamer, calcium acetate). Calcium supplementation if symptomatic hypocalcemia or severe hyperkalemia. |
D. Serum Creatinine Trends
- Baseline SCr: Crucial for diagnosis. Use recent outpatient labs if available. If unknown, back-calculation using the MDRD equation assuming a GFR of 75 mL/min/1.73m² can be attempted but has limitations.
- Lag Time: Recognize the 48–72 hour lag between the actual kidney injury and the subsequent rise in SCr.
- Confounders: Low muscle mass (e.g., elderly, malnourished) can lead to a lower baseline SCr and mask significant GFR decline. Fluid overload can dilute SCr, underestimating AKI severity.
III. Laboratory and Imaging Evaluation
Laboratory tests and imaging studies are essential to confirm AKI, help differentiate its etiology (prerenal, intrinsic, postrenal), and guide management steps.
A. Serum Creatinine and BUN
- BUN/SCr Ratio: A ratio >20:1 may suggest prerenal azotemia (due to increased urea reabsorption) but is not definitive and can be influenced by other factors (e.g., GI bleed, catabolic states, high protein intake).
- Nonrenal Influences: SCr is influenced by muscle mass, age, sex, and certain medications (e.g., trimethoprim, cimetidine). BUN is affected by protein intake, catabolism, and liver function.
B. Urine Output Metrics
- Hourly UO: Essential for early detection and staging of AKI in acute settings.
- 24-hour Totals: Useful for trending overall kidney function and fluid balance management.
- Accuracy vs. Risk: While an indwelling catheter provides the most accurate UO, balance this against the increased risk of catheter-associated urinary tract infections (CAUTI).
C. Urinalysis and Sediment Examination
Microscopic examination of urine sediment can provide valuable clues to the type of AKI.
| AKI Type | Typical Sediment Findings |
|---|---|
| Prerenal AKI | Bland sediment (few cells or casts), possibly hyaline casts (concentrated urine). |
| Intrinsic AKI (Acute Tubular Necrosis – ATN) | Muddy brown granular casts (pathognomonic for ATN), renal tubular epithelial cells and casts. |
| Intrinsic AKI (Acute Interstitial Nephritis – AIN) | White blood cells (especially eosinophils, if stained), WBC casts, +/- red blood cells. |
| Intrinsic AKI (Glomerulonephritis) | Red blood cells (often dysmorphic), RBC casts, proteinuria. |
| Postrenal AKI | Often bland initially; may see crystals, RBCs, or WBCs if infection or inflammation present due to obstruction. |
D. Imaging Modalities
- Renal Ultrasound: First-line imaging to exclude obstructive uropathy (e.g., hydronephrosis) and assess kidney size (small kidneys suggest chronicity).
- Doppler Ultrasound: Can assess renal blood flow and resistive indices.
- CT/MRI: Reserved for specific concerns (e.g., complex cysts, masses, renal vein thrombosis) or when ultrasound is inconclusive. Avoid intravenous contrast agents if possible in patients with AKI, or use with appropriate preventative measures if essential.
Clinical Pearl
Point-of-care ultrasound (POCUS) by trained clinicians can expedite the exclusion of postrenal causes (hydronephrosis) at the bedside and can also assist in guiding fluid management by assessing IVC diameter and collapsibility.
IV. AKI Classification Systems
Standardized staging systems like RIFLE and KDIGO are used to classify the severity of AKI based on changes in SCr and UO. These classifications correlate with prognosis and help inform the timing of interventions, including RRT.
A. RIFLE Criteria (Risk, Injury, Failure, Loss, End-stage kidney disease)
| RIFLE Class | Serum Creatinine Criteria | Urine Output Criteria |
|---|---|---|
| Risk | Increased SCr ×1.5 OR GFR decrease >25% | UO <0.5 mL/kg/h for 6 hours |
| Injury | Increased SCr ×2 OR GFR decrease >50% | UO <0.5 mL/kg/h for 12 hours |
| Failure | Increased SCr ×3 OR GFR decrease >75% OR SCr ≥4.0 mg/dL with an acute rise ≥0.5 mg/dL | UO <0.3 mL/kg/h for 24 hours OR Anuria for 12 hours |
| Loss | Persistent AKI = complete loss of kidney function >4 weeks | |
| End-Stage Kidney Disease (ESKD) | ESKD >3 months | |
B. KDIGO Staging (Kidney Disease: Improving Global Outcomes)
Definition of AKI by KDIGO: Any of the following:
- Increase in SCr by ≥0.3 mg/dL (≥26.5 µmol/L) within 48 hours; 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 <0.5 mL/kg/h for 6 hours.
| Stage | Serum Creatinine Criteria | Urine Output Criteria |
|---|---|---|
| Stage 1 | 1.5–1.9 times baseline OR ≥0.3 mg/dL (≥26.5 µmol/L) increase | <0.5 mL/kg/h for 6–12 hours |
| Stage 2 | 2.0–2.9 times baseline | <0.5 mL/kg/h for ≥12 hours |
| Stage 3 | 3.0 times baseline OR Increase in serum creatinine to ≥4.0 mg/dL (≥353.6 µmol/L) OR Initiation of RRT | <0.3 mL/kg/h for ≥24 hours OR Anuria for ≥12 hours |
C. Comparison and Implications
- KDIGO criteria integrate aspects of both RIFLE and AKIN (Acute Kidney Injury Network) classifications and are generally considered more sensitive for detecting early AKI.
