CKM Staging and the Kidney Axis - Nephrology Lectures 2025

Two staging systems, one patient. A nephrology patient carries a CKD stage (KDIGO, G × A) and a CKM stage (0–4). They are not the same axis and they answer different questions. This page works through both, then shows exactly where one becomes the other — and why albuminuria, not eGFR, is doing most of the work.

🧬 Part 1 — The CKM stages in detail

Stage 0No CKM syndrome. Normal weight, glucose, blood pressure, lipids and kidney function; no subclinical or clinical CVD.

Stage 1Excess or dysfunctional adiposity, and/or prediabetes, with no other metabolic risk factors, no CKD and no CVD.

Stage 2Metabolic risk factors and/or CKD.

Stage 3Subclinical CVD, or a CKM risk equivalent.

Stage 4Clinical CVD, substaged 4a / 4b.

Defining criteria by stage, verified against the 2026 guideline text.
Stage	Qualifying criteria
1	BMI at or above 25 kg/m² (or 23 if Asian ancestry), or waist circumference at or above 88 cm (women) / 102 cm (men) — or 80 / 90 cm if Asian ancestry — or fasting blood glucose 100–125 mg/dL or HbA1c 5.7–6.4%, without other metabolic risk factors or CKD
2	Metabolic risk factors — hypertriglyceridemia, hypertension, metabolic syndrome or type 2 diabetes — and/or moderate-to-high-risk CKD. Hypertriglyceridemia is defined by the guideline as fasting triglycerides at or above 150 mg/dL, or nonfasting at or above 175 mg/dL.
3	Subclinical ASCVD (elevated coronary calcium, or nonobstructive plaque on CTA); subclinical HF / pre-HF (elevated natriuretic peptide and/or hs-troponin, or echocardiographic abnormality); or a risk equivalent — very-high-risk CKD, or 10-year PREVENT-CVD at or above 20%
4	ASCVD: acute coronary syndrome, MI, stable or unstable angina, coronary or other arterial revascularization, stroke, TIA, peripheral artery disease. Heart failure: symptomatic HF at any ejection fraction. Atrial fibrillation — an independent qualifier needing no ischemic or structural disease.

Stage 4 substaging — verified against the guideline text.
Substage	Definition
4a	Clinical CVD without kidney failure
4b	Clinical CVD with kidney failure — eGFR below 15 mL/min/1.73 m², or chronic kidney replacement therapy

Any NYHA class qualifies for stage 4. The boundary that matters is against ACC/AHA heart failure stage B: asymptomatic structural or biomarker abnormality is pre-HF and sits at CKM stage 3. Symptom onset moves the patient to stage 4 permanently — it does not revert when symptoms resolve on guideline-directed medical therapy.

🥬 Part 2 — The CKD stages (KDIGO)

KDIGO stages CKD on two independent axes, and this is the part most often collapsed to a single number in conversation. "Stage 3 CKD" names only the G axis and is an incomplete description of the patient.

G — glomerular filtration rate

G1 — eGFR 90 or above
G2 — 60 to 89
G3a — 45 to 59
G3b — 30 to 44
G4 — 15 to 29
G5 — below 15

A — albuminuria (UACR, mg/g)

A1 — below 30 · normal to mildly increased
A2 — 30 to 300 · moderately increased
A3 — above 300 · severely increased

G1 and G2 are only CKD at all if something else is abnormal — albuminuria, structural disease, or another marker of damage. A normal-eGFR patient with A1 does not have CKD.

📏 Part 3 — Where CKD staging becomes CKM staging

CKM stage on the kidney axis is set by the G × A cell, not by G stage alone:

Green = no CKD on this axis. Orange = CKM stage 2 (KDIGO moderate-to-high risk). Red-orange = CKM stage 3 (KDIGO very-high risk, treated as a subclinical-CVD risk equivalent). Mapping verified verbatim against the guideline.
eGFR	A1 — below 30	A2 — 30 to 300	A3 — above 300
G1 — 90+	No CKD → stage 0/1	Stage 2	Stage 2
G2 — 60–89	No CKD → stage 0/1	Stage 2	Stage 2
G3a — 45–59	Stage 2	Stage 2	Stage 3
G3b — 30–44	Stage 2	Stage 3	Stage 3
G4 — 15–29	Stage 3	Stage 3	Stage 3
G5 — below 15	Stage 3	Stage 3	Stage 3

                Albuminuria is doing the staging work, not eGFR. Look at the two rows that
                straddle the stage 2/3 boundary. G3a crosses at UACR above 300; G3b crosses at UACR above 30 —
                a tenfold difference in threshold for one eGFR band's difference. Two patients with an identical
                eGFR of 50 sit in different CKM stages depending on a urine test that costs a few dollars and is
                still not ordered reliably.
            

Clinical CVD overrides the entire grid. A patient with symptomatic heart failure and G5 CKD is stage 4b, not stage 3. Kidney severity does not cap the stage — it substages it.

🧪 Part 4 — Laboratory thresholds by stage

Stage	eGFR	UACR	HF biomarkers	HbA1c
1	60 or above, A1 (no CKD)	Not required	Not indicated	5.7–6.4% — defines the stage
2	Per grid; measure with UACR annually	30 mg/g or above qualifies	Test if PREVENT-HF at or above 5%	6.5% or above — defines the stage
3	Very-high-risk CKD per grid	Value determines G3a/G3b assignment	Elevation defines pre-HF	Not a stage criterion
4	Full KDIGO staging	Same add-on thresholds	Diagnostic and prognostic, not staging	Not a stage criterion

Pre-HF biomarkers — what the guideline actually specifies

Worth stating plainly, because secondary summaries often attach numbers here that the guideline does not publish: the 2026 guideline sets no numeric pre-HF biomarker cut points. Its criterion is qualitative — "elevations of cardiac biomarkers (BNP, NT-proBNP, or hs-cTn) or structural or functional abnormalities on cardiac imaging identify individuals with pre-HF who are at increased HF risk, with the co-occurrence of the 2 indicating greatest absolute HF risk."

The only numeric biomarker values anywhere in the document belong to individual studies, not to the recommendation: BNP at or above 50 pg/mL was the screening threshold in the STOP-HF trial, and NT-proBNP above 40 pg/mL was an entry criterion in a single 46-patient exercise study. Neither is a guideline cut point, and neither should be taught as one.

                What the guideline does give you is a testing trigger, not a threshold. When a
                diagnosis of pre-HF is not known, a 10-year PREVENT-HF risk estimate at or above 5%
                can be considered as the trigger for selected cardiac biomarker testing — because that
                corresponds to roughly the same 3–5% 10-year incident HF risk that an elevated biomarker
                itself confers. Interpretation of the resulting value is left to the HF guidelines and to local
                assay reference ranges.
            

These cut points misbehave in exactly the population nephrology sees. Both natriuretic peptides and hs-troponin rise as eGFR falls, so the stage 3 pre-HF thresholds systematically overcall subclinical heart failure in G3b–G4. The opposite problem occurs in obesity, where natriuretic peptides read falsely low despite genuine cardiac dysfunction — and the guideline explicitly permits hs-troponin in that setting. On dialysis, the cut points are uninterpretable altogether.

⚠️ Part 5 — Two structural weaknesses worth teaching

The framework is useful, but it buys its simplicity with two real compressions. Both matter most in nephrology, and both are worth saying out loud to students rather than letting them discover the hard way.

1. HbA1c is a switch, not a dial

CKM staging treats diabetes as binary. HbA1c of 6.5% assigns stage 2. HbA1c of 13% also assigns stage 2. Glycemic severity never escalates the stage — there is no mechanism in the staging system by which worse diabetes produces a worse stage.

Two patients, same stage, wildly different disease. A 55-year-old with an HbA1c of 6.6% controlled on metformin, and a 55-year-old with an HbA1c of 13%, osmotic symptoms and catabolic weight loss, are both CKM stage 2. The stage label conceals the entire difference between them.

Severity does re-enter, but only in two indirect places: agent selection — "severe hyperglycemia" is named among the comorbidities steering the choice of cardioprotective antihyperglycemic, and uncontrolled diabetes favors a GLP-1 RA over finerenone in the albuminuria add-on decision — and PREVENT, which takes HbA1c as a continuous input and will register the excess risk the stage label hides. If you stage without running PREVENT, that risk simply disappears from the assessment. This is worked through in the glycemic management deep dive.

2. Severe albuminuria with a preserved eGFR is under-staged

This one is sharper, and it cuts against the entire CKD literature. Look back at the grid: a patient at G1 or G2 with A3 — say eGFR 95 with a UACR of 1,200 mg/g — is CKM stage 2. That is the same stage as a patient whose only qualifying feature is uncomplicated hypertension, and the same stage as a G3a A1 patient with an eGFR of 50 and no albuminuria.

Set that against how KDIGO itself grades those cells. The KDIGO heat map has four risk bands, and the CKM grid collapses two of them:

CKM stage 2 spans both the moderate and high KDIGO risk bands; only the very-high band becomes stage 3. Mapping derived from the grid as stated above.
Cell	KDIGO risk band	CKM stage	Consequence
G3a A1 (eGFR 50, UACR 12)	Moderately increased	Stage 2	—
G1–G2 A3 (eGFR 95, UACR 1,200)	High	Stage 2	Higher KDIGO risk, identical CKM stage
G3a A3	Very high	Stage 3	Escalates only once eGFR has fallen too

                Why this is the wrong way round. In the CKD prognosis literature, severe
                albuminuria is among the strongest available predictors of both kidney progression and
                cardiovascular death, and it carries that weight across the full eGFR range —
                including at a normal eGFR. Heavy proteinuria with preserved filtration is not a mild state; it is
                frequently the steepest trajectory in the clinic. The CKM grid escalates that patient to stage 3
                only after the eGFR has already fallen, which is to say only after the damage the albuminuria was
                predicting has occurred.
            

And the other tool does not cover the gap. The obvious answer — run KFRE instead — fails here, because KFRE is not validated above an eGFR of 60 and will not run at all in G1–G2. So for the young patient with nephrotic-range proteinuria and a normal creatinine, CKM staging says "stage 2" and KFRE says nothing. Neither instrument sees them. Only the UACR value itself does, which is an argument for reading the number rather than the category.

The practical rule. In G1–G2 with A3, ignore the stage and treat the albuminuria. Full RASi titration, SGLT2 inhibition, and the finerenone or semaglutide add-on decision are all driven by the UACR threshold directly — the CKM stage adds nothing to that decision and may falsely reassure.

So why did a guideline endorsed by ASN do this?

The obvious suspicion — that nephrology was not in the room, or that KDIGO was not consulted — does not survive contact with the document. The guideline states verbatim that "the writing committee included representatives from the AHA, ACC, American Diabetes Association (ADA), including ADA Obesity Alliance representation, and the American Society of Nephrology." KDIGO is cited 39 times throughout, and the kidney axis is imported from the KDIGO heat map directly.

The published roster bears that out. Nephrology on the writing committee included Ian H. de Boer, David H. Ellison (FASN), Janani Rangaswami, Katherine R. Tuttle (FASN), and nephrology pharmacist Wendy St. Peter. And the KDIGO link is personal, not just bibliographic: de Boer and Tuttle are both KDIGO diabetes-and-CKD work-group principals — de Boer is first author on KDIGO's own consensus output on incretin therapies in CKD. The claim that no KDIGO figure sat on the panel is false.

One organization is genuinely absent, though. The National Kidney Foundation is not a partner or endorsing society on this guideline, and the string "National Kidney Foundation" does not appear anywhere in the document. The kidney voice here is ASN and KDIGO; NKF is not part of it.

The compression happens somewhere more interesting: at the translation step between KDIGO's risk bands and CKM's stages. KDIGO grades the G × A grid into four risk bands. The CKM framework imports them as two:

The guideline's own wording, verbatim: "KDIGO risk classification for moderate-high–risk CKD: stages G1-G2 with A2-A3, stage G3a with A1-A2, or stage G3b with A1; for very high-risk CKD: stages G3a with A3, stage G3b with A2-A3, or stages G4-G5 CKD."
KDIGO bands	Collapsed into	Effect
Moderately increased + high	CKM stage 2	Two bands become one stage — G1–G2 A3 lands here
Very high	CKM stage 3	Reserved for the top band only

Read as a cardiovascular instrument, that collapse is defensible. A 35-year-old with an eGFR of 95 and a UACR of 1,200 genuinely does carry lower 10-year absolute cardiovascular risk than a 75-year-old at G4 — which is the quantity CKM staging exists to grade. The framework is not wrong about its own question. It is only wrong when borrowed to answer a kidney question it never claimed to answer.

And the guideline's answer to both critiques is the same: PREVENT

Neither limitation is stated as a limitation anywhere in the guideline. But both have the same structural resolution, and the text is explicit about the mechanism:

                Verbatim from the guideline: "The PREVENT base equations include traditional CVD
                risk factors, and newly include predictors relevant to CKM syndrome (BMI and eGFR), with
                add-on models incorporating UACR, HbA1c, and the social deprivation index."
            

So both severities that the stage throws away — how heavy the albuminuria is, and how bad the diabetes is — re-enter as continuous inputs to the PREVENT add-on models. The stage is deliberately coarse; PREVENT is where the granularity lives. That is the framework's answer, and it is a coherent one.

Two caveats keep it from being a complete answer. First, it only works if you actually run an add-on model with a UACR — the base equation does not include it, and most calculator front-ends default to the base. Second, and more fundamentally, PREVENT recovers cardiovascular risk only. Nothing in either instrument recovers the kidney-progression risk of heavy albuminuria at a preserved eGFR, because KFRE does not run above an eGFR of 60. For that patient the framework is complete on cardiac risk and silent on renal trajectory — and a search of the guideline for an acknowledgment of that turns up nothing beyond Table 21's note that the PREVENT calculator needs "refinement."

🔗 Where to go next

⚖️ How this compares to KFRE 🧪 The HbA1c problem in CKD

🔍 Source and verification

Primary source: the 2026 AHA/ACC/ADA/ASN guideline for the prevention, detection, evaluation, and management of cardiovascular-kidney-metabolic syndrome (Circulation. 2026;154(4):e50–e158, PMID 42263157), published Free Access and read in full for these pages. Glycemic triggers are from the ADA Standards of Care in Diabetes — 2026, Section 9 (PMID 41358900), read in full via PubMed Central. Kidney staging and glycemic targets in CKD are from KDIGO 2024 and KDIGO 2022 (PMID 36272764), the latter verified against its peer-reviewed synopsis (PMID 36623286).

Every numeric threshold on this page was checked against the source text. Figures that could not be confirmed in a primary source were removed rather than published with a caveat — including a set of pre-HF biomarker cut points that circulate in secondary summaries but appear nowhere in the guideline.

🧬 CKM Staging and the Kidney Axis