Aldosterone Inhibition in CKD

What Happens Over 10 Years — RAAS Alone vs. Layered Add-On Therapy

An interactive model of mortality, CKD progression, dialysis, and cardiovascular risk under three treatment scenarios.

MODELED PROJECTION, NOT MEASURED TRIAL DATA. No trial has directly randomized these three regimens against each other or followed patients for 10 years — trial follow-up was 2.0–3.0 years. This tool extrapolates each drug class's own hazard ratio (from FIDELITY, DAPA-CKD, EMPA-KIDNEY, CREDENCE) forward assuming a constant annual hazard and independent, multiplicative effects of add-on drugs — an assumption, not a proven result. Use this to illustrate the shape and scale of benefit to patients and colleagues, not as an individual risk calculator.

Outcome

Baseline CKD Risk (KDIGO-style)

Modeled cumulative incidence over 10 years

At Year 10 (modeled)

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Number needed to treat (RAAS-only vs. full add-on) to prevent one additional event over 10 years, at this baseline risk.

Model assumptions & where the numbers come from

Baseline annual event hazards for the "RAAS only" arm are illustrative, back-calculated from the control/placebo arms of FIDELITY (kidney and CV composite, all-cause mortality), DAPA-CKD (kidney composite), and EMPA-KIDNEY (kidney/CV composite) for a CKD + type 2 diabetes population with albuminuria — not a single patient's measured risk.

+ SGLT2i hazard ratios are averaged across DAPA-CKD, EMPA-KIDNEY, and CREDENCE (kidney progression ≈0.68, dialysis/ESKD ≈0.65, CV composite ≈0.78, all-cause mortality ≈0.80).
+ Finerenone hazard ratios are layered on top from the FIDELITY pooled analysis and FINE-HEART (kidney composite 0.77, CV composite 0.86, all-cause mortality 0.82–0.91 depending on analysis) — applied multiplicatively to the SGLT2i-adjusted hazard.
Cumulative incidence is modeled as 1 − e^(−λt), i.e. a constant-hazard (exponential) survival model — real risk is rarely perfectly constant over 10 years, especially as eGFR declines.
Key limitation: FIGARO-DKD already had substantial background SGLT2i use, so treating the SGLT2i and finerenone effects as fully independent likely overstates the combined benefit somewhat. Competing risk of death (which reduces observed progression/dialysis events) is not separately modeled.
"Risk profile" buttons scale the baseline hazard (Moderate ×0.7, High ×1.0, Very High ×1.4) to approximate KDIGO risk categories — this is a illustrative scaling, not derived from a validated risk equation (e.g. KFRE).