- The ≥0.3 mg/dL SCr increase in KDIGO Stage 1 may detect transient SCr fluctuations, potentially risking overdiagnosis if not interpreted in clinical context. However, it also enhances sensitivity for smaller, prognostically important changes.
- Uniform staging facilitates communication among healthcare providers, guides escalation of care, helps standardize research, and informs decisions regarding nephrology consultation and initiation of RRT.
Clinical Pearl
In patients receiving diuretics, urine output criteria for AKI staging may be misleading (falsely reassuring). In such cases, rely more heavily on SCr trends and adjunctive diagnostic indices like FENa or FEUrea (if appropriate) to assess kidney function.
V. Integration of Diagnostic Data
A structured approach combining clinical risk assessment, serial laboratory monitoring, urine sediment analysis, imaging, and standardized staging optimizes AKI assessment and subsequent management decisions.
A. Fractional Excretion of Sodium (FENa) and Urea (FEUrea)
These indices can help differentiate prerenal AKI from intrinsic AKI (specifically ATN), particularly when the cause is unclear.
| Index | Prerenal AKI | Intrinsic AKI (ATN) | Notes |
|---|---|---|---|
| FENa (UNa × PCr) / (PNa × UCr) × 100 |
<1% | >2% | Most reliable when oliguric and not on diuretics. Values between 1-2% are indeterminate. Less reliable in CKD, glomerulonephritis, or contrast nephropathy. |
| FEUrea (UUrea × PCr) / (PUrea × UCr) × 100 |
<35% | >50% | Useful in patients receiving diuretics, as urea reabsorption is less affected by loop diuretics than sodium. Similar limitations as FENa in other contexts. |
Interpret FENa and FEUrea within the overall clinical context. They should not be used in isolation to diagnose AKI etiology, especially in patients with underlying chronic kidney disease (CKD) or mixed etiologies.
B. Trend Analysis and Risk Scores
- Serial changes in SCr and UO over hours to days provide superior prognostic insight compared to single measurements.
- Dynamic assessment is key. Rapidly rising SCr or worsening oliguria despite interventions signals a more severe injury.
- Incorporate AKI data into validated risk prediction tools or electronic alerts when available to enhance early recognition and standardized care.
C. Diagnostic Algorithm for AKI
A systematic approach is crucial for timely and effective AKI management:
AKI Diagnostic Algorithm
1. Identify Risk Factors (Sepsis,
Hypotension, Nephrotoxins)
2. Initiate Hourly UO &
Daily/Serial SCr Monitoring
3. Perform Urinalysis &
Urine Sediment Exam
4. Renal Ultrasound to
Exclude Obstruction
5. Etiology Unclear? Calculate
FENa/FEUrea (if applicable)
6. Stage AKI per KDIGO
7. KDIGO Stage 2-3 or
Rapid Progression?
→ Consult Nephrology
8. Evaluate Need/Timing of RRT
Clinical Vignette: A 70-year-old diabetic ICU patient has a urine output of 0.4 mL/kg/h over the past 8 hours. Serum creatinine has risen from a baseline of 1.0 mg/dL to 1.4 mg/dL in the last 24 hours. Based on these findings, KDIGO Stage 1 AKI is diagnosed (SCr increase of 0.4 mg/dL and UO <0.5 mL/kg/h for 6-12h). A FENa is calculated and found to be 0.6%, suggesting a prerenal etiology. Initial management focuses on cautious fluid resuscitation to improve renal perfusion and meticulous avoidance of nephrotoxic medications.
Clinical Pearl
Early nephrology involvement for patients with KDIGO Stage 2–3 AKI, or those with rapid progression of AKI, may improve outcomes. Nephrologists can assist in diagnostic workup, optimize medical management, and help determine the appropriate timing and modality of RRT if needed.
References
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- Bellomo R, Ronco C, Kellum JA, Mehta RL, et al. Acute renal failure—Definition, outcome measures, and fluid therapy: ADQI consensus. Crit Care. 2004;8:R204–R212.
- Khwaja A. KDIGO clinical practice guideline for acute kidney injury. Nephron Clin Pract. 2012;120:c179–c184.
- Pereira M, Rodrigues N, Godinho I, et al. AKI in septic shock: RIFLE vs AKIN vs KDIGO. Clin Kidney J. 2017;10:332–340.
- Zeng X, McMahon GM, Brunelli SM, et al. Incidence and outcomes across AKI definitions. Clin J Am Soc Nephrol. 2014;9:12–20.
- Vanmassenhove J, Vanholder R, Nagler E, et al. Urinary and serum biomarkers for AKI: In-depth review. Nephrol Dial Transplant. 2013;28:254–273.
- Hobson CE, Darmon M, Mohan S, et al. E-alerts for AKI detection: ADQI consensus. Can J Kidney Health Dis. 2016;3:9.
