Albuminuria as a treatment-response biomarker during layered kidney-protective therapy for albuminuric chronic kidney disease

Albuminuria is a major prognostic marker in chronic kidney disease and a useful treatment-response biomarker during outcome-supported therapy.In selected trial contexts, treatment effects on urinary albumin-to-creatinine ratio may also serve as a surrogate endpoint for kidney outcomes.These roles do not establish albuminuria as a conventional treat-to-target parameter: no universal ratio threshold, required percentage reduction, or validated escalation rule has been defined for individual care.A reproducible reduction in albuminuria during layered therapy with a renin-angiotensin system inhibitor, a sodium-glucose cotransporter 2 inhibitor, and, when indicated, finerenone can provide supportive evidence that the regimen is producing an expected biological response.However, trial-level surrogacy does not guarantee individual benefit; kidney protection may occur despite minimal baseline albuminuria or little change in albuminuria, albuminuria is biologically variable, and biomarker and clinical responses may be discordant.Interpretation is especially difficult when albuminuria decreases while serum creatinine rises or estimated glomerular filtration rate falls after rapid layering.This review defines the evidentiary roles and boundaries of albuminuria and proposes an evidence-informed framework integrating serial albuminuria measurements with kidney-function trajectory, potassium, blood pressure, volume status, and clinical context.The framework is not a prospectively validated decision rule.Progressive kidney dysfunction, symptomatic hypotension, volume depletion, uncontrolled hyperkalemia, active intrinsic kidney disease, nephrotoxin exposure, or acute kidney injury should take precedence over a favorable albuminuria response.Albuminuria should inform treatment assessment but should not dictate treatment in isolation.