Does mild kidney impairment ruin AD blood tests?
In 242 TRIAD participants, eGFR related to some plasma AD biomarkers, but adding eGFR did not improve Aβ-positivity prediction beyond age/sex and the biomarker itself.
Source
The impact of kidney function on Alzheimer's disease blood biomarkers: implications for predicting amyloid-β positivity
What they did
Measured eGFR from plasma creatinine and multiple Simoa plasma biomarkers (Aβ42/40, GFAP, NfL, p-tau isoforms, NTA-tau) in 242 TRIAD participants, then tested associations and Aβ-positivity models with/without eGFR.
What they found
Levels were highest in CKD stage 3 for some markers (significant for NfL, Aβ42, Aβ40). Many eGFR associations shrank after age/sex/Aβ-PET adjustment; adding eGFR did not improve AIC or AUC for Aβ-positivity. Authors conclude normal-to-mild renal impairment is not clinically decisive for accurate markers like p-tau217.
The limits
What it doesn't show
Few participants had advanced CKD, so results do not rule out clinically important confounding in severe kidney disease.
Key terms
- eGFR
- Estimated glomerular filtration rate from plasma creatinine indexing kidney function.
- Aβ-positivity
- Amyloid-positive status used as the prediction target.
- p-tau217
- Plasma phosphorylated tau species highlighted as a highly accurate AD blood biomarker.
- NfL
- Neurofilament light chain, a neurodegeneration marker sensitive to kidney function in this study.
- GFAP
- Glial fibrillary acidic protein measured in plasma as an astrocytic injury marker.
- TRIAD
- Translational Biomarkers in Aging and Dementia cohort.
Flashcards
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TRIAD sample size:
Common questions
Sample size?
242 TRIAD participants.
Did eGFR improve Aβ prediction?
No meaningful AIC/AUC gains after adding eGFR.
Which markers stayed linked after covariates?
Notably Aβ40, Aβ42, NfL, and GFAP in adjusted models.
Clinical takeaway?
Normal-to-mild renal impairment seems less critical for accurate markers like p-tau217.