Updated kdigo classification
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KDIGO 2024 2025 updated classification AKI CKD staging
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https://kdigo.org/wp-content/uploads/2026/03/KDIGO-2026-AKI-…
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"KDIGO" AND "acute kidney injury" AND "classification"
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I now have comprehensive data from the 2026 AKI/AKD draft, the 2024 CKD guideline, and textbook references. Here is the full updated KDIGO classification:
KDIGO Classification - Updated (2024/2026)
There are two major KDIGO classifications: CKD (updated 2024) and AKI/AKD (2026 draft update). Both have significant changes from the 2012 originals.
Part 1: KDIGO 2024 - Chronic Kidney Disease (CKD)
Definition
CKD = abnormalities in kidney structure or function lasting ≥3 months, with implications for health.
CGA Framework (Cause, GFR, Albuminuria)
The 2024 update retains the CGA framework but with key revisions.
GFR Categories (G-stages)
| Category | eGFR (mL/min/1.73 m²) | Description |
|---|---|---|
| G1 | ≥90 | Normal or high |
| G2 | 60-89 | Mildly decreased |
| G3a | 45-59 | Mildly to moderately decreased |
| G3b | 30-44 | Moderately to severely decreased |
| G4 | 15-29 | Severely decreased |
| G5 | <15 | Kidney failure |
Albuminuria Categories (A-stages)
| Category | ACR (mg/mmol) | ACR (mg/g) | Description |
|---|---|---|---|
| A1 | <3 | <30 | Normal to mildly increased |
| A2 | 3-29 | 30-299 | Moderately increased |
| A3 | ≥30 | ≥300 | Severely increased |
Key 2024 Updates vs. 2012
- Dual GFR estimation: The 2024 guideline recommends using both creatinine AND cystatin C for more accurate eGFR estimation (cystatin C is not confounded by muscle mass).
- Risk prediction models: Promotes models incorporating CKD-related variables (age, sex, comorbidities) beyond just eGFR and albuminuria - reflecting precision medicine principles.
- Updated heat map: The risk stratification heat map (green = low, yellow = moderate, orange = high, red = very high) for CKD progression, cardiovascular disease, and mortality is refined based on data from 27+ million participants across 114 global cohorts (CKD Prognosis Consortium).
- Monitoring frequency guidance: The CGA classification now incorporates recommended monitoring frequency ("Screen" vs. "Treat 1/2/3" categories based on combined G- and A-stage).
- Focused update announced March 2026: KDIGO has initiated a further update to Chapter 3 (delaying progression/managing complications), specifically addressing SGLT2 inhibitors, GLP-1-based therapies, and nonsteroidal MRAs in non-diabetic CKD.
Part 2: KDIGO 2026 Draft - AKI / AKD
This is a major overhaul from the 2012 KDIGO AKI guideline, published as a public review draft in March 2026, incorporating evidence through June 2025.
The Biggest Change: 3-Dimensional Staging System
The 2026 draft moves from a single-axis staging (just SCr + urine output) to a 3-component staging system that adds damage biomarkers:
| Component | Marker | Stages |
|---|---|---|
| C (Creatinine/Functional) | Serum creatinine | C0, C1, C2, C3 |
| U (Urine output/Functional) | Urine output | U0, U1, U2, U3 |
| B (Biomarker/Structural) | Damage biomarkers | B0 (negative), B1 (positive) |
AKI Staging Criteria (Adults)
Serum Creatinine (C-criteria)
| Stage | Criteria |
|---|---|
| C0 | No rise - baseline |
| C1 | ≥0.3 mg/dL (≥26.5 µmol/L) increase or 1.5-1.9× baseline |
| C2 | 2.0-2.9× baseline |
| C3 | ≥3.0× baseline or SCr ≥4.0 mg/dL (≥353.6 µmol/L) or initiation of RRT |
Urine Output (U-criteria)
| Stage | Criteria |
|---|---|
| U0 | Normal |
| U1 | <0.5 mL/kg/h for 6-12 hours |
| U2 | <0.5 mL/kg/h for >12 hours |
| U3 | <0.3 mL/kg/h for >24 hours or anuria for >12 hours |
Damage Biomarker (B-criteria)
| Stage | Criteria |
|---|---|
| B0 | Negative damage biomarker |
| B1 | Positive damage biomarker |
Structural biomarkers include: NGAL (urinary), CCL14 (identifies persistent Stage 3 AKI risk in critically ill patients with KDIGO 2012 Stage 2-3), cystatin C, and others reflecting cellular stress, damage, or inflammation.
Example staging: A patient could be staged as "C1, U1, B1" - meaning Stage 1 by creatinine, Stage 1 by urine output, with a positive damage biomarker.
Why the Biomarker Dimension Was Added
- Biomarkers detect kidney cellular stress/damage earlier than functional markers alone
- Enables earlier intervention and potentially better outcomes
- Cystatin C overcomes some limitations of SCr (not affected by muscle mass)
- B1 classification upgrades clinical risk even when functional criteria are mild
- SCr combined with urinary NGAL predicts RRT requirement better than either alone (in mechanically ventilated patients)
Neonatal AKI Staging (Special Population - also updated)
| Stage | SCr Criteria | Urine Output |
|---|---|---|
| C1 | 1.5-1.9× baseline | U1: >0.5 and ≤1.0 mL/kg/h for 24 h |
| C2 | 2.0-2.9× baseline | U2: >0.3 and ≤0.5 mL/kg/h for 24 h |
| C3 | ≥3× baseline or SCr ≥2.5 mg/dL (220 µmol/L) or RRT | U3: ≤0.3 mL/kg/h for 24 h |
(Neonatal thresholds differ because absolute SCr changes are small due to low muscle mass and physiologically low baseline GFR.)
AKD (Acute Kidney Disease) - Retained & Clarified
AKD occupies the temporal gap between AKI and CKD:
- AKI: onset <7 days
- AKD: kidney disease 7 days to <3 months duration
- CKD: structural damage or dysfunction for ≥3 months
Comparison: 2012 vs. 2026 AKI Staging
| Feature | KDIGO 2012 | KDIGO 2026 |
|---|---|---|
| Staging axes | 2 (SCr, UO) | 3 (SCr, UO, biomarker) |
| Biomarkers | Not included | B0/B1 dimension added |
| Cystatin C | Not mentioned | Recognized as alternative functional marker |
| Neonatal criteria | Same as adult | Separate, age-specific thresholds |
| Evidence cutoff | ~2011 | June 2025 |
Summary of Key KDIGO Updates
- CKD (2024): Retain CGA framework; add dual creatinine + cystatin C eGFR; refine heat map with large population data; incorporate precision medicine risk models.
- AKI/AKD (2026 draft): Major change - add damage biomarker (B0/B1) as a third staging dimension alongside creatinine (C) and urine output (U); separate neonatal staging; incorporate NGAL, cystatin C, CCL14.
- Ongoing update (2026): KDIGO is reviewing new data on SGLT2 inhibitors, GLP-1 agonists, and nonsteroidal MRAs for CKD progression in non-diabetic patients.
Sources: KDIGO 2026 AKI/AKD Draft Guideline | 2024 CKD Guideline summary (CCJM) | Brenner & Rector's The Kidney, 10e | Current Surgical Therapy 14e
IMG_2238.jpg
IMG_2239.jpg
Interpret
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analyse_media
Both ECGs are from the same patient (dates 14-07-2026 and nearby), and the second image already contains handwritten clinical notes with a differential. Here is a structured interpretation of both:
ECG 1 (IMG_2238) - BPL Machine, 14-07-2026, 05:07 AM
Technical: 25 mm/s, 10 mm/mV, machine rate shown as 133 bpm
| Parameter | Finding |
|---|---|
| Rate | ~133 bpm (tachycardic) |
| Rhythm | Regular |
| P waves | Upright P waves visible before each QRS |
| PR interval | Normal (~120-140 ms), 1:1 AV conduction |
| QRS | Narrow (<100 ms) |
| Axis | Normal (I positive, aVF positive) |
| ST segments | Isoelectric in all territories |
| T waves | Upright and normal |
| Q waves | No pathological Q waves |
Interpretation: Sinus Tachycardia at ~133 bpm - no acute ischemic changes, no conduction abnormality.
ECG 2 (IMG_2239) - GE MAC Machine
Technical: 25 mm/s, 10 mm/mV, 50 Hz filter, 0.56-20 Hz ZPD
Automated measurements printed:
- Heart rate: ~140 bpm
- QRS duration: 66 ms (narrow)
- QT/QTc: 270/412 ms
- P-R-T axes: 269° / 25° / -41°
- Machine flag: "Cannot rule out Anterior infarct, age undetermined" | "Abnormal ECG"
Handwritten Notes (by clinician):
Rate = 1500/11 = ~140 bpm | REGULAR RHYTHM | P-wave: Absent | Narrow QRS | Low voltage in II, aVF | No ST elevation/depression | Sinus Tachycardia vs Regular Rhythm with Absent P wave → Atrial Flutter
My Interpretation:
| Parameter | Finding |
|---|---|
| Rate | ~136-140 bpm |
| Rhythm | Regular |
| P waves | Not clearly identifiable - continuous undulating baseline in inferior leads (II, III, aVF) and V1, consistent with sawtooth flutter waves |
| PR interval | Not measurable |
| QRS | Narrow (66 ms) - normal intraventricular conduction |
| Axis | Left axis deviation (~-41°, QRS positive in I, negative/isoelectric in aVF) |
| Voltage | Low voltage in limb leads (QRS <5 mm in II, III, aVF) |
| ST-T | No diagnostic ST elevation or depression |
| Q waves | No definite pathological Q waves |
Diagnostic Conclusion
Atrial Flutter with 2:1 AV Conduction
The second ECG is the more diagnostic tracing. The key findings are:
- Regular tachycardia at ~140 bpm with absent discrete sinus P waves
- Continuous sawtooth undulation of the baseline in inferior leads and V1 - these are flutter (F) waves at an atrial rate of ~280-300 bpm
- 2:1 block: every other flutter wave is conducted, giving ventricular rate ~140-150 bpm (this is the classic "regular tachycardia with absent P waves" pattern)
- Narrow QRS confirms the ventricular conduction is via the normal His-Purkinje system
- Left axis deviation (P-T axis discordance, axis ~-41°)
- Low limb lead voltage - consider causes: pericardial effusion, obesity, hypothyroidism, COPD, or anasarca
Comparing Both ECGs
The first ECG (133 bpm) could represent an earlier stage or slightly different rate of the same flutter, or truly sinus tachycardia - the absence of clearly visible flutter waves vs. the overt sawtooth in the second makes the first appear more like sinus tachycardia. This could represent:
- Evolution: sinus tachycardia converting to atrial flutter, or
- Rate-dependent concealment: at 133 bpm, flutter waves may be partially hidden within T waves (a well-known trap in 2:1 flutter)
Clinical Correlations Needed
- Check for underlying causes of flutter: thyroid disease, heart failure, valvular disease, pulmonary embolism, post-cardiac surgery
- Address the low voltage: rule out pericardial effusion (urgent echo if clinical concern)
- The machine flag of "cannot rule out anterior infarct" likely reflects low voltage/poor R-wave progression - clinical and troponin correlation required
- Rate control first (beta-blocker, non-DHP CCB, or digoxin), then rhythm control (cardioversion or antiarrhythmic) per clinical context
- Anticoagulation per CHA₂DS₂-VASc score if flutter is new-onset or duration uncertain
⚠️ This interpretation is for educational/clinical support purposes. Confirm with a treating physician, especially regarding the pericardial effusion/low voltage concern and anticoagulation decisions.
